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1. Homologous Recombination Deficiency (HRD) in Cutaneous Oncology.

Author

Akinjiyan, Favour, Morecroft, Renee, Phillipps, Jordan, Adeyelu, Tolulope, Elliott, Andrew, Park, Soo, Butt, Omar, Zhou, Alice, and Ansstas, George

Subjects
DNA repair, PARP inhibitors, genomic scars, homologous recombination deficiency, immunotherapy, melanoma, skin cancer, synthetic lethality, Humans, Female, Poly(ADP-ribose) Polymerase Inhibitors, BRCA1 Protein, Homologous Recombination, Carcinoma, Squamous Cell, BRCA2 Protein, Skin Neoplasms, Poly(ADP-ribose) Polymerases, Melanoma, Ovarian Neoplasms
Abstract

Skin cancers, including basal cell carcinoma (BCC), cutaneous squamous cell carcinoma (SCC), and melanoma, are the most common malignancies in the United States. Loss of DNA repair pathways in the skin plays a significant role in tumorigenesis. In recent years, targeting DNA repair pathways, particularly homologous recombination deficiency (HRD), has emerged as a potential therapeutic approach in cutaneous malignancies. This review provides an overview of DNA damage and repair pathways, with a focus on HRD, and discusses major advances in targeting these pathways in skin cancers. Poly(ADP-ribose) polymerase (PARP) inhibitors have been developed to exploit HRD in cancer cells. PARP inhibitors disrupt DNA repair mechanisms by inhibiting PARP enzymatic activity, leading to the accumulation of DNA damage and cell death. The concept of synthetic lethality has been demonstrated in HR-deficient cells, such as those with BRCA1/2 mutations, which exhibit increased sensitivity to PARP inhibitors. HRD assessment methods, including genomic scars, RAD51 foci formation, functional assays, and BRCA1/2 mutation analysis, are discussed as tools for identifying patients who may benefit from PARP inhibitor therapy. Furthermore, HRD has been implicated in the response to immunotherapy, and the combination of PARP inhibitors with immunotherapy has shown promising results. The frequency of HRD in melanoma ranges from 18% to 57%, and studies investigating the use of PARP inhibitors as monotherapy in melanoma are limited. Further research is warranted to explore the potential of PARP inhibition in melanoma treatment.

Published
2023

2. Mapping age- and sex-specific HIV prevalence in adults in sub-Saharan Africa, 2000–2018

Author

Haeuser, Emily, Serfes, Audrey L, Cork, Michael A, Yang, Mingyou, Abbastabar, Hedayat, Abhilash, ES, Adabi, Maryam, Adebayo, Oladimeji M, Adekanmbi, Victor, Adeyinka, Daniel Adedayo, Afzal, Saira, Ahinkorah, Bright Opoku, Ahmadi, Keivan, Ahmed, Muktar Beshir, Akalu, Yonas, Akinyemi, Rufus Olusola, Akunna, Chisom Joyqueenet, Alahdab, Fares, Alanezi, Fahad Mashhour, Alanzi, Turki M, Alene, Kefyalew Addis, Alhassan, Robert Kaba, Alipour, Vahid, Almasi-Hashiani, Amir, Alvis-Guzman, Nelson, Ameyaw, Edward Kwabena, Amini, Saeed, Amugsi, Dickson A, Ancuceanu, Robert, Anvari, Davood, Appiah, Seth Christopher Yaw, Arabloo, Jalal, Aremu, Olatunde, Asemahagn, Mulusew A, Jafarabadi, Mohammad Asghari, Awedew, Atalel Fentahun, Quintanilla, Beatriz Paulina Ayala, Ayanore, Martin Amogre, Aynalem, Yared Asmare, Azari, Samad, Azene, Zelalem Nigussie, Darshan, BB, Babalola, Tesleem Kayode, Baig, Atif Amin, Banach, Maciej, Bärnighausen, Till Winfried, Bell, Arielle Wilder, Bhagavathula, Akshaya Srikanth, Bhardwaj, Nikha, Bhardwaj, Pankaj, Bhattacharyya, Krittika, Bijani, Ali, Bitew, Zebenay Workneh, Bohlouli, Somayeh, Bolarinwa, Obasanjo Afolabi, Boloor, Archith, Bozicevic, Ivana, Butt, Zahid A, Cárdenas, Rosario, Carvalho, Felix, Charan, Jaykaran, Chattu, Vijay Kumar, Chowdhury, Mohiuddin Ahsanul Kabir, Chu, Dinh-Toi, Cowden, Richard G, Dahlawi, Saad MA, Damiani, Giovanni, Darteh, Eugene Kofuor Maafo, Darwesh, Aso Mohammad, das Neves, José, Weaver, Nicole Davis, De Leo, Diego, De Neve, Jan-Walter, Deribe, Kebede, Deuba, Keshab, Dharmaratne, Samath, Dianatinasab, Mostafa, Diaz, Daniel, Didarloo, Alireza, Djalalinia, Shirin, Dorostkar, Fariba, Dubljanin, Eleonora, Duko, Bereket, El Tantawi, Maha, El-Jaafary, Shaimaa I, Eshrati, Babak, Eskandarieh, Sharareh, Eyawo, Oghenowede, Ezeonwumelu, Ifeanyi Jude, Ezzikouri, Sayeh, Farzadfar, Farshad, Fattahi, Nazir, Fauk, Nelsensius Klau, Fernandes, Eduarda, Filip, Irina, Fischer, Florian, Foigt, Nataliya A, Foroutan, Masoud, Fukumoto, Takeshi, and Gad, Mohamed M

Subjects
Biomedical and Clinical Sciences, Public Health, Health Sciences, Clinical Sciences, HIV/AIDS, Infectious Diseases, Prevention, Pediatric, Clinical Research, 2.4 Surveillance and distribution, Aetiology, Infection, Good Health and Well Being, Male, Female, Adult, Humans, Pregnancy, Adolescent, Young Adult, Middle Aged, HIV, Acquired Immunodeficiency Syndrome, Prevalence, Seroepidemiologic Studies, HIV Infections, Africa South of the Sahara, Mapping, Africa, Geostatistics, Spatial statistics, HIV prevalence, Demographics, Local Burden of Disease sub-Saharan Africa HIV Prevalence Collaborators, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundHuman immunodeficiency virus and acquired immune deficiency syndrome (HIV/AIDS) is still among the leading causes of disease burden and mortality in sub-Saharan Africa (SSA), and the world is not on track to meet targets set for ending the epidemic by the Joint United Nations Programme on HIV/AIDS (UNAIDS) and the United Nations Sustainable Development Goals (SDGs). Precise HIV burden information is critical for effective geographic and epidemiological targeting of prevention and treatment interventions. Age- and sex-specific HIV prevalence estimates are widely available at the national level, and region-wide local estimates were recently published for adults overall. We add further dimensionality to previous analyses by estimating HIV prevalence at local scales, stratified into sex-specific 5-year age groups for adults ages 15-59 years across SSA.MethodsWe analyzed data from 91 seroprevalence surveys and sentinel surveillance among antenatal care clinic (ANC) attendees using model-based geostatistical methods to produce estimates of HIV prevalence across 43 countries in SSA, from years 2000 to 2018, at a 5 × 5-km resolution and presented among second administrative level (typically districts or counties) units.ResultsWe found substantial variation in HIV prevalence across localities, ages, and sexes that have been masked in earlier analyses. Within-country variation in prevalence in 2018 was a median 3.5 times greater across ages and sexes, compared to for all adults combined. We note large within-district prevalence differences between age groups: for men, 50% of districts displayed at least a 14-fold difference between age groups with the highest and lowest prevalence, and at least a 9-fold difference for women. Prevalence trends also varied over time; between 2000 and 2018, 70% of all districts saw a reduction in prevalence greater than five percentage points in at least one sex and age group. Meanwhile, over 30% of all districts saw at least a five percentage point prevalence increase in one or more sex and age group.ConclusionsAs the HIV epidemic persists and evolves in SSA, geographic and demographic shifts in prevention and treatment efforts are necessary. These estimates offer epidemiologically informative detail to better guide more targeted interventions, vital for combating HIV in SSA.

Published
2022

3. Global, regional, and national burden of stroke and its risk factors, 1990–2019: a systematic analysis for the Global Burden of Disease Study 2019

Author

Collaborators, GBD 2019 Stroke, Feigin, Valery L, Stark, Benjamin A, Johnson, Catherine Owens, Roth, Gregory A, Bisignano, Catherine, Abady, Gdiom Gebreheat, Abbasifard, Mitra, Abbasi-Kangevari, Mohsen, Abd-Allah, Foad, Abedi, Vida, Abualhasan, Ahmed, Abu-Rmeileh, Niveen ME, Abushouk, Abdelrahman I, Adebayo, Oladimeji M, Agarwal, Gina, Agasthi, Pradyumna, Ahinkorah, Bright Opoku, Ahmad, Sohail, Ahmadi, Sepideh, Salih, Yusra Ahmed, Aji, Budi, Akbarpour, Samaneh, Akinyemi, Rufus Olusola, Hamad, Hanadi Al, Alahdab, Fares, Alif, Mohammad, Alipour, Vahid, Aljunid, Syed Mohamed, Almustanyir, Sami, Al-Raddadi, Rajaa M, Salman, Rustam Al-Shahi, Alvis-Guzman, Nelson, Ancuceanu, Robert, Anderlini, Deanna, Anderson, Jason A, Ansar, Adnan, Antonazzo, Ippazio Cosimo, Arabloo, Jalal, Ärnlöv, Johan, Artanti, Kurnia Dwi, Aryan, Zahra, Asgari, Samaneh, Ashraf, Tahira, Athar, Mohammad, Atreya, Alok, Ausloos, Marcel, Baig, Atif Amin, Baltatu, Ovidiu Constantin, Banach, Maciej, Barboza, Miguel A, Barker-Collo, Suzanne Lyn, Bärnighausen, Till Winfried, Barone, Mark Thomaz Ugliara, Basu, Sanjay, Bazmandegan, Gholamreza, Beghi, Ettore, Beheshti, Mahya, Béjot, Yannick, Bell, Arielle Wilder, Bennett, Derrick A, Bensenor, Isabela M, Bezabhe, Woldesellassie Mequanint, Bezabih, Yihienew Mequanint, Bhagavathula, Akshaya Srikanth, Bhardwaj, Pankaj, Bhattacharyya, Krittika, Bijani, Ali, Bikbov, Boris, Birhanu, Mulugeta M, Boloor, Archith, Bonny, Aime, Brauer, Michael, Brenner, Hermann, Bryazka, Dana, Butt, Zahid A, dos Santos, Florentino Luciano Caetano, Campos-Nonato, Ismael R, Cantu-Brito, Carlos, Carrero, Juan J, Castañeda-Orjuela, Carlos A, Catapano, Alberico L, Chakraborty, Promit Ananyo, Charan, Jaykaran, Choudhari, Sonali Gajanan, Chowdhury, Enayet Karim, Chu, Dinh-Toi, Chung, Sheng-Chia, Colozza, David, Costa, Vera Marisa, Costanzo, Simona, Criqui, Michael H, Dadras, Omid, Dagnew, Baye, Dai, Xiaochen, Dalal, Koustuv, Damasceno, Albertino Antonio Moura, D'Amico, Emanuele, Dandona, Lalit, and Dandona, Rakhi

Subjects
Brain Disorders, Aging, Prevention, Stroke, Clinical Research, 2.4 Surveillance and distribution, Aetiology, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Body Mass Index, Cerebral Hemorrhage, Female, Global Burden of Disease, Humans, Incidence, Income, Ischemic Stroke, Male, Middle Aged, Prevalence, Quality-Adjusted Life Years, Risk Factors, Subarachnoid Hemorrhage, GBD 2019 Stroke Collaborators, Clinical Sciences, Neurosciences, Neurology & Neurosurgery
Abstract

BackgroundRegularly updated data on stroke and its pathological types, including data on their incidence, prevalence, mortality, disability, risk factors, and epidemiological trends, are important for evidence-based stroke care planning and resource allocation. The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) aims to provide a standardised and comprehensive measurement of these metrics at global, regional, and national levels.MethodsWe applied GBD 2019 analytical tools to calculate stroke incidence, prevalence, mortality, disability-adjusted life-years (DALYs), and the population attributable fraction (PAF) of DALYs (with corresponding 95% uncertainty intervals [UIs]) associated with 19 risk factors, for 204 countries and territories from 1990 to 2019. These estimates were provided for ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and all strokes combined, and stratified by sex, age group, and World Bank country income level.FindingsIn 2019, there were 12·2 million (95% UI 11·0-13·6) incident cases of stroke, 101 million (93·2-111) prevalent cases of stroke, 143 million (133-153) DALYs due to stroke, and 6·55 million (6·00-7·02) deaths from stroke. Globally, stroke remained the second-leading cause of death (11·6% [10·8-12·2] of total deaths) and the third-leading cause of death and disability combined (5·7% [5·1-6·2] of total DALYs) in 2019. From 1990 to 2019, the absolute number of incident strokes increased by 70·0% (67·0-73·0), prevalent strokes increased by 85·0% (83·0-88·0), deaths from stroke increased by 43·0% (31·0-55·0), and DALYs due to stroke increased by 32·0% (22·0-42·0). During the same period, age-standardised rates of stroke incidence decreased by 17·0% (15·0-18·0), mortality decreased by 36·0% (31·0-42·0), prevalence decreased by 6·0% (5·0-7·0), and DALYs decreased by 36·0% (31·0-42·0). However, among people younger than 70 years, prevalence rates increased by 22·0% (21·0-24·0) and incidence rates increased by 15·0% (12·0-18·0). In 2019, the age-standardised stroke-related mortality rate was 3·6 (3·5-3·8) times higher in the World Bank low-income group than in the World Bank high-income group, and the age-standardised stroke-related DALY rate was 3·7 (3·5-3·9) times higher in the low-income group than the high-income group. Ischaemic stroke constituted 62·4% of all incident strokes in 2019 (7·63 million [6·57-8·96]), while intracerebral haemorrhage constituted 27·9% (3·41 million [2·97-3·91]) and subarachnoid haemorrhage constituted 9·7% (1·18 million [1·01-1·39]). In 2019, the five leading risk factors for stroke were high systolic blood pressure (contributing to 79·6 million [67·7-90·8] DALYs or 55·5% [48·2-62·0] of total stroke DALYs), high body-mass index (34·9 million [22·3-48·6] DALYs or 24·3% [15·7-33·2]), high fasting plasma glucose (28·9 million [19·8-41·5] DALYs or 20·2% [13·8-29·1]), ambient particulate matter pollution (28·7 million [23·4-33·4] DALYs or 20·1% [16·6-23·0]), and smoking (25·3 million [22·6-28·2] DALYs or 17·6% [16·4-19·0]).InterpretationThe annual number of strokes and deaths due to stroke increased substantially from 1990 to 2019, despite substantial reductions in age-standardised rates, particularly among people older than 70 years. The highest age-standardised stroke-related mortality and DALY rates were in the World Bank low-income group. The fastest-growing risk factor for stroke between 1990 and 2019 was high body-mass index. Without urgent implementation of effective primary prevention strategies, the stroke burden will probably continue to grow across the world, particularly in low-income countries.FundingBill & Melinda Gates Foundation.

Published
2021

4. Trauma and nontrauma damage-control laparotomy: The difference is delirium (data from the Eastern Association for the Surgery of Trauma SLEEP-TIME multicenter trial).

Author

McArthur, Kaitlin, Krause, Cassandra, Kwon, Eugenia, Luo-Owen, Xian, Cochran-Yu, Meghan, Swentek, Lourdes, Burruss, Sigrid, Turay, David, Krasnoff, Chloe, Grigorian, Areg, Nahmias, Jeffry, Butt, Ahsan, Gutierrez, Adam, LaRiccia, Aimee, Kincaid, Michelle, Fiorentino, Michele N, Glass, Nina, Toscano, Samantha, Ley, Eric, Lombardo, Sarah R, Guillamondegui, Oscar D, Bardes, James M, DeLa'O, Connie, Wydo, Salina M, Leneweaver, Kyle, Duletzke, Nicholas T, Nunez, Jade, Moradian, Simon, Posluszny, Joseph, Naar, Leon, Kaafarani, Haytham, Kemmer, Heidi, Lieser, Mark J, Dorricott, Alexa, Chang, Grace, Nemeth, Zoltan, and Mukherjee, Kaushik

Subjects
Humans, Delirium, Abdominal Injuries, Postoperative Complications, Analgesics, Opioid, Length of Stay, Laparotomy, Injury Severity Score, Incidence, Linear Models, Risk Factors, Retrospective Studies, Sleep, Adult, Middle Aged, Intensive Care Units, United States, Female, Male, Young Adult, Physical Injury - Accidents and Adverse Effects, Traumatic Head and Spine Injury, Infectious Diseases, Clinical Research, Patient Safety, Clinical Trials and Supportive Activities, Trauma, damage-control laparotomy, sedation, delirium, nontrauma, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Nursing, Emergency & Critical Care Medicine
Abstract

BackgroundDamage-control laparotomy (DCL) has been used for traumatic and nontraumatic indications. We studied factors associated with delirium and outcome in this population.MethodsWe reviewed DCL patients at 15 centers for 2 years, including demographics, Charlson Comorbidity Index (CCI), diagnosis, operations, and outcomes. We compared 30-day mortality; renal failure requiring dialysis; number of takebacks; hospital, ventilator, and intensive care unit (ICU) days; and delirium-free and coma-free proportion of the first 30 ICU days (DF/CF-ICU-30) between trauma (T) and nontrauma (NT) patients. We performed linear regression for DF/CF-ICU-30, including age, sex, CCI, achievement of primary fascial closure (PFC), small and large bowel resection, bowel discontinuity, abdominal vascular procedures, and trauma as covariates. We performed one-way analysis of variance for DF/CF-ICU-30 against traumatic brain injury severity as measured by Abbreviated Injury Scale for the head.ResultsAmong 554 DCL patients (25.8% NT), NT patients were older (58.9 ± 15.8 vs. 39.7 ± 17.0 years, p < 0.001), more female (45.5% vs. 22.1%, p < 0.001), and had higher CCI (4.7 ± 3.3 vs. 1.1 ± 2.2, p < 0.001). The number of takebacks (1.7 ± 2.6 vs. 1.5 ± 1.2), time to first takeback (32.0 hours), duration of bowel discontinuity (47.0 hours), and time to PFC were similar (63.2 hours, achieved in 73.5%). Nontrauma and T patients had similar ventilator, ICU, and hospital days and mortality (31.0% NT, 29.8% T). Nontrauma patients had higher rates of renal failure requiring dialysis (36.6% vs. 14.1%, p < 0.001) and postoperative abdominal sepsis (40.1% vs. 17.1%, p < 0.001). Trauma and NT patients had similar number of hours of sedative (89.9 vs. 65.5 hours, p = 0.064) and opioid infusions (106.9 vs. 96.7 hours, p = 0.514), but T had lower DF/CF-ICU-30 (51.1% vs. 73.7%, p = 0.029), indicating more delirium. Linear regression analysis indicated that T was associated with a 32.1% decrease (95% CI, 14.6%-49.5%; p < 0.001) in DF/CF-ICU-30, while achieving PFC was associated with a 25.1% increase (95% CI, 10.2%-40.1%; p = 0.001) in DF/CFICU-30. Increasing Abbreviated Injury Scale for the head was associated with decreased DF/CF-ICU-30 by analysis of variance (p < 0.001).ConclusionNontrauma patients had higher incidence of postoperative abdominal sepsis and need for dialysis, while T was independently associated with increased delirium, perhaps because of traumatic brain injury.Level of evidenceTherapeutic study, level IV.

Published
2021

5. Statin exposure and risk of cancer in people with and without HIV infection.

Author

Bedimo, Roger J, Park, Lesley S, Shebl, Fatima M, Sigel, Keith, Rentsch, Christopher T, Crothers, Kristina, Rodriguez-Barradas, Maria C, Goetz, Matthew Bidwell, Butt, Adeel A, Brown, Sheldon T, Gibert, Cynthia, Justice, Amy C, and Tate, Janet P

Subjects
Clinical Research, HIV/AIDS, Prevention, Cancer, Infectious Diseases, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Aetiology, Infection, Good Health and Well Being, Cohort Studies, Female, HIV Infections, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Male, Neoplasms, Proportional Hazards Models, cancer, HIV, hypolipidemic agents, neoplasms, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Virology
Abstract

ObjectiveTo determine whether statin exposure is associated with decreased cancer and mortality risk among persons with HIV (PWH) and uninfected persons. Statins appear to have immunomodulatory and anti-inflammatory effects and may reduce cancer risk, particularly among PWH as they experience chronic inflammation and immune activation.DesignPropensity score-matched cohort of statin-exposed and unexposed patients from 2002 to 2017 in the Veterans Aging Cohort Study (VACS), a large cohort with cancer registry linkage and detailed pharmacy data.MethodsWe calculated Cox regression hazard ratios (HRs) and 95% confidence intervals (CI) associated with statin use for all cancers, microbial cancers (associated with bacterial or oncovirus coinfection), nonmicrobial cancers, and mortality.Results:The propensity score-matched sample (N = 47 940) included 23 970 statin initiators (31% PWH). Incident cancers were diagnosed in 1160 PWH and 2116 uninfected patients. Death was reported in 1667 (7.0%) statin-exposed, and 2215 (9.2%) unexposed patients. Statin use was associated with 24% decreased risk of microbial-associated cancers (hazard ratio 0.76; 95% CI 0.69-0.85), but was not associated with nonmicrobial cancer risk (hazard ratio 1.00; 95% CI 0.92-1.09). Statin use was associated with 33% lower risk of death overall (hazard ratio 0.67; 95% CI 0.63-0.72). Results were similar in analyses stratified by HIV status, except for non-Hodgkin lymphoma where statin use was associated with reduced risk (hazard ratio 0.56; 95% CI 0.38-0.83) for PWH, but not for uninfected (P interaction = 0.012).ConclusionIn both PWH and uninfected, statin exposure was associated with lower risk of microbial, but not nonmicrobial cancer incidence, and with decreased mortality.

Published
2021

6. Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in HIV: Veterans Aging Cohort Study

Author

Polanka, Brittanny M, Kundu, Suman, So-Armah, Kaku A, Freiberg, Matthew S, Gupta, Samir K, Zapolski, Tamika CB, Hirsh, Adam T, Bedimo, Roger J, Budoff, Matthew J, Butt, Adeel A, Chang, Chung-Chou H, Gottlieb, Stephen S, Marconi, Vincent C, Womack, Julie A, and Stewart, Jesse C

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Health Sciences, Heart Disease, Cardiovascular, Clinical Trials and Supportive Activities, Clinical Research, Aging, Mental Health, HIV/AIDS, Prevention, Good Health and Well Being, Biomarkers, Blood Coagulation, Cohort Studies, Female, Fibrin Fibrinogen Degradation Products, HIV Infections, Humans, Inflammation, Interleukin-6, Lipopolysaccharide Receptors, Male, Middle Aged, Monocytes, Sleep Initiation and Maintenance Disorders, Veterans, General Science & Technology
Abstract

BackgroundInsomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated.MethodsWe examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, "Difficulty falling or staying asleep?," with the following response options: "I do not have this symptom" or "I have this symptom and…" "it doesn't bother me," "it bothers me a little," "it bothers me," "it bothers me a lot." Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI).ResultsWe observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the "Bothers a Lot" group had, on average, 17% higher D-dimer than veterans in the "No Difficulty Falling or Staying Asleep" group in the demographic-adjusted model (exp[b] = 1.17, 95%CI = 1.01-1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI = 0.94-1.26, p = .27).ConclusionWe observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.

Published
2021

7. A Core Outcome Set for Pediatric Critical Care.

Author

Fink, Ericka L, Maddux, Aline B, Pinto, Neethi, Sorenson, Samuel, Notterman, Daniel, Dean, J Michael, Carcillo, Joseph A, Berg, Robert A, Zuppa, Athena, Pollack, Murray M, Meert, Kathleen L, Hall, Mark W, Sapru, Anil, McQuillen, Patrick S, Mourani, Peter M, Wessel, David, Amey, Deborah, Argent, Andrew, Brunow de Carvalho, Werther, Butt, Warwick, Choong, Karen, Curley, Martha AQ, Del Pilar Arias Lopez, Maria, Demirkol, Demet, Grosskreuz, Ruth, Houtrow, Amy J, Knoester, Hennie, Lee, Jan Hau, Long, Debbie, Manning, Joseph C, Morrow, Brenda, Sankar, Jhuma, Slomine, Beth S, Smith, McKenna, Olson, Lenora M, and Watson, R Scott

Subjects
Clinical Research, Behavioral and Social Science, Pediatric, Good Health and Well Being, Adult, Aged, Child, Child Health, Critical Care, Critical Illness, Delphi Technique, Female, Humans, Intensive Care Units, Pediatric, Male, Middle Aged, Stakeholder Participation, Treatment Outcome, Young Adult, child, critical care, family, outcome assessment, postintensive care syndrome, Pediatric Outcomes STudies after PICU (POST-PICU) Investigators of the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network and the Eunice Kennedy Shriver National Institute of Child Health and Human Development Collaborative Pediatric Critical Care Research Network, Clinical Sciences, Nursing, Public Health and Health Services, Emergency & Critical Care Medicine
Abstract

ObjectivesMore children are surviving critical illness but are at risk of residual or new health conditions. An evidence-informed and stakeholder-recommended core outcome set is lacking for pediatric critical care outcomes. Our objective was to create a multinational, multistakeholder-recommended pediatric critical care core outcome set for inclusion in clinical and research programs.DesignA two-round modified Delphi electronic survey was conducted with 333 invited research, clinical, and family/advocate stakeholders. Stakeholders completing the first round were invited to participate in the second. Outcomes scoring greater than 69% "critical" and less than 15% "not important" advanced to round 2 with write-in outcomes considered. The Steering Committee held a virtual consensus conference to determine the final components.SettingMultinational survey.PatientsStakeholder participants from six continents representing clinicians, researchers, and family/advocates.Measurements and main resultsOverall response rates were 75% and 82% for each round. Participants voted on seven Global Domains and 45 Specific Outcomes in round 1, and six Global Domains and 30 Specific Outcomes in round 2. Using overall (three stakeholder groups combined) results, consensus was defined as outcomes scoring greater than 90% "critical" and less than 15% "not important" and were included in the final PICU core outcome set: four Global Domains (Cognitive, Emotional, Physical, and Overall Health) and four Specific Outcomes (Child Health-Related Quality of Life, Pain, Survival, and Communication). Families (n = 21) suggested additional critically important outcomes that did not meet consensus, which were included in the PICU core outcome set-extended.ConclusionsThe PICU core outcome set and PICU core outcome set-extended are multistakeholder-recommended resources for clinical and research programs that seek to improve outcomes for children with critical illness and their families.

Published
2020

8. Community-Acquired Pneumonia and Risk of Cardiovascular Events in People Living With HIV.

Author

Zifodya, Jerry S, Duncan, Meredith S, So-Armah, Kaku A, Attia, Engi F, Akgün, Kathleen M, Rodriguez-Barradas, Maria C, Marconi, Vincent C, Budoff, Matthew J, Bedimo, Roger J, Alcorn, Charles W, Soo Hoo, Guy W, Butt, Adeel A, Kim, Joon W, Sico, Jason J, Tindle, Hilary A, Huang, Laurence, Tate, Janet P, Justice, Amy C, Freiberg, Matthew S, and Crothers, Kristina

Subjects
Humans, Community-Acquired Infections, HIV Infections, Pneumonia, Cardiovascular Diseases, Hospitalization, Incidence, Survival Rate, Cohort Studies, Adult, Aged, Middle Aged, Veterans, United States, Female, Male, AIDS, HIV, cardiovascular disease, community‐acquired pneumonia, community&#8208, acquired pneumonia, Cardiorespiratory Medicine and Haematology
Abstract

Background Hospitalization with community-acquired pneumonia (CAP) is associated with an increased risk of cardiovascular disease (CVD) events in patients uninfected with HIV. We evaluated whether people living with HIV (PLWH) have a higher risk of CVD or mortality than individuals uninfected with HIV following hospitalization with CAP. Methods and Results We analyzed data from the Veterans Aging Cohort Study on US veterans admitted with their first episode of CAP from April 2003 through December 2014. We used Cox regression analyses to determine whether HIV status was associated with incident CVD events and mortality from date of admission through 30 days after discharge (30-day mortality), adjusting for known CVD risk factors. We included 4384 patients (67% [n=2951] PLWH). PLWH admitted with CAP were younger, had less severe CAP, and had fewer CVD risk factors than patients with CAP who were uninfected with HIV. In multivariable-adjusted analyses, CVD risk was similar in PLWH compared with HIV-uninfected (hazard ratio [HR], 0.89; 95% CI, 0.70-1.12), but HIV infection was associated with higher mortality risk (HR, 1.49; 95% CI, 1.16-1.90). In models stratified by HIV status, CAP severity was significantly associated with incident CVD and 30-day mortality in PLWH and patients uninfected with HIV. Conclusions In this study, the risk of CVD events during or after hospitalization for CAP was similar in PLWH and patients uninfected with HIV, after adjusting for known CVD risk factors and CAP severity. HIV infection, however, was associated with increased 30-day mortality after CAP hospitalization in multivariable-adjusted models. PLWH should be included in future studies evaluating mechanisms and prevention of CVD events after CAP.

Published
2020

9. FIB-4 stage of liver fibrosis is associated with incident heart failure with preserved, but not reduced, ejection fraction among people with and without HIV or hepatitis C.

Author

So-Armah, Kaku A, Lim, Joseph K, Lo Re, Vincent, Tate, Janet P, Chang, Chung-Chou H, Butt, Adeel A, Gibert, Cynthia L, Rimland, David, Marconi, Vincent C, Goetz, Matthew Bidwell, Ramachandran, Vasan, Brittain, Evan, Long, Michelle, Nguyen, Kim-Lien, Rodriguez-Barradas, Maria C, Budoff, Matthew J, Tindle, Hilary A, Samet, Jeffrey H, Justice, Amy C, Freiberg, Matthew S, and VACS Project Team

Subjects
VACS Project Team, Humans, Hepatitis C, HIV Infections, Liver Cirrhosis, Anti-HIV Agents, Stroke Volume, Prognosis, Viral Load, Severity of Illness Index, Incidence, Risk Assessment, Risk Factors, Health Status, Ventricular Function, Left, Time Factors, Adult, Middle Aged, HIV Long-Term Survivors, United States, Female, Male, Heart Failure, Veterans Health, Cohort, Ejection fraction, HIV, Heart failure, Hepatitis, Liver fibrosis, Clinical Research, Heart Disease, Chronic Liver Disease and Cirrhosis, Liver Disease, Cardiovascular, Digestive Diseases, Cardiovascular System & Hematology, Cardiorespiratory Medicine and Haematology
Abstract

BackgroundLiver fibrosis, is independently associated with incident heart failure (HF). Investigating the association between liver fibrosis and type of HF, specifically HF with reduced ejection fraction (EF; HFrEF) or HF with preserved ejection fraction (HFpEF), may provide mechanistic insight into this association. We sought to determine the association between liver fibrosis score (FIB-4) and type of HF, and to assess whether HIV or hepatitis C status modified this association.MethodsWe included patients alive on or after 4/1/2003 from the Veterans Aging Cohort Study. We followed patients without prevalent cardiovascular disease until their first HF event, death, last clinic visit, or 9/30/2015. We defined liver fibrosis as: likely advanced fibrosis (FIB-4 > 3.25), indeterminate (FIB-4 range 1.45-3.25), unlikely advanced fibrosis (FIB-4

Published
2020

10. Mapping disparities in education across low- and middle-income countries

Author

Graetz, Nicholas, Woyczynski, Lauren, Wilson, Katherine F, Hall, Jason B, Abate, Kalkidan Hassen, Abd-Allah, Foad, Adebayo, Oladimeji M, Adekanmbi, Victor, Afshari, Mahdi, Ajumobi, Olufemi, Akinyemiju, Tomi, Alahdab, Fares, Al-Aly, Ziyad, Alcalde Rabanal, Jacqueline Elizabeth, Alijanzadeh, Mehran, Alipour, Vahid, Altirkawi, Khalid, Amiresmaili, Mohammadreza, Anber, Nahla Hamed, Andrei, Catalina Liliana, Anjomshoa, Mina, Antonio, Carl Abelardo T, Arabloo, Jalal, Aremu, Olatunde, Aryal, Krishna K, Asadi-Aliabadi, Mehran, Atique, Suleman, Ausloos, Marcel, Awasthi, Ashish, Ayala Quintanilla, Beatriz Paulina, Azari, Samad, Badawi, Alaa, Banoub, Joseph Adel Mattar, Barker-Collo, Suzanne Lyn, Barnett, Anthony, Bedi, Neeraj, Bennett, Derrick A, Bhattacharjee, Natalia V, Bhattacharyya, Krittika, Bhattarai, Suraj, Bhutta, Zulfiqar A, Bijani, Ali, Bikbov, Boris, Britton, Gabrielle, Burstein, Roy, Butt, Zahid A, Cardenas, Rosario, Carvalho, Felix, Castaneda-Orjuela, Carlos A, Castro, Franz, Cerin, Ester, Chang, Jung-Chen, Collison, Michael L, Cooper, Cyrus, Cork, Michael A, Daoud, Farah, Das Gupta, Rajat, Weaver, Nicole Davis, De Neve, Jan-Walter, Deribe, Kebede, Desalegn, Beruk Berhanu, Deshpande, Aniruddha, Desta, Melaku, Dhimal, Meghnath, Diaz, Daniel, Dinberu, Mesfin Tadese, Djalalinia, Shirin, Dubey, Manisha, Dubljanin, Eleonora, Duraes, Andre R, Dwyer-Lindgren, Laura, Earl, Lucas, Kalan, Mohammad Ebrahimi, El-Khatib, Ziad, Eshrati, Babak, Faramarzi, Mahbobeh, Fareed, Mohammad, Faro, Andre, Fereshtehnejad, Seyed-Mohammad, Fernandes, Eduarda, Filip, Irina, Fischer, Florian, Fukumoto, Takeshi, Garcia, Jose A, Gill, Paramjit Singh, Gill, Tiffany K, Gona, Philimon N, Gopalani, Sameer Vali, Grada, Ayman, Guo, Yuming, Gupta, Rajeev, Gupta, Vipin, Haj-Mirzaian, Arvin, Haj-Mirzaian, Arya, Hamadeh, Randah R, Hamidi, Samer, Hasan, Mehedi, Hassen, Hamid Yimam, Hendrie, Delia, and Henok, Andualem

Subjects
Pediatric, Aetiology, 2.3 Psychological, social and economic factors, Good Health and Well Being, Bayes Theorem, Developing Countries, Education, Female, Health Status, Humans, Male, Socioeconomic Factors, Local Burden of Disease Educational Attainment Collaborators, General Science & Technology
Abstract

Educational attainment is an important social determinant of maternal, newborn, and child health1-3. As a tool for promoting gender equity, it has gained increasing traction in popular media, international aid strategies, and global agenda-setting4-6. The global health agenda is increasingly focused on evidence of precision public health, which illustrates the subnational distribution of disease and illness7,8; however, an agenda focused on future equity must integrate comparable evidence on the distribution of social determinants of health9-11. Here we expand on the available precision SDG evidence by estimating the subnational distribution of educational attainment, including the proportions of individuals who have completed key levels of schooling, across all low- and middle-income countries from 2000 to 2017. Previous analyses have focused on geographical disparities in average attainment across Africa or for specific countries, but-to our knowledge-no analysis has examined the subnational proportions of individuals who completed specific levels of education across all low- and middle-income countries12-14. By geolocating subnational data for more than 184 million person-years across 528 data sources, we precisely identify inequalities across geography as well as within populations.

Published
2020

11. Comparison of the prevalence, severity, and risk factors for hepatic steatosis in HIV-infected and uninfected people

Author

Torgersen, Jessie, So-Armah, Kaku, Freiberg, Matthew S, Goetz, Matthew B, Budoff, Matthew J, Lim, Joseph K, Taddei, Tamar, Butt, Adeel A, Rodriguez-Barradas, Maria C, Justice, Amy C, Kostman, Jay R, and Lo Re, Vincent

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Liver Disease, Clinical Research, HIV/AIDS, Infectious Diseases, Digestive Diseases, Cardiovascular, Chronic Liver Disease and Cirrhosis, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Comorbidity, Cross-Sectional Studies, Fatty Liver, Female, HIV Infections, Humans, Male, Middle Aged, Prevalence, Prospective Studies, Risk Factors, Severity of Illness Index, Tomography, X-Ray Computed, United States, Hepatic steatosis, HIV, Liver fibrosis, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Abstract

BackgroundHepatic steatosis is prevalent in Western countries, but few studies have evaluated whether the frequency and severity of steatosis are greater in the setting of HIV infection. We compared the prevalence and severity of hepatic steatosis between HIV-infected (HIV+) and uninfected persons and identified factors associated with greater steatosis severity within both groups.MethodsWe performed a cross-sectional study among participants without cardiovascular disease who participated in a substudy of the Veterans Aging Cohort Study. Hepatic steatosis was defined by noncontrast computed tomography (CT) liver-to-spleen (L/S) attenuation ratio

Published
2019

12. Global, regional, and national burden of neurological disorders, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

Author

Collaborators, GBD 2016 Neurology, Feigin, Valery L, Nichols, Emma, Alam, Tahiya, Bannick, Marlena S, Beghi, Ettore, Blake, Natacha, Culpepper, William J, Dorsey, E Ray, Elbaz, Alexis, Ellenbogen, Richard G, Fisher, James L, Fitzmaurice, Christina, Giussani, Giorgia, Glennie, Linda, James, Spencer L, Johnson, Catherine Owens, Kassebaum, Nicholas J, Logroscino, Giancarlo, Marin, Benoît, Mountjoy-Venning, W Cliff, Nguyen, Minh, Ofori-Asenso, Richard, Patel, Anoop P, Piccininni, Marco, Roth, Gregory A, Steiner, Timothy J, Stovner, Lars Jacob, Szoeke, Cassandra EI, Theadom, Alice, Vollset, Stein Emil, Wallin, Mitchell Taylor, Wright, Claire, Zunt, Joseph Raymond, Abbasi, Nooshin, Abd-Allah, Foad, Abdelalim, Ahmed, Abdollahpour, Ibrahim, Aboyans, Victor, Abraha, Haftom Niguse, Acharya, Dilaram, Adamu, Abdu A, Adebayo, Oladimeji M, Adeoye, Abiodun Moshood, Adsuar, Jose C, Afarideh, Mohsen, Agrawal, Sutapa, Ahmadi, Alireza, Ahmed, Muktar Beshir, Aichour, Amani Nidhal, Aichour, Ibtihel, Aichour, Miloud Taki Eddine, Akinyemi, Rufus Olusola, Akseer, Nadia, Al-Eyadhy, Ayman, Salman, Rustam Al-Shahi, Alahdab, Fares, Alene, Kefyalew Addis, Aljunid, Syed Mohamed, Altirkawi, Khalid, Alvis-Guzman, Nelson, Anber, Nahla Hamed, Antonio, Carl Abelardo T, Arabloo, Jalal, Aremu, Olatunde, Ärnlöv, Johan, Asayesh, Hamid, Asghar, Rana Jawad, Atalay, Hagos Tasew, Awasthi, Ashish, Quintanilla, Beatriz Paulina Ayala, Ayuk, Tambe B, Badawi, Alaa, Banach, Maciej, Banoub, Joseph Adel Mattar, Barboza, Miguel A, Barker-Collo, Suzanne Lyn, Bärnighausen, Till Winfried, Baune, Bernhard T, Bedi, Neeraj, Behzadifar, Masoud, Behzadifar, Meysam, Béjot, Yannick, Bekele, Bayu Begashaw, Belachew, Abate Bekele, Bennett, Derrick A, Bensenor, Isabela M, Berhane, Adugnaw, Beuran, Mircea, Bhattacharyya, Krittika, Bhutta, Zulfiqar A, Biadgo, Belete, Bijani, Ali, Bililign, Nigus, Bin Sayeed, Muhammad Shahdaat, Blazes, Christopher Kynrint, Brayne, Carol, Butt, Zahid A, Campos-Nonato, Ismael R, and Cantu-Brito, Carlos

Subjects
Neurosciences, Headaches, Pain Research, Aging, Brain Disorders, Prevention, Neurodegenerative, Aetiology, 2.1 Biological and endogenous factors, Neurological, Good Health and Well Being, Adult, Age Factors, Aged, Aged, 80 and over, Cause of Death, Dementia, Disability Evaluation, Female, Global Burden of Disease, Humans, Incidence, Male, Middle Aged, Nervous System Diseases, Prevalence, Quality-Adjusted Life Years, Risk Factors, Sex Factors, Socioeconomic Factors, GBD 2016 Neurology Collaborators, Clinical Sciences, Neurology & Neurosurgery
Abstract

BackgroundNeurological disorders are increasingly recognised as major causes of death and disability worldwide. The aim of this analysis from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2016 is to provide the most comprehensive and up-to-date estimates of the global, regional, and national burden from neurological disorders.MethodsWe estimated prevalence, incidence, deaths, and disability-adjusted life-years (DALYs; the sum of years of life lost [YLLs] and years lived with disability [YLDs]) by age and sex for 15 neurological disorder categories (tetanus, meningitis, encephalitis, stroke, brain and other CNS cancers, traumatic brain injury, spinal cord injury, Alzheimer's disease and other dementias, Parkinson's disease, multiple sclerosis, motor neuron diseases, idiopathic epilepsy, migraine, tension-type headache, and a residual category for other less common neurological disorders) in 195 countries from 1990 to 2016. DisMod-MR 2.1, a Bayesian meta-regression tool, was the main method of estimation of prevalence and incidence, and the Cause of Death Ensemble model (CODEm) was used for mortality estimation. We quantified the contribution of 84 risks and combinations of risk to the disease estimates for the 15 neurological disorder categories using the GBD comparative risk assessment approach.FindingsGlobally, in 2016, neurological disorders were the leading cause of DALYs (276 million [95% UI 247-308]) and second leading cause of deaths (9·0 million [8·8-9·4]). The absolute number of deaths and DALYs from all neurological disorders combined increased (deaths by 39% [34-44] and DALYs by 15% [9-21]) whereas their age-standardised rates decreased (deaths by 28% [26-30] and DALYs by 27% [24-31]) between 1990 and 2016. The only neurological disorders that had a decrease in rates and absolute numbers of deaths and DALYs were tetanus, meningitis, and encephalitis. The four largest contributors of neurological DALYs were stroke (42·2% [38·6-46·1]), migraine (16·3% [11·7-20·8]), Alzheimer's and other dementias (10·4% [9·0-12·1]), and meningitis (7·9% [6·6-10·4]). For the combined neurological disorders, age-standardised DALY rates were significantly higher in males than in females (male-to-female ratio 1·12 [1·05-1·20]), but migraine, multiple sclerosis, and tension-type headache were more common and caused more burden in females, with male-to-female ratios of less than 0·7. The 84 risks quantified in GBD explain less than 10% of neurological disorder DALY burdens, except stroke, for which 88·8% (86·5-90·9) of DALYs are attributable to risk factors, and to a lesser extent Alzheimer's disease and other dementias (22·3% [11·8-35·1] of DALYs are risk attributable) and idiopathic epilepsy (14·1% [10·8-17·5] of DALYs are risk attributable).InterpretationGlobally, the burden of neurological disorders, as measured by the absolute number of DALYs, continues to increase. As populations are growing and ageing, and the prevalence of major disabling neurological disorders steeply increases with age, governments will face increasing demand for treatment, rehabilitation, and support services for neurological disorders. The scarcity of established modifiable risks for most of the neurological burden demonstrates that new knowledge is required to develop effective prevention and treatment strategies.FundingBill & Melinda Gates Foundation.

Published
2019

13. Depression and all‐cause mortality risk in HIV‐infected and HIV‐uninfected US veterans: a cohort study

Author

So‐Armah, K, Gupta, SK, Kundu, S, Stewart, JC, Goulet, JL, Butt, AA, Sico, JJ, Marconi, Crystal, S, Rodriguez‐Barradas, MC, Budoff, M, Gibert, CL, Chang, C‐CH, Bedimo, R, and Freiberg

Subjects
Biomedical and Clinical Sciences, Epidemiology, Public Health, Clinical Sciences, Health Sciences, Medical Microbiology, Brain Disorders, Prevention, HIV/AIDS, Depression, Mental Health, Clinical Research, Infectious Diseases, Behavioral and Social Science, Aetiology, 2.4 Surveillance and distribution, Infection, Good Health and Well Being, Adult, Case-Control Studies, Depressive Disorder, Major, Female, HIV Infections, Humans, Longitudinal Studies, Male, Middle Aged, Mortality, Prospective Studies, United States, Veterans, depression, HIV, mortality, Virology, Clinical sciences
Abstract

ObjectivesThe contribution of depression to mortality in adults with and without HIV infection is unclear. We hypothesized that depression increases mortality risk and that this association is stronger among those with HIV infection.MethodsVeterans Aging Cohort Study (VACS) data were analysed from the first clinic visit on or after 1 April 2003 (baseline) to 30 September 2015. Depression definitions were: (1) major depressive disorder defined using International Classification of Diseases, Ninth Revision (ICD-9) codes; (2) depressive symptoms defined as Patient Health Questionnaire (PHQ)-9 scores ≥ 10. The outcome was all-cause mortality. Covariates were demographics, comorbid conditions and health behaviours.ResultsAmong 129 140 eligible participants, 30% had HIV infection, 16% had a major depressive disorder diagnosis, and 24% died over a median follow-up time of 11 years. The death rate was 25.3 [95% confidence interval (CI) 25.0-25.6] deaths per 1000 person-years. Major depressive disorder was associated with mortality [hazard ratio (HR) 1.04; 95% CI 1.01, 1.07]. This association was modified by HIV status (interaction P-value = 0.02). In HIV-stratified analyses, depression was significantly associated with mortality among HIV-uninfected veterans but not among those with HIV infection. Among those with PHQ-9 data (n = 7372), 50% had HIV infection, 22% had PHQ-9 scores ≥ 10, and 28% died over a median follow-up time of 12 years. The death rate was 27.3 (95% CI 26.1-28.5) per 1000 person-years. Depressive symptoms were associated with mortality (HR 1.16; 95% CI 1.04, 1.28). This association was modified by HIV status (interaction P-value = 0.05). In HIV-stratified analyses, depressive symptoms were significantly associated with mortality among veterans with HIV infection but not among those without HIV infection.ConclusionsDepression was associated with all-cause mortality. This association was modified by HIV status and method of depression ascertainment.

Published
2019

14. Paediatric acute respiratory distress syndrome incidence and epidemiology (PARDIE): an international, observational study

Author

Khemani, Robinder G, Smith, Lincoln, Lopez-Fernandez, Yolanda M, Kwok, Jeni, Morzov, Rica, Klein, Margaret J, Yehya, Nadir, Willson, Douglas, Kneyber, Martin CJ, Lillie, Jon, Fernandez, Analia, Newth, Christopher JL, Jouvet, Philippe, Thomas, Neal J, Investigators, Pediatric Acute Respiratory Distress syndrome Incidence and Epidemiology, Abaleke, Eugenia, Ackerman, Kate G, Acuña, Carlos, Adu-Darko, Michelle, Affolter, Jeremy T, Agbeko, Rachel, Amoudi, Ahmed Al, Alahmadti, Ahmad, Aldairi, Nedaa, Alibrahim, Omar, Allen, Kiona, Allen, Christine, Al-Subu, Awni, Althabe, María, Alvear, Jimena, Anil, Ayse Berna, Anthony, Heather, Aramburo, Angela, Villanueva, David Arjona, Ashtari, Neda, Vera, Antonio Ávila, Baines, Paul, Bales, Melissa, Barr, Samantha, Barry, Dana, Baudin, Florent, Beca, John, Belfield, Holly, Beltramo, Fernando, Benken, Laura, Bhalla, Anoopindar, Blom, Andrea, Botta, Priscila, Bourgoin, Pierre, Brezmes, Marta, Briassoulis, George, Bridier, Armelle, Brierley, Joe, Sanagustin, Sonia Brio, Broden, Elizabeth, Butt, Warwick, Bysani, Kris, Camilo, Cristina, Camporesi, Anna, Campos-Miño, Santiago, Can, Fulya Kamit, Capocasa, Patricia, Caro, Daniel, Carroll, Christopher, Castellani, Pablo, Castillo, Andres E, Chen, Yang, Chima, Ranjit S, Chiusolo, Fabrizio, Cinquegrani, Karina, Coates, Bria, Coronado-Munoz, Alvaro, Cortéz, Ambar, Romero, Pablo Cruces, Cullimore, Melissa, Cvijanovich, Natalie, Dahmer, Mary K, Deep, Akash, Delzoppo, Carmel, Di Nardo, Matteo, Díaz, Franco, Dijkstra, Sandra, Dockery, W Keith, Dominguez, Troy E, Dumitrascu, Mariana, Dursun, Oguz, Dwarakanathan, Buvana, Elghuwael, Ismail, Emeriaud, Guillaume, Erickson, Simon, Español, Segundo Fernando, Estil, Jim Brian, Feather, Calandra, Feinstein, Yael, Fernández, Analía, Ferreyra, Marcela, Flori, Heidi, Fortini, Yanina Vanesa, Fortune, Peter-Marc, and French, Mary Ellen

Subjects
Biomedical and Clinical Sciences, Cardiovascular Medicine and Haematology, Clinical Sciences, Pediatric, Lung, Clinical Research, 4.1 Discovery and preclinical testing of markers and technologies, Detection, screening and diagnosis, Respiratory, Good Health and Well Being, Acute Lung Injury, Age Factors, Area Under Curve, Cause of Death, Child, Child, Preschool, Combined Modality Therapy, Cross-Sectional Studies, Female, Hospital Mortality, Humans, Intensive Care Units, Pediatric, Internationality, Kaplan-Meier Estimate, Male, Prognosis, Prospective Studies, Respiratory Distress Syndrome, Severity of Illness Index, Sex Factors, Survival Analysis, United States, Pediatric Acute Respiratory Distress syndrome Incidence and Epidemiology (PARDIE) Investigators, Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network, Public Health and Health Services, Other Medical and Health Sciences, Cardiovascular medicine and haematology, Clinical sciences
Abstract

BackgroundPaediatric acute respiratory distress syndrome (PARDS) is associated with high mortality in children, but until recently no paediatric-specific diagnostic criteria existed. The Pediatric Acute Lung Injury Consensus Conference (PALICC) definition was developed to overcome limitations of the Berlin definition, which was designed and validated for adults. We aimed to determine the incidence and outcomes of children who meet the PALICC definition of PARDS.MethodsIn this international, prospective, cross-sectional, observational study, 145 paediatric intensive care units (PICUs) from 27 countries were recruited, and over a continuous 5 day period across 10 weeks all patients were screened for enrolment. Patients were included if they had a new diagnosis of PARDS that met PALICC criteria during the study week. Exclusion criteria included meeting PARDS criteria more than 24 h before screening, cyanotic heart disease, active perinatal lung disease, and preparation or recovery from a cardiac intervention. Data were collected on the PICU characteristics, patient demographics, and elements of PARDS (ie, PARDS risk factors, hypoxaemia severity metrics, type of ventilation), comorbidities, chest imaging, arterial blood gas measurements, and pulse oximetry. The primary outcome was PICU mortality. Secondary outcomes included 90 day mortality, duration of invasive mechanical and non-invasive ventilation, and cause of death.FindingsBetween May 9, 2016, and June 16, 2017, during the 10 study weeks, 23 280 patients were admitted to participating PICUs, of whom 744 (3·2%) were identified as having PARDS. 95% (708 of 744) of patients had complete data for analysis, with 17% (121 of 708; 95% CI 14-20) mortality, whereas only 32% (230 of 708) of patients met Berlin criteria with 27% (61 of 230) mortality. Based on hypoxaemia severity at PARDS diagnosis, mortality was similar among those who were non-invasively ventilated and with mild or moderate PARDS (10-15%), but higher for those with severe PARDS (33% [54 of 165; 95% CI 26-41]). 50% (80 of 160) of non-invasively ventilated patients with PARDS were subsequently intubated, with 25% (20 of 80; 95% CI 16-36) mortality. By use of PALICC PARDS definition, severity of PARDS at 6 h after initial diagnosis (area under the curve [AUC] 0·69, 95% CI 0·62-0·76) discriminates PICU mortality better than severity at PARDS diagnosis (AUC 0·64, 0·58-0·71), and outperforms Berlin severity groups at 6 h (0·64, 0·58-0·70; p=0·01).InterpretationThe PALICC definition identified more children as having PARDS than the Berlin definition, and PALICC PARDS severity groupings improved the stratification of mortality risk, particularly when applied 6 h after PARDS diagnosis. The PALICC PARDS framework should be considered for use in future epidemiological and therapeutic research among children with PARDS.FundingUniversity of Southern California Clinical Translational Science Institute, Sainte Justine Children's Hospital, University of Montreal, Canada, Réseau en Santé Respiratoire du Fonds de Recherche Quebec-Santé, and Children's Hospital Los Angeles, Department of Anesthesiology and Critical Care Medicine.

Published
2019

15. Medical Intensive Care Unit Admission Among Patients With and Without HIV, Hepatitis C Virus, and Alcohol-Related Diagnoses in the United States

Author

Rentsch, Christopher T, Tate, Janet P, Steel, Tessa, Butt, Adeel A, Gibert, Cynthia L, Huang, Laurence, Pisani, Margaret, Soo Hoo, Guy W, Crystal, Stephen, Rodriguez-Barradas, Maria C, Brown, Sheldon T, Freiberg, Matthew S, Graber, Christopher J, Kim, Joon W, Rimland, David, Justice, Amy C, Fiellin, David A, Crothers, Kristina A, and Akgün, Kathleen M

Subjects
Liver Disease, Hepatitis - C, Hepatitis, Chronic Liver Disease and Cirrhosis, HIV/AIDS, Infectious Diseases, Substance Misuse, Digestive Diseases, Clinical Research, Alcoholism, Alcohol Use and Health, Emerging Infectious Diseases, Aetiology, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, Adult, Alcohol Drinking, Alcohol-Related Disorders, Coinfection, Female, HIV Infections, Hepatitis C, Humans, Intensive Care Units, Male, Middle Aged, Patient Admission, Retrospective Studies, Risk Factors, United States, intensive care units, HIV, hepatitis C, alcoholism, electronic health records, veterans, Clinical Sciences, Public Health and Health Services, Virology
Abstract

BackgroundHIV, hepatitis C virus (HCV), and alcohol-related diagnoses (ARD) independently contribute increased risk of all-cause hospitalization. We sought to determine annual medical intensive care unit (MICU) admission rates and relative risk of MICU admission between 1997 and 2014 among people with and without HIV, HCV, and ARD, using data from the largest HIV and HCV care provider in the United States.SettingVeterans Health Administration.MethodsAnnual MICU admission rates were calculated among 155,550 patients in the Veterans Aging Cohort Study by HIV, HCV, and ARD status. Adjusted rate ratios and 95% confidence intervals (CIs) were estimated with Poisson regression. Significance of trends in age-adjusted admission rates were tested with generalized linear regression. Models were stratified by calendar period to identify shifts in MICU admission risk over time.ResultsCompared to HIV-/HCV-/ARD- patients, relative risk of MICU admission decreased among HIV-mono-infected patients from 61% (95% CI: 1.56 to 1.65) in 1997-2009% to 21% (95% CI: 1.16 to 1.27) in 2010-2014, increased among HCV-mono-infected patients from 22% (95% CI: 1.16 to 1.29) in 1997-2009% to 54% (95% CI: 1.43 to 1.67) in 2010-2014, and remained consistent among patients with ARD only at 46% (95% CI: 1.42 to 1.50). MICU admission rates decreased by 48% among HCV-uninfected patients (P-trend

Published
2019

16. FREQUENCY OF 25-HYDROXY VITAMIN D DEFICIENCY IN PATIENTS WITH MULTIPLE SCLEROSIS

Author

Mehwish Arif Butt, Asma Arman, and Tahir Ansari

Subjects
multiple sclerosis, vitamin d, risk, vitamin d deficiency, educational status, socioeconomic factors, female, male, Medicine
Abstract

OBJECTIVE: To determine the frequency of 25-hydroxy vitamin-D deficiency in Patients with multiple sclerosis (MS). METHODS: This cross-sectional study was conducted at Civil Hospital Karachi, Pakistan from January to December 2019. One hundred and sixty five diagnosed cases of MS of either gender, aging 20-55 years, not taking vitamin-D supplements, steroids and could go outside in the sun were selected through non-probability consecutive sampling technique. Patients having history of rickets, parathyroid disease, chronic liver or renal diseases were excluded. Blood sample was taken to measure 25-hydroxyl vitamin D3 levels. A level of

Published
2022
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17. Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016

Author

Griswold, Max G, Fullman, Nancy, Hawley, Caitlin, Arian, Nicholas, Zimsen, Stephanie RM, Tymeson, Hayley D, Venkateswaran, Vidhya, Tapp, Austin Douglas, Forouzanfar, Mohammad H, Salama, Joseph S, Abate, Kalkidan Hassen, Abate, Degu, Abay, Solomon M, Abbafati, Cristiana, Abdulkader, Rizwan Suliankatchi, Abebe, Zegeye, Aboyans, Victor, Abrar, Mohammed Mehdi, Acharya, Pawan, Adetokunboh, Olatunji O, Adhikari, Tara Ballav, Adsuar, Jose C, Afarideh, Mohsen, Agardh, Emilie Elisabet, Agarwal, Gina, Aghayan, Sargis Aghasi, Agrawal, Sutapa, Ahmed, Muktar Beshir, Akibu, Mohammed, Akinyemiju, Tomi, Akseer, Nadia, Asfoor, Deena H Al, Al-Aly, Ziyad, Alahdab, Fares, Alam, Khurshid, Albujeer, Ammar, Alene, Kefyalew Addis, Ali, Raghib, Ali, Syed Danish, Alijanzadeh, Mehran, Aljunid, Syed Mohamed, Alkerwi, Ala'a, Allebeck, Peter, Alvis-Guzman, Nelson, Amare, Azmeraw T, Aminde, Leopold N, Ammar, Walid, Amoako, Yaw Ampem, Amul, Gianna Gayle Herrera, Andrei, Catalina Liliana, Angus, Colin, Ansha, Mustafa Geleto, Antonio, Carl Abelardo T, Aremu, Olatunde, Ärnlöv, Johan, Artaman, Al, Aryal, Krishna K, Assadi, Reza, Ausloos, Marcel, Avila-Burgos, Leticia, Avokpaho, Euripide F, Awasthi, Ashish, Ayele, Henok Tadesse, Ayer, Rakesh, Ayuk, Tambe B, Azzopardi, Peter S, Badali, Hamid, Badawi, Alaa, Banach, Maciej, Barker-Collo, Suzanne Lyn, Barrero, Lope H, Basaleem, Huda, Baye, Estifanos, Bazargan-Hejazi, Shahrzad, Bedi, Neeraj, Béjot, Yannick, Belachew, Abate Bekele, Belay, Saba Abraham, Bennett, Derrick A, Bensenor, Isabela M, Bernabe, Eduardo, Bernstein, Robert S, Beyene, Addisu Shunu, Beyranvand, Tina, Bhaumik, Soumyadeeep, Bhutta, Zulfiqar A, Biadgo, Belete, Bijani, Ali, Bililign, Nigus, Birlik, Sait Mentes, Birungi, Charles, Bizuneh, Hailemichael, Bjerregaard, Peter, Bjørge, Tone, Borges, Guilherme, Bosetti, Cristina, Boufous, Soufiane, Bragazzi, Nicola Luigi, Brenner, Hermann, and Butt, Zahid A

Subjects
Epidemiology, Public Health, Health Sciences, Alcoholism, Alcohol Use and Health, Aging, Prevention, Behavioral and Social Science, Substance Misuse, Women's Health, 2.4 Surveillance and distribution, Cancer, Oral and gastrointestinal, Stroke, Good Health and Well Being, Adolescent, Adult, Age Distribution, Aged, Aged, 80 and over, Alcohol Drinking, Cause of Death, Commerce, Female, Global Burden of Disease, Global Health, Humans, Male, Middle Aged, Observational Studies as Topic, Population Surveillance, Prevalence, Prospective Studies, Quality-Adjusted Life Years, Retrospective Studies, Risk Assessment, Risk Factors, Sex Distribution, Young Adult, GBD 2016 Alcohol Collaborators, Medical and Health Sciences, General & Internal Medicine, Biomedical and clinical sciences, Health sciences
Abstract

BackgroundAlcohol use is a leading risk factor for death and disability, but its overall association with health remains complex given the possible protective effects of moderate alcohol consumption on some conditions. With our comprehensive approach to health accounting within the Global Burden of Diseases, Injuries, and Risk Factors Study 2016, we generated improved estimates of alcohol use and alcohol-attributable deaths and disability-adjusted life-years (DALYs) for 195 locations from 1990 to 2016, for both sexes and for 5-year age groups between the ages of 15 years and 95 years and older.MethodsUsing 694 data sources of individual and population-level alcohol consumption, along with 592 prospective and retrospective studies on the risk of alcohol use, we produced estimates of the prevalence of current drinking, abstention, the distribution of alcohol consumption among current drinkers in standard drinks daily (defined as 10 g of pure ethyl alcohol), and alcohol-attributable deaths and DALYs. We made several methodological improvements compared with previous estimates: first, we adjusted alcohol sales estimates to take into account tourist and unrecorded consumption; second, we did a new meta-analysis of relative risks for 23 health outcomes associated with alcohol use; and third, we developed a new method to quantify the level of alcohol consumption that minimises the overall risk to individual health.FindingsGlobally, alcohol use was the seventh leading risk factor for both deaths and DALYs in 2016, accounting for 2·2% (95% uncertainty interval [UI] 1·5-3·0) of age-standardised female deaths and 6·8% (5·8-8·0) of age-standardised male deaths. Among the population aged 15-49 years, alcohol use was the leading risk factor globally in 2016, with 3·8% (95% UI 3·2-4·3) of female deaths and 12·2% (10·8-13·6) of male deaths attributable to alcohol use. For the population aged 15-49 years, female attributable DALYs were 2·3% (95% UI 2·0-2·6) and male attributable DALYs were 8·9% (7·8-9·9). The three leading causes of attributable deaths in this age group were tuberculosis (1·4% [95% UI 1·0-1·7] of total deaths), road injuries (1·2% [0·7-1·9]), and self-harm (1·1% [0·6-1·5]). For populations aged 50 years and older, cancers accounted for a large proportion of total alcohol-attributable deaths in 2016, constituting 27·1% (95% UI 21·2-33·3) of total alcohol-attributable female deaths and 18·9% (15·3-22·6) of male deaths. The level of alcohol consumption that minimised harm across health outcomes was zero (95% UI 0·0-0·8) standard drinks per week.InterpretationAlcohol use is a leading risk factor for global disease burden and causes substantial health loss. We found that the risk of all-cause mortality, and of cancers specifically, rises with increasing levels of consumption, and the level of consumption that minimises health loss is zero. These results suggest that alcohol control policies might need to be revised worldwide, refocusing on efforts to lower overall population-level consumption.FundingBill & Melinda Gates Foundation.

Published
2018

18. Fatigue, Pain, and Other Physical Symptoms of Living Liver Donors in the Adult‐to‐Adult Living Donor Liver Transplantation Cohort Study

Author

Butt, Zeeshan, DiMartini, Andrea F, Liu, Qian, Simpson, Mary Ann, Smith, Abigail R, Zee, Jarcy, Gillespie, Brenda W, Holtzman, Susan, Ladner, Daniela, Olthoff, Kim, Fisher, Robert A, Hafliger, Silvia, Freise, Chris E, Mandell, Mercedes Susan, Sherker, Averell H, and Dew, Mary Amanda

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Pain, Digestive Diseases, Patient Safety, Pain Research, Liver Disease, Organ Transplantation, Transplantation, Clinical Research, 7.1 Individual care needs, Management of diseases and conditions, Oral and gastrointestinal, Donor Selection, Fatigue, Female, Health Status, Hepatectomy, Humans, Liver Transplantation, Living Donors, Longitudinal Studies, Male, North America, Pain Measurement, Pain, Postoperative, Patient Reported Outcome Measures, Prospective Studies, Quality of Life, Recovery of Function, Risk Assessment, Risk Factors, Time Factors, Treatment Outcome, Surgery, Clinical sciences
Abstract

Little is known about living liver donors' perceptions of their physical well-being following the procedure. We collected data on donor fatigue, pain, and other relevant physical outcomes as part of the prospective, multicenter Adult-to-Adult Living Donor Liver Transplantation Cohort Study consortium. A total of 271 (91%) of 297 eligible donors were interviewed at least once before donation and 3, 6, 12, and 24 months after donation using validated measures when available. Repeated measures regression models were used to identify potential predictors of worse physical outcomes. We found that donors reported more fatigue immediately after surgery that improved by 2 years after donation, but not to predonation levels. A similar pattern was seen across a number of other physical outcomes. Abdominal or back pain and interference from their pain were rated relatively low on average at all study points. However, 21% of donors did report clinically significant pain at some point during postdonation study follow-up. Across multiple outcomes, female donors, donors whose recipients died, donors with longer hospital stays after surgery, and those whose families discouraged donation were at risk for worse physical well-being outcomes. In conclusion, although not readily modifiable, we have identified risk factors that may help identify donors at risk for worse physical outcomes for targeted intervention. Liver Transplantation 00 000-000 2018 AASLD.

Published
2018

19. Association of Human Immunodeficiency Virus Infection and Risk of Peripheral Artery Disease

Author

Beckman, Joshua A, Duncan, Meredith S, Alcorn, Charles W, So-Armah, Kaku, Butt, Adeel A, Goetz, Matthew Bidwell, Tindle, Hilary A, Sico, Jason J, Tracy, Russel P, Justice, Amy C, and Freiberg, Matthew S

Subjects
Clinical Research, Heart Disease, HIV/AIDS, Prevention, Cardiovascular, Infectious Diseases, Infection, Good Health and Well Being, Adult, CD4 Lymphocyte Count, Cohort Studies, Female, Follow-Up Studies, HIV Infections, HIV-1, Humans, Male, Middle Aged, Peripheral Arterial Disease, Prognosis, Risk, Survival Analysis, United States, Veterans, amputation, antiretroviral therapy, CD4 cells, human immunodeficiency virus, mortality, peripheral artery disease, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Public Health and Health Services, Cardiovascular System & Hematology
Abstract

BACKGROUND:The effect of human immunodeficiency virus (HIV) on the development of peripheral artery disease (PAD) remains unclear. We investigated whether HIV infection is associated with an increased risk of PAD after adjustment for traditional atherosclerotic risk factors in a large cohort of HIV-infected (HIV+) and demographically similar HIV-uninfected veterans. METHODS:We studied participants in the Veterans Aging Cohort Study from April 1, 2003 through December 31, 2014. We excluded participants with known prior PAD or prevalent cardiovascular disease (myocardial infarction, stroke, coronary heart disease, and congestive heart failure) and analyzed the effect of HIV status on the risk of incident PAD events after adjusting for demographics, PAD risk factors, substance use, CD4 cell count, HIV-1 ribonucleic acid, and antiretroviral therapy. The primary outcome is incident peripheral artery disease events. Secondary outcomes include mortality and amputation in subjects with incident PAD events by HIV infection status, viral load, and CD4 count. RESULTS:Among 91 953 participants, over a median follow up of 9.0 years, there were 7708 incident PAD events. Rates of incident PAD events per 1000 person-years were higher among HIV+ (11.9; 95% confidence interval [CI], 11.5-12.4) than uninfected veterans (9.9; 95% CI, 9.6-10.1). After adjustment for demographics, PAD risk factors, and other covariates, HIV+ veterans had an increased risk of incident PAD events compared with uninfected veterans (hazard ratio [HR], 1.19; 95% CI, 1.13-1.25). This risk was highest among those with time-updated HIV viral load >500 copies/mL (HR, 1.51; 95% CI, 1.38-1.65) and CD4 cell counts

Published
2018

20. Validation of the ICD-9 Diagnostic Code for Palliative Care in Patients Hospitalized With Heart Failure Within the Veterans Health Administration

Author

Feder, Shelli L, Redeker, Nancy S, Jeon, Sangchoon, Schulman-Green, Dena, Womack, Julie A, Tate, Janet P, Bedimo, Roger J, Budoff, Matthew J, Butt, Adeel A, Crothers, Kristina, and Akgün, Kathleen M

Subjects
Health Services and Systems, Health Sciences, Heart Disease, Health Services, Aging, Clinical Research, Cardiovascular, Pain Research, Management of diseases and conditions, 7.2 End of life care, Adult, Aged, Electronic Health Records, Female, Heart Failure, Humans, International Classification of Diseases, Male, Middle Aged, Palliative Care, Severity of Illness Index, United States, United States Department of Veterans Affairs, Veterans Health, heart failure, palliative care, hospitalization, Ninth Revision (ICD-9) code, hospice, Nursing, Gerontology, Health services and systems
Abstract

BACKGROUND:Patients with heart failure (HF) are at increased risk of unmet palliative care needs. The International Classification of Diseases, Ninth Revision ( ICD-9) code, V66.7, can identify palliative care services. However, code validity for specialist palliative care in the Veterans Health Administration (VHA) has not been determined. OBJECTIVE:To validate the ICD-9 code for specialist palliative care and determine common reasons for specialist palliative care consultation among VHA patients hospitalized with HF. DESIGN:Electronic health record review of data from the Veterans Aging Cohort Study. SETTING/PARTICIPANTS:The sample included 100 patients hospitalized with HF from 2003 to 2012. MEASUREMENTS:Data from 50 patients with V66.7 were matched by age, race, site of care, hospital length of stay, intensive care unit admission, and fiscal year of study discharge to 50 patients with HF without V66.7 who had died within a year of hospitalization. We calculated positive and negative predictive values (PPV, NPV), sensitivity, and specificity. RESULTS:All patients included in the sample were male, 66% black ethnicity, and mean age = 65 years (standard deviations [SD] ± 10.5 for cases; SD ± 9.8 for matches). Specialist palliative care was documented for 49 of 50 patients with V66.7 (PPV = 98%, 95% confidence interval [CI]: 88-99) and 9 of 50 patients without the code (NPV = 82%, 95% CI: 68-91). Sensitivity was 84% (95% CI: 72-92), and specificity was 98% (95% CI: 86-99). Establishing goals of care was the most frequent reason for palliative care consultation (43% of the sample). CONCLUSION:The ICD-9 code V66.7 identifies specialist palliative care for hospitalized patients with HF in the VHA. Replication of findings in other data sources and populations is needed.

Published
2018

21. Bilirubin Is Inversely Associated With Cardiovascular Disease Among HIV‐Positive and HIV‐Negative Individuals in VACS (Veterans Aging Cohort Study)

Author

Marconi, Vincent C, Duncan, Meredith S, So‐Armah, Kaku, Re, Vincent Lo, Lim, Joseph K, Butt, Adeel A, Goetz, Matthew Bidwell, Rodriguez‐Barradas, Maria C, Alcorn, Charles W, Lennox, Jeffrey, Beckman, Joshua A, Justice, Amy, and Freiberg, Matthew

Subjects
Heart Disease - Coronary Heart Disease, Clinical Research, Cardiovascular, Prevention, Heart Disease, Aging, Good Health and Well Being, Adult, Age Factors, Bilirubin, Biomarkers, Cardiovascular Diseases, Female, HIV Infections, Humans, Incidence, Male, Middle Aged, Prognosis, Prospective Studies, Protective Factors, Risk Assessment, Risk Factors, Time Factors, United States, Up-Regulation, Veterans Health, cardiovascular disease, bilirubin, HIV, stroke, myocardial infarction, heart failure, HIV, Cardiorespiratory Medicine and Haematology
Abstract

Bilirubin may protect against cardiovascular disease (CVD) by reducing oxidative stress. Whether elevated bilirubin reduces the risk of CVD events among HIV+ individuals and if this differs from uninfected individuals remain unclear. We assessed whether bilirubin independently predicted the risk of CVD events among HIV+ and uninfected participants in VACS (Veterans Aging Cohort Study). We conducted a prospective cohort study using VACS participants free of baseline CVD. Total bilirubin was categorized by quartiles. CVD as well as acute myocardial infarction, heart failure, and ischemic stroke events were assessed. Cox regression was used to evaluate hazard ratios of outcomes associated with quartiles of total bilirubin in HIV+ and uninfected people after adjusting for multiple risk factors. There were 96 381 participants (30 427 HIV+); mean age was 48 years, 48% were black, and 97% were men. There were 6603 total incident CVD events over a mean of 5.7 years. In adjusted models, increasing quartiles of baseline total bilirubin were associated with decreased hazards of all outcomes (hazard ratio, 0.86; 95% confidence interval, 0.80-0.91). Among HIV+ participants, results persisted for heart failure, ischemic stroke, and total CVD, but nonsignificant associations were observed for acute myocardial infarction. VACS participants (regardless of HIV status) with elevated bilirubin levels had a lower risk of incident total CVD, acute myocardial infarction, heart failure, and ischemic stroke events after adjusting for known risk factors. Future studies should investigate how this apparently protective effect of elevated bilirubin could be harnessed to reduce CVD risk or improve risk estimation among HIV+ individuals.

Published
2018

22. Current-use flame retardants: Maternal exposure and neurodevelopment in children of the CHAMACOS cohort

Author

Castorina, Rosemary, Bradman, Asa, Stapleton, Heather M, Butt, Craig, Avery, Dylan, Harley, Kim G, Gunier, Robert B, Holland, Nina, and Eskenazi, Brenda

Subjects
Biomedical and Clinical Sciences, Environmental Sciences, Pollution and Contamination, Clinical Research, Endocrine Disruptors, Women's Health, Health Effects of Indoor Air Pollution, Pediatric, Neurosciences, Social Determinants of Health, 2.2 Factors relating to the physical environment, Good Health and Well Being, Adult, Animals, Biphenyl Compounds, Child, Cohort Studies, Data Collection, Environmental Pollutants, Female, Flame Retardants, Halogenated Diphenyl Ethers, Humans, Insecticides, Intelligence Tests, Male, Maternal Exposure, Memory, Short-Term, Nervous System, Organophosphates, Organophosphorus Compounds, Phosphates, Phosphoric Acids, Polybrominated Biphenyls, Pregnancy, Flame retardants, PFRs, Exposure, Children, Neurodevelopment, FM 550, FM 550(®), Meteorology & Atmospheric Sciences
Abstract

Flame retardants are commonly used in consumer products found in U.S. households. Restrictions on the use of polybrominated diphenyl ether flame retardants have resulted in increased use of replacement chemicals, including Firemaster 550® (FM 550®) and organophosphate flame retardants (PFRs): tris(1,3- dichloro-2-propyl) phosphate (TDCIPP); tris(chloropropyl) phosphate (TCIPP); tris(2-chloroethyl) phosphate (TCEP); and triphenyl phosphate (TPHP). Animal research suggests that PFRs may affect neurodevelopment through noncholinergic mechanisms similar to some organophosphate (OP) pesticides. Despite the widespread presence of these compounds in home environments, and their structural similarity to neurotoxic OP pesticides, understanding of human exposure and health effects of PFRs is limited. We measured four urinary PFR metabolites from pregnant women in the CHAMACOS birth cohort study (n = 310) and assessed neurodevelopment of their children at age 7. Metabolites of TDCIPP (BDCIPP: bis(1,3-dichloro-2-propyl) phosphate) and TPHP (DPHP: diphenyl phosphate) were detected in >75% of urine samples, and isopropylphenyl phenyl phosphate (ip-PPP), a metabolite of one component of FM 550®, was detected in 72% of urine samples. We observed decreases of 2.9 points (95% Confidence Interval (CI): -6.3, 0.5) and 3.9 points (95% CI: -7.3,-0.5) in Full-Scale intelligence quotient and Working Memory, respectively, for each ten-fold increase in DPHP in adjusted regression models (n = 248). Decreases in Full-Scale IQ and Working Memory were greater in models of the molar sum of the PFR metabolites compared to the DPHP models. This is the first study to examine PFR and FM 550® exposures and potential neurodevelopmental outcomes in pregnant women and children. Additional research is warranted.

Published
2017

23. Risk of Acute Liver Injury After Statin Initiation by Human Immunodeficiency Virus and Chronic Hepatitis C Virus Infection Status.

Author

Byrne, Dana D, Tate, Janet P, Forde, Kimberly A, Lim, Joseph K, Goetz, Matthew Bidwell, Rimland, David, Rodriguez-Barradas, Maria C, Butt, Adeel A, Gibert, Cynthia L, Brown, Sheldon T, Bedimo, Roger, Freiberg, Matthew S, Justice, Amy C, Kostman, Jay R, Roy, Jason A, and Lo Re, Vincent

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Emerging Infectious Diseases, Rare Diseases, Genetics, Hepatitis - C, Infectious Diseases, Hepatitis, Clinical Research, Liver Disease, Chronic Liver Disease and Cirrhosis, Digestive Diseases, HIV/AIDS, Infection, Good Health and Well Being, Chemical and Drug Induced Liver Injury, Female, HIV Infections, Hepatitis C, Chronic, Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Incidence, Male, Middle Aged, Retrospective Studies, Risk Factors, statins, HIV, hepatitis C, hepatotoxicity, acute liver injury, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

BackgroundPatients with human immunodeficiency virus (HIV) and/or chronic hepatitis C virus (HCV) infection may be prescribed statins as treatment for metabolic/cardiovascular disease, but it remains unclear if the risk of acute liver injury (ALI) is increased for statin initiators compared to nonusers in groups classified by HIV/HCV status.MethodsWe conducted a cohort study to compare rates of ALI in statin initiators vs nonusers among 7686 HIV/HCV-coinfected, 8155 HCV-monoinfected, 17739 HIV-monoinfected, and 36604 uninfected persons in the Veterans Aging Cohort Study (2000-2012). We determined development of (1) liver aminotransferases >200 U/L, (2) severe ALI (coagulopathy with hyperbilirubinemia), and (3) death, all within 18 months. Cox regression was used to determine propensity score-adjusted hazard ratios (HRs) with 95% confidence intervals (CIs) of outcomes in statin initiators compared to nonusers across the groups.ResultsAmong HIV/HCV-coinfected patients, statin initiators had lower risks of aminotransferase levels >200 U/L (HR, 0.66 [95% CI, .53-.83]), severe ALI (HR, 0.23 [95% CI, .12-.46]), and death (HR, 0.36 [95% CI, .28-.46]) compared with statin nonusers. In the setting of chronic HCV alone, statin initiators had reduced risks of aminotransferase elevations (HR, 0.57 [95% CI, .45-.72]), severe ALI (HR, 0.15 [95% CI, .06-.37]), and death (HR, 0.42 [95% CI, .32-.54]) than nonusers. Among HIV-monoinfected patients, statin initiators had lower risks of aminotransferase increases (HR, 0.52 [95% CI, .40-.66]), severe ALI (HR, 0.26 [95% CI, .13-.55]), and death (HR, 0.19 [95% CI, .16-.23]) compared with nonusers. Results were similar among uninfected persons.ConclusionsRegardless of HIV and/or chronic HCV status, statin initiators had a lower risk of ALI and death within 18 months compared with statin nonusers.

Published
2017

24. Associations between flame retardant applications in furniture foam, house dust levels, and residents' serum levels

Author

Hammel, Stephanie C, Hoffman, Kate, Lorenzo, Amelia M, Chen, Albert, Phillips, Allison L, Butt, Craig M, Sosa, Julie Ann, Webster, Thomas F, and Stapleton, Heather M

Subjects
Environmental Sciences, Pollution and Contamination, Cohort Studies, Dust, Environmental Monitoring, Environmental Pollutants, Female, Flame Retardants, Halogenated Diphenyl Ethers, Humans, Interior Design and Furnishings, Male, Middle Aged, North Carolina, Organophosphates, Organophosphorus Compounds, Polybrominated Biphenyls, Polyurethanes, Brominated flame retardants, Polyurethane foam, House dust, Exposure, Serum biomarkers
Abstract

Polyurethane foam (PUF) in upholstered furniture frequently is treated with flame retardant chemicals (FRs) to reduce its flammability and adhere to rigorous flammability standards. For decades, a commercial mixture of polybrominated diphenyl ethers (PBDEs) called PentaBDE was commonly applied to foam to fulfill these regulations; however, concerns over toxicity, bioaccumulation, and persistence led to a global phase-out in the mid-2000s. Although PentaBDE is still detected in older furniture, other FR compounds such as tris(1,3-dichloroisopropyl) phosphate (TDCIPP) and Firemaster® 550 (FM550) have been increasingly used as replacements. While biomonitoring studies suggest exposure is widespread, the primary sources of exposure are not clearly known. Here, we investigated the relationships between specific FR applications in furniture foam and human exposure. Paired samples of furniture foam, house dust and serum samples were collected from a cohort in North Carolina, USA and analyzed for FRs typically used in PUF. In general, the presence of a specific FR in the sofa of a home was associated with an increase in the concentration of that FR in house dust. For example, the presence of PentaBDE in sofas was associated with significantly higher levels of BDE-47, a major component of PentaBDE, in house dust (10β=6.4, p

Published
2017

25. Performance of the Pooled Cohort atherosclerotic cardiovascular disease risk score in hepatitis C virus‐infected persons

Author

Chew, KW, Bhattacharya, D, Horwich, TB, Yan, P, McGinnis, KA, Tseng, C, Freiberg, MS, Currier, JS, and Butt, AA

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Clinical Sciences, Atherosclerosis, Heart Disease, Prevention, Cardiovascular, Aging, Chronic Liver Disease and Cirrhosis, Minority Health, Infectious Diseases, Digestive Diseases, Hepatitis - C, Hepatitis, Emerging Infectious Diseases, Liver Disease, Aetiology, 2.2 Factors relating to the physical environment, Infection, Good Health and Well Being, Aged, Cardiovascular Diseases, Comorbidity, Female, Hepacivirus, Hepatitis C, Humans, Incidence, Male, Middle Aged, Population Surveillance, Proportional Hazards Models, Reproducibility of Results, Retrospective Studies, Risk Assessment, Risk Factors, atherosclerotic cardiovascular disease score, cardiovascular disease, cardiovascular risk assessment, hepatitis C virus, Microbiology, Gastroenterology & Hepatology, Clinical sciences, Medical microbiology
Abstract

Chronic hepatitis C virus (HCV) infection has been associated with an increased risk for cardiovascular disease (CVD). The recommended Pooled Cohort atherosclerotic cardiovascular disease (ASCVD) risk equation for estimation of 10-year CVD risk has not been validated in HCV-infected populations. We examined the performance of the ASCVD risk score in HCV-infected persons, using the national Electronically Retrieved Cohort of HCV Infected Veterans to derive a cohort of HCV-infected and uninfected subjects without baseline ASCVD, hepatitis B, or HIV infection, and with low-density lipoprotein cholesterol level

Published
2017

26. FIB-4 stage of liver fibrosis predicts incident heart failure among HIV-infected and uninfected patients.

Author

So-Armah, Kaku A, Lim, Joseph K, Lo Re, Vincent, Tate, Janet P, Chang, Chung-Chou H, Butt, Adeel A, Gibert, Cynthia L, Rimland, David, Marconi, Vincent C, Goetz, Matthew B, Rodriguez-Barradas, Maria C, Budoff, Matthew J, Tindle, Hilary A, Samet, Jeffrey H, Justice, Amy C, Freiberg, Matthew S, and Veterans Aging Cohort Study Project Team

Subjects
Veterans Aging Cohort Study Project Team, Humans, HIV Infections, Liver Cirrhosis, Severity of Illness Index, Case-Control Studies, Cohort Studies, Adult, Middle Aged, Female, Male, Heart Failure, Heart Disease, Infectious Diseases, Hepatitis - C, Digestive Diseases, HIV/AIDS, Chronic Liver Disease and Cirrhosis, Liver Disease, Aging, Hepatitis, Clinical Research, Cardiovascular, Emerging Infectious Diseases, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Medical Biochemistry and Metabolomics, Clinical Sciences, Immunology, Gastroenterology & Hepatology
Abstract

Liver fibrosis is common, particularly in individuals who are infected with human immunodeficiency virus (HIV). HIV-infected individuals have excess congestive heart failure (CHF) risk compared with uninfected people. It remains unknown whether liver fibrosis stage influences the CHF risk or if HIV or hepatitis C virus (HCV) infection modifies this association. Our objectives were to assess whether 1) stage of liver fibrosis is independently associated with incident CHF and 2) the association between stage of liver fibrosis and incident CHF is modified by HIV/HCV status. Participants alive on or after April 1, 2003, in the Veterans Aging Cohort Study were included. Those without prevalent cardiovascular disease were followed until their first CHF event, death, last follow-up date, or December 31, 2011. Liver fibrosis was measured using the fibrosis 4 index (FIB-4), which is calculated using age, aminotransferases, and platelets. Cox proportional hazards regression models were adjusted for cardiovascular disease risk factors. Among 96,373 participants over 6.9 years, 3844 incident CHF events occurred. FIB-4 between 1.45 and 3.25 (moderate fibrosis) and FIB-4 > 3.25 (advanced fibrosis/cirrhosis) were associated with CHF (hazard ratio [95% confidence interval], 1.17 [1.07-1.27] and 1.65 [1.43-1.92], respectively). The association of advanced fibrosis/cirrhosis and incident CHF persisted regardless of HIV/HCV status.ConclusionModerate and advanced liver fibrosis/cirrhosis are associated with an increased risk of CHF. The association for advanced fibrosis/cirrhosis persists even among participants without hepatitis C and/or HIV infection. Assessing liver health may be important for reducing the risk of future CHF events, particularly among HIV and hepatitis C infected people among whom cardiovascular disease risk is elevated and liver disease is common. (Hepatology 2017;66:1286-1295).

Published
2017

27. Insular and cingulate attenuation during decision making is associated with future transition to stimulant use disorder

Author

Stewart, Jennifer L, Butt, Mamona, May, April C, Tapert, Susan F, and Paulus, Martin P

Subjects
Biological Psychology, Psychology, Drug Abuse (NIDA only), Substance Misuse, Clinical Research, Neurosciences, Brain Disorders, Mental health, Adult, Amphetamine-Related Disorders, Brain Mapping, California, Central Nervous System Stimulants, Cerebral Cortex, Decision Making, Female, Gyrus Cinguli, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Risk, Young Adult, Addiction, anterior cingulate, functional neuroimaging, insula, marijuana, reward, stimulants, Medical and Health Sciences, Psychology and Cognitive Sciences, Substance Abuse, Public health, Clinical and health psychology
Abstract

AimsTo understand processes placing individuals at risk for stimulant (amphetamine and cocaine) use disorder.DesignLongitudinal study.SettingUniversity of California, San Diego Department of Psychiatry, CA, USA.ParticipantsOccasional stimulant users (OSU; n = 184) underwent a baseline clinical interview and a functional magnetic resonance imaging (fMRI) session. On the basis of a follow-up clinical interview completed 3 years later, OSU (n = 147) were then categorized as problem stimulant users (PSU: n = 36; those who developed stimulant use disorders in the interim) or desisted stimulant users (DSU: n = 74; those who stopped using). OSU who did not meet criteria for PSU or DSU (n = 37) were included in dimensional analyses.MeasurementsfMRI blood oxygen level-dependent (BOLD) contrast percentage signal change from baseline collected during a Paper-Scissors-Rock task was examined during three decision-making conditions, those resulting in: (1) wins, (2) ties and (3) losses. These data were used as dependent variables in categorical analyses comparing PSU and DSU, as well as dimensional analyses including interim drug use as predictors, controlling for baseline drug use.FindingsPSU exhibited lower anterior cingulate, middle insula, superior temporal, inferior parietal, precuneus and cerebellum activation than DSU across all three conditions (significant brain clusters required > 19 neighboring voxels to exceed F(1,108)  = 5.58, P  0.83). Higher interim marijuana use was linked to lower pre-central and superior temporal activation during choices resulting in wins (> 19 neighboring voxels to exceed t = 2.61, P  0.11).ConclusionsIndividuals who transition from stimulant use to stimulant use disorder appear to show alterations in neural processing of stimulus valuation and outcome monitoring, patterns also evident in chronic stimulant use disorder. Attenuated anterior cingulate and insular processing may constitute a high-risk neural processing profile, which could be used to calculate risk scores for individuals experimenting with stimulants.

Published
2017

28. Global, regional, and national age-sex specific mortality for 264 causes of death, 1980–2016: a systematic analysis for the Global Burden of Disease Study 2016

Author

Collaborators, GBD 2016 Causes of Death, Naghavi, Mohsen, Abajobir, Amanuel Alemu, Abbafati, Cristiana, Abbas, Kaja M, Abd-Allah, Foad, Abera, Semaw Ferede, Aboyans, Victor, Adetokunboh, Olatunji, Afshin, Ashkan, Agrawal, Anurag, Ahmadi, Alireza, Ahmed, Muktar Beshir, Aichour, Amani Nidhal, Aichour, Miloud Taki Eddine, Aichour, Ibtihel, Aiyar, Sneha, Alahdab, Fares, Al-Aly, Ziyad, Alam, Khurshid, Alam, Noore, Alam, Tahiya, Alene, Kefyalew Addis, Al-Eyadhy, Ayman, Ali, Syed Danish, Alizadeh-Navaei, Reza, Alkaabi, Juma M, Alkerwi, Ala'a, Alla, François, Allebeck, Peter, Allen, Christine, Al-Raddadi, Rajaa, Alsharif, Ubai, Altirkawi, Khalid A, Alvis-Guzman, Nelson, Amare, Azmeraw T, Amini, Erfan, Ammar, Walid, Amoako, Yaw Ampem, Anber, Nahla, Andersen, Hjalte H, Andrei, Catalina Liliana, Androudi, Sofia, Ansari, Hossein, Antonio, Carl Abelardo T, Anwari, Palwasha, Ärnlöv, Johan, Arora, Megha, Artaman, Al, Aryal, Krishna Kumar, Asayesh, Hamid, Asgedom, Solomon W, Atey, Tesfay Mehari, Avila-Burgos, Leticia, Avokpaho, Euripide Frinel G, Awasthi, Ashish, Babalola, Tesleem Kayode, Bacha, Umar, Balakrishnan, Kalpana, Barac, Aleksandra, Barboza, Miguel A, Barker-Collo, Suzanne L, Barquera, Simon, Barregard, Lars, Barrero, Lope H, Baune, Bernhard T, Bedi, Neeraj, Beghi, Ettore, Béjot, Yannick, Bekele, Bayu Begashaw, Bell, Michelle L, Bennett, James R, Bensenor, Isabela M, Berhane, Adugnaw, Bernabé, Eduardo, Betsu, Balem Demtsu, Beuran, Mircea, Bhatt, Samir, Biadgilign, Sibhatu, Bienhoff, Kelly, Bikbov, Boris, Bisanzio, Donal, Bourne, Rupert RA, Breitborde, Nicholas JK, Bulto, Lemma Negesa Bulto, Bumgarner, Blair R, Butt, Zahid A, Cahuana-Hurtado, Lucero, Cameron, Ewan, Campuzano, Julio Cesar, Car, Josip, Cárdenas, Rosario, Carrero, Juan Jesus, Carter, Austin, Casey, Daniel C, Castañeda-Orjuela, Carlos A, Catalá-López, Ferrán, Charlson, Fiona J, Chibueze, Chioma Ezinne, and Chimed-Ochir, Odgerel

Subjects
Pediatric, Clinical Research, Infant Mortality, Infectious Diseases, 2.4 Surveillance and distribution, Aetiology, Infection, Cardiovascular, Good Health and Well Being, Adolescent, Adult, Age Distribution, Aged, Aged, 80 and over, Cause of Death, Child, Child, Preschool, Communicable Diseases, Disasters, Female, Global Burden of Disease, Global Health, Humans, Infant, Infant, Newborn, Male, Middle Aged, Noncommunicable Diseases, Nutrition Disorders, Pregnancy, Pregnancy Complications, Socioeconomic Factors, Wounds and Injuries, Young Adult, GBD 2016 Causes of Death Collaborators, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundMonitoring levels and trends in premature mortality is crucial to understanding how societies can address prominent sources of early death. The Global Burden of Disease 2016 Study (GBD 2016) provides a comprehensive assessment of cause-specific mortality for 264 causes in 195 locations from 1980 to 2016. This assessment includes evaluation of the expected epidemiological transition with changes in development and where local patterns deviate from these trends.MethodsWe estimated cause-specific deaths and years of life lost (YLLs) by age, sex, geography, and year. YLLs were calculated from the sum of each death multiplied by the standard life expectancy at each age. We used the GBD cause of death database composed of: vital registration (VR) data corrected for under-registration and garbage coding; national and subnational verbal autopsy (VA) studies corrected for garbage coding; and other sources including surveys and surveillance systems for specific causes such as maternal mortality. To facilitate assessment of quality, we reported on the fraction of deaths assigned to GBD Level 1 or Level 2 causes that cannot be underlying causes of death (major garbage codes) by location and year. Based on completeness, garbage coding, cause list detail, and time periods covered, we provided an overall data quality rating for each location with scores ranging from 0 stars (worst) to 5 stars (best). We used robust statistical methods including the Cause of Death Ensemble model (CODEm) to generate estimates for each location, year, age, and sex. We assessed observed and expected levels and trends of cause-specific deaths in relation to the Socio-demographic Index (SDI), a summary indicator derived from measures of average income per capita, educational attainment, and total fertility, with locations grouped into quintiles by SDI. Relative to GBD 2015, we expanded the GBD cause hierarchy by 18 causes of death for GBD 2016.FindingsThe quality of available data varied by location. Data quality in 25 countries rated in the highest category (5 stars), while 48, 30, 21, and 44 countries were rated at each of the succeeding data quality levels. Vital registration or verbal autopsy data were not available in 27 countries, resulting in the assignment of a zero value for data quality. Deaths from non-communicable diseases (NCDs) represented 72·3% (95% uncertainty interval [UI] 71·2-73·2) of deaths in 2016 with 19·3% (18·5-20·4) of deaths in that year occurring from communicable, maternal, neonatal, and nutritional (CMNN) diseases and a further 8·43% (8·00-8·67) from injuries. Although age-standardised rates of death from NCDs decreased globally between 2006 and 2016, total numbers of these deaths increased; both numbers and age-standardised rates of death from CMNN causes decreased in the decade 2006-16-age-standardised rates of deaths from injuries decreased but total numbers varied little. In 2016, the three leading global causes of death in children under-5 were lower respiratory infections, neonatal preterm birth complications, and neonatal encephalopathy due to birth asphyxia and trauma, combined resulting in 1·80 million deaths (95% UI 1·59 million to 1·89 million). Between 1990 and 2016, a profound shift toward deaths at older ages occurred with a 178% (95% UI 176-181) increase in deaths in ages 90-94 years and a 210% (208-212) increase in deaths older than age 95 years. The ten leading causes by rates of age-standardised YLL significantly decreased from 2006 to 2016 (median annualised rate of change was a decrease of 2·89%); the median annualised rate of change for all other causes was lower (a decrease of 1·59%) during the same interval. Globally, the five leading causes of total YLLs in 2016 were cardiovascular diseases; diarrhoea, lower respiratory infections, and other common infectious diseases; neoplasms; neonatal disorders; and HIV/AIDS and tuberculosis. At a finer level of disaggregation within cause groupings, the ten leading causes of total YLLs in 2016 were ischaemic heart disease, cerebrovascular disease, lower respiratory infections, diarrhoeal diseases, road injuries, malaria, neonatal preterm birth complications, HIV/AIDS, chronic obstructive pulmonary disease, and neonatal encephalopathy due to birth asphyxia and trauma. Ischaemic heart disease was the leading cause of total YLLs in 113 countries for men and 97 countries for women. Comparisons of observed levels of YLLs by countries, relative to the level of YLLs expected on the basis of SDI alone, highlighted distinct regional patterns including the greater than expected level of YLLs from malaria and from HIV/AIDS across sub-Saharan Africa; diabetes mellitus, especially in Oceania; interpersonal violence, notably within Latin America and the Caribbean; and cardiomyopathy and myocarditis, particularly in eastern and central Europe. The level of YLLs from ischaemic heart disease was less than expected in 117 of 195 locations. Other leading causes of YLLs for which YLLs were notably lower than expected included neonatal preterm birth complications in many locations in both south Asia and southeast Asia, and cerebrovascular disease in western Europe.InterpretationThe past 37 years have featured declining rates of communicable, maternal, neonatal, and nutritional diseases across all quintiles of SDI, with faster than expected gains for many locations relative to their SDI. A global shift towards deaths at older ages suggests success in reducing many causes of early death. YLLs have increased globally for causes such as diabetes mellitus or some neoplasms, and in some locations for causes such as drug use disorders, and conflict and terrorism. Increasing levels of YLLs might reflect outcomes from conditions that required high levels of care but for which effective treatments remain elusive, potentially increasing costs to health systems.FundingBill & Melinda Gates Foundation.

Published
2017

29. HIV and Obesity Comorbidity Increase Interleukin 6 but Not Soluble CD14 or D-Dimer

Author

Taylor, Barbara S, So-Armah, Kaku, Tate, Janet P, Marconi, Vincent C, Koethe, John R, Bedimo, Roger J, Butt, Adeel A, Gibert, Cynthia L, Goetz, Matthew B, Rodriguez-Barradas, Maria C, Womack, Julie A, Gerschenson, Mariana, Re, Vincent Lo, Rimland, David, Yin, Michael T, Leaf, David, Tracy, Russell P, Justice, Amy C, and Freiberg, Matthew S

Subjects
Obesity, Clinical Research, HIV/AIDS, Nutrition, Cardiovascular, Stroke, Metabolic and endocrine, Adult, Aging, Biomarkers, Comorbidity, Cross-Sectional Studies, Female, Fibrin Fibrinogen Degradation Products, HIV Infections, Humans, Inflammation, Interleukin-6, Lipopolysaccharide Receptors, Male, Middle Aged, Prospective Studies, United States, Veterans, HIV, obesity, inflammation, monocyte activation, coagulation, VACS, Clinical Sciences, Public Health and Health Services, Virology
Abstract

ObjectivesObesity prevalence among people living with HIV (HIV+) is rising. HIV and obesity are proinflammatory states, but their combined effect on inflammation (measured by interleukin 6, IL-6), altered coagulation (D-dimer), and monocyte activation (soluble CD14, sCD14) is unknown. We hypothesized inflammation increases when obesity and HIV infection co-occur.MethodsThe Veterans Aging Cohort Study survey cohort is a prospective, observational study of predominantly male HIV+ veterans and veterans uninfected with HIV; a subset provided blood samples. Inclusion criteria for this analysis were body mass index ≥ 18.5 kg/m and biomarker measurement. Dependent variables were IL-6, sCD14, and D-dimer quartiles. Obesity/HIV status was the primary predictor. Unadjusted and adjusted logistic regression models were constructed.ResultsData were analyzed for 1477 HIV+ and 823 uninfected participants. Unadjusted median IL-6 levels were significantly higher and sCD14 levels significantly lower in obese/HIV+ compared with nonobese/uninfected (P

Published
2017

30. Risk of End‐Stage Renal Disease in HIV‐Positive Potential Live Kidney Donors

Author

Muzaale, AD, Althoff, KN, Sperati, CJ, Abraham, AG, Kucirka, LM, Massie, AB, Kitahata, MM, Horberg, MA, Justice, AC, Fischer, MJ, Silverberg, MJ, Butt, AA, Boswell, SL, Rachlis, AR, Mayor, AM, Gill, MJ, Eron, JJ, Napravnik, S, Drozd, DR, Martin, JN, Bosch, RJ, Durand, CM, Locke, JE, Moore, RD, Lucas, GM, and Segev, DL

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, HIV/AIDS, Infectious Diseases, Sexually Transmitted Infections, Kidney Disease, Aetiology, 2.2 Factors relating to the physical environment, Renal and urogenital, Infection, Good Health and Well Being, Adult, Case-Control Studies, Female, Follow-Up Studies, Glomerular Filtration Rate, Graft Rejection, Graft Survival, HIV Infections, HIV Seropositivity, HIV-1, Humans, Incidence, Kidney Failure, Chronic, Kidney Function Tests, Kidney Transplantation, Living Donors, Male, Middle Aged, Nephrectomy, North America, Prognosis, Risk Factors, Viral Load, clinical research/practice, donors and donation: living, infection and infectious agents, infectious disease, kidney transplantation/nephrology, viral: human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome, Medical and Health Sciences, Surgery, Clinical sciences, Immunology
Abstract

New federal regulations allow HIV-positive individuals to be live kidney donors; however, potential candidacy for donation is poorly understood given the increased risk of end-stage renal disease (ESRD) associated with HIV infection. To better understand this risk, we compared the incidence of ESRD among 41 968 HIV-positive participants of North America AIDS Cohort Collaboration on Research and Design followed for a median of 5 years with the incidence of ESRD among comparable HIV-negative participants of National Health and Nutrition Examination III followed for a median of 14 years. We used risk associations from multivariable Cox proportional hazards regression to derive cumulative incidence estimates for selected HIV-positive scenarios (no history of diabetes, hypertension, AIDS, or hepatitis C virus coinfection) and compared these estimates with those from similarly selected HIV-negative scenarios. For 40-year-old HIV-positive individuals with health characteristics that were similar to those of age-matched kidney donors, viral load

Published
2017

31. Flame retardants and their metabolites in the homes and urine of pregnant women residing in California (the CHAMACOS cohort)

Author

Castorina, Rosemary, Butt, Craig, Stapleton, Heather M, Avery, Dylan, Harley, Kim G, Holland, Nina, Eskenazi, Brenda, and Bradman, Asa

Subjects
Biomedical and Clinical Sciences, Environmental Sciences, Pollution and Contamination, Clinical Research, Health Effects of Indoor Air Pollution, Endocrine Disruptors, Social Determinants of Health, Good Health and Well Being, Adult, California, Cohort Studies, Dust, Environmental Pollutants, Female, Flame Retardants, Halogenated Diphenyl Ethers, Humans, Organophosphates, Phosphates, Pregnancy, Urine, Young Adult, Flame retardants, Exposure, Pregnant women, Urinary metabolites, Meteorology & Atmospheric Sciences
Abstract

Organophosphate flame retardants (PFRs), used in consumer products since the 1970s, persist in the environment. Restrictions on penta-polybrominated diphenyl ether (PBDE) flame retardants resulted in increased use of Firemaster® 550 (FM® 550), and the organophosphate triesters: tris(1,3- dichloro-2-propyl) phosphate (TDCIPP); tris(chloropropyl) phosphate (TCIPP); tris(2-chloroethyl) phosphate (TCEP); and triphenyl phosphate (TPHP). The objectives of this study were to (1) identify determinants of flame retardants (4 PFRs, PentaBDEs and FM® 550) in house dust, (2) measure urinary PFR metabolites in pregnant women, and (3) estimate health risks from PFR exposure. We measured flame retardants in house dust (n = 125) and metabolites in urine (n = 310) collected in 2000-2001 from Mexican American women participating in the CHAMACOS birth cohort study in California. We detected FM® 550 and PFRs, including two (TCEP and TDCIPP) known to the state of California to cause cancer, in most dust samples. The maximum TCEP and TDCIPP dust levels were among the highest ever reported although the median levels were generally lower compared to other U.S. cohorts. Metabolites of TDCIPP (BDCIPP: bis(1,3-dichloro-2-propyl) phosphate) and TPHP (DPHP: diphenyl phosphate) were detected in 78% and 79% of prenatal urine samples, respectively. We found a weak but positive correlation between TPHP in dust and DPHP in 124 paired prenatal urine samples (Spearman rho = 0.17; p = 0.06). These results provide information on PFR exposure and risk in pregnant women from the early 2000's and are also valuable to assess trends in exposure and risk given changing fire safety regulations and concomitant changes in chemical flame retardant use.

Published
2017

32. Association Between HIV Infection and the Risk of Heart Failure With Reduced Ejection Fraction and Preserved Ejection Fraction in the Antiretroviral Therapy Era: Results From the Veterans Aging Cohort Study

Author

Freiberg, Matthew S, Chang, Chung-Chou H, Skanderson, Melissa, Patterson, Olga V, DuVall, Scott L, Brandt, Cynthia A, So-Armah, Kaku A, Vasan, Ramachandran S, Oursler, Kris Ann, Gottdiener, John, Gottlieb, Stephen, Leaf, David, Rodriguez-Barradas, Maria, Tracy, Russell P, Gibert, Cynthia L, Rimland, David, Bedimo, Roger J, Brown, Sheldon T, Goetz, Matthew Bidwell, Warner, Alberta, Crothers, Kristina, Tindle, Hilary A, Alcorn, Charles, Bachmann, Justin M, Justice, Amy C, and Butt, Adeel A

Subjects
HIV/AIDS, Heart Disease, Aging, Clinical Research, Cardiovascular, Infectious Diseases, Infection, Good Health and Well Being, Adult, Anti-HIV Agents, CD4 Lymphocyte Count, Case-Control Studies, Cohort Studies, Female, HIV Infections, Heart Failure, Humans, Male, Middle Aged, Proportional Hazards Models, Risk Assessment, Risk Factors, Risk Reduction Behavior, Stroke Volume, United States, United States Department of Veterans Affairs, Veterans, Viral Load
Abstract

ImportanceWith improved survival, heart failure (HF) has become a major complication for individuals with human immunodeficiency virus (HIV) infection. It is unclear if this risk extends to different types of HF in the antiretroviral therapy (ART) era. Determining whether HIV infection is associated with HF with reduced ejection fraction (HFrEF), HF with preserved ejection fraction (HFpEF), or both is critical because HF types differ with respect to underlying mechanism, treatment, and prognosis.ObjectivesTo investigate whether HIV infection increases the risk of future HFrEF and HFpEF and to assess if this risk varies by sociodemographic and HIV-specific factors.Design, setting, and participantsThis study evaluated 98 015 participants without baseline cardiovascular disease from the Veterans Aging Cohort Study, an observational cohort of HIV-infected veterans and uninfected veterans matched by age, sex, race/ethnicity, and clinical site, enrolled on or after April 1, 2003, and followed up through September 30, 2012. The dates of the analysis were October 2015 to November 2016.ExposureHuman immunodeficiency virus infection.Main outcomes and measuresOutcomes included HFpEF (EF≥50%), borderline HFpEF (EF 40%-49%), HFrEF (EF

Published
2017

33. Baseline, Time-Updated, and Cumulative HIV Care Metrics for Predicting Acute Myocardial Infarction and All-Cause Mortality

Author

Salinas, Jorge L, Rentsch, Christopher, Marconi, Vincent C, Tate, Janet, Budoff, Matthew, Butt, Adeel A, Freiberg, Matthew S, Gibert, Cynthia L, Goetz, Matthew Bidwell, Leaf, David, Rodriguez-Barradas, Maria C, Justice, Amy C, and Rimland, David

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Heart Disease, HIV/AIDS, Prevention, Cardiovascular, Infectious Diseases, Clinical Research, Heart Disease - Coronary Heart Disease, Genetics, Good Health and Well Being, Adult, Aged, Aging, Biomarkers, CD4 Lymphocyte Count, Cohort Studies, Female, HIV Infections, HIV-1, Humans, Male, Middle Aged, Myocardial Infarction, Predictive Value of Tests, Proportional Hazards Models, Risk Assessment, Risk Factors, United States, Veterans, Viremia, acute myocardial infarction, HIV, mortality, VACS Index, Biological Sciences, Medical and Health Sciences, Microbiology, Clinical sciences
Abstract

Background After adjustment for cardiovascular risk factors and despite higher mortality, those with human immunodeficiency virus (HIV+) have a greater risk of acute myocardial infarction (AMI) than uninfected individuals.Methods We included HIV+ individuals who started combination antiretroviral therapy (cART) in the Veterans Aging Cohort Study (VACS) from 1996 to 2012. We fit multivariable proportional hazards models for baseline, time-updated and cumulative measures of HIV-1 RNA, CD4 counts, and the VACS Index. We used the trapezoidal rule to build the following cumulative measures: viremia copy-years, CD4-years, and VACS Index score-years, captured 180 days after cART initiation until AMI, death, last clinic visit, or 30 September 2012. The primary outcomes were incident AMI (Medicaid, Medicare, and Veterans Affairs International Classification of Diseases-9 codes) and death.Results A total of 8168 HIV+ individuals (53 861 person-years) were analyzed with 196 incident AMIs and 1710 deaths. Controlling for known cardiovascular risk factors, 6 of the 9 metrics predicted AMI and all metrics predicted mortality. Time-updated VACS Index had the lowest Akaike information criterion among all models for both outcomes. A time-updated VACS Index score of 55+ was associated with a hazard ratio (HR) of 3.31 (95% confidence interval [CI], 2.11-5.20) for AMI and a HR of 31.77 (95% CI, 26.17-38.57) for mortality.Conclusions Time-updated VACS Index provided better AMI and mortality prediction than CD4 count and HIV-1 RNA, suggesting that current health determines risk more accurately than prior history and that risk assessment can be improved by biomarkers of organ injury.

Published
2016

34. Association Between Depressive Disorders and Incident Acute Myocardial Infarction in Human Immunodeficiency Virus–Infected Adults: Veterans Aging Cohort Study

Author

Khambaty, Tasneem, Stewart, Jesse C, Gupta, Samir K, Chang, Chung-Chou H, Bedimo, Roger J, Budoff, Matthew J, Butt, Adeel A, Crane, Heidi, Gibert, Cynthia L, Leaf, David A, Rimland, David, Tindle, Hilary A, So-Armah, Kaku A, Justice, Amy C, and Freiberg, Matthew S

Subjects
HIV/AIDS, Clinical Research, Mental Health, Aging, Cardiovascular, Brain Disorders, Depression, Heart Disease, Prevention, Good Health and Well Being, Adult, Cohort Studies, Depressive Disorder, Major, Female, HIV Infections, Humans, Male, Middle Aged, Myocardial Infarction, Veterans
Abstract

ImportanceWith the advent of highly effective antiretroviral therapy and improved survival, human immunodeficiency virus (HIV)-infected people are living longer and are now at an increased risk for cardiovascular disease (CVD). There is an urgent need to identify novel risk factors and primary prevention approaches for CVD in HIV. Although depression is prevalent in HIV-infected adults and is associated with future CVD in the general population, its association with CVD events has not been examined in the HIV-infected population.ObjectiveTo examine whether depressive disorders are prospectively associated with incident acute myocardial infarction (AMI) in a large cohort of adults with HIV.Design, setting, and participantsIncluded in this cohort study were 26 144 HIV-infected veterans without CVD at baseline (1998-2003) participating in the US Department of Veterans Affairs Veterans Aging Cohort Study from April 1, 2003, through December 31, 2009. At baseline, 4853 veterans (19%) with major depressive disorder (MDD; International Classification of Diseases, Ninth Revision [ICD-9] codes 296.2 and 296.3) and 2296 (9%) with dysthymic disorder (ICD-9 code 300.4) were identified. The current analysis was conducted from January 2015 to November 2015.Main outcomes and measuresIncident AMI (defined by discharge summary documentation, enzyme/electrocardiography evidence of AMI, inpatient ICD-9 code for AMI (410), or AMI as underlying cause of death [International Statistical Classification of Diseases and Related Health Problems, Tenth Revision code 121]) between the enrollment date and December 31, 2009.ResultsThe mean (SD) age of those with MDD was 47.3 (7.9) years and for those without MDD was 48.2 (9.7) years. During 5.8 years of follow-up, 490 AMI events (1.9%) occurred. Baseline MDD was associated with incident AMI after adjusting for demographics (hazard ratio [HR], 1.31; 95% CI, 1.05-1.62), CVD risk factors (HR, 1.29; 95% CI, 1.04-1.60), and HIV-specific factors (HR, 1.30; 95% CI, 1.05-1.62). Further adjustment for hepatitis C, renal disease, substance abuse, and hemoglobin level (HR, 1.25; 95% CI, 1.00-1.56) and antidepressant use (HR, 1.12; 95% CI, 0.87-1.42) attenuated associations. Baseline dysthymic disorder was not associated with incident AMI.Conclusions and relevanceWe report novel evidence that HIV-infected adults with MDD have a 30% increased risk for AMI than HIV-infected adults without MDD after adjustment for many potential confounders. Our findings raise the possibility that MDD may be independently associated with incident atherosclerotic CVD in the HIV-infected population.

Published
2016

35. Do Biomarkers of Inflammation, Monocyte Activation, and Altered Coagulation Explain Excess Mortality Between HIV Infected and Uninfected People?

Author

So-Armah, Kaku A, Tate, Janet P, Chang, Chung-Chou H, Butt, Adeel A, Gerschenson, Mariana, Gibert, Cynthia L, Leaf, David, Rimland, David, Rodriguez-Barradas, Maria C, Budoff, Matthew J, Samet, Jeffrey H, Kuller, Lewis H, Deeks, Steven G, Crothers, Kristina, Tracy, Russell P, Crane, Heidi M, Sajadi, Mohammad M, Tindle, Hilary A, Justice, Amy C, Freiberg, Matthew S, and VACS Project Team

Subjects
VACS Project Team, Monocytes, Humans, HIV-1, HIV Infections, Blood Coagulation Disorders, Inflammation, Fibrin Fibrinogen Degradation Products, Interleukin-6, Analysis of Variance, Logistic Models, Longitudinal Studies, Aging, Adult, Middle Aged, Veterans, United States, Female, Male, Biomarkers, Lipopolysaccharide Receptors, Clinical Sciences, Public Health and Health Services, Virology
Abstract

BackgroundHIV infection and biomarkers of inflammation [measured by interleukin-6 (IL-6)], monocyte activation [soluble CD14 (sCD14)], and coagulation (D-dimer) are associated with morbidity and mortality. We hypothesized that these immunologic processes mediate (explain) some of the excess risk of mortality among HIV infected (HIV+) versus uninfected people independently of comorbid diseases.MethodsAmong 2350 (1521 HIV+) participants from the Veterans Aging Cohort Study Biomarker Cohort (VACS BC), we investigated whether the association between HIV and mortality was altered by adjustment for IL-6, sCD14, and D-dimer, accounting for confounders. Participants were followed from date of blood draw for biomarker assays (baseline) until death or July 25, 2013. Analyses included ordered logistic regression and Cox Proportional Hazards regression.ResultsDuring 6.9 years (median), 414 deaths occurred. The proportional odds of being in a higher quartile of IL-6, sCD14, or D-dimer were 2-3 fold higher for viremic HIV+ versus uninfected people. Mortality rates were higher among HIV+ compared with uninfected people [incidence rate ratio (95% CI): 1.31 (1.06 to 1.62)]. Mortality risk increased with increasing quartiles of IL-6, sCD14, and D-dimer regardless of HIV status. Adjustment for IL-6, sCD14, and D-dimer partially attenuated mortality risk among HIV+ people with unsuppressed viremia (HIV-1 RNA ≥10,000 copies per milliliter) compared with uninfected people-hazard ratio (95% CI) decreased from 2.18 (1.60 to 2.99) to 2.00 (1.45 to 2.76).ConclusionsHIV infection is associated with elevated IL-6, sCD14, and D-dimer, which are in turn associated with mortality. Baseline measures of these biomarkers partially mediate excess mortality risk among HIV+ versus uninfected people.

Published
2016

36. Isolated Hepatitis B Core Antibody is Associated With Advanced Hepatic Fibrosis in HIV/HCV Infection But Not in HIV Infection Alone

Author

Bhattacharya, Debika, Tseng, Chi-hong, Tate, Janet P, Re, Vincent Lo, Gibert, Cynthia L, Butt, Adeel A, Brown, Sheldon T, Lim, Joseph K, Rodriguez-Barradas, Maria C, Rimland, David, Kaufman, Erica, Justice, Amy C, and Goetz, Matthew Bidwell

Subjects
Medical Microbiology, Biomedical and Clinical Sciences, Immunology, Good Health and Well Being, Adult, Aspartate Aminotransferases, CD4 Lymphocyte Count, Coinfection, Cross-Sectional Studies, Female, HIV Infections, Hepatitis B Antibodies, Hepatitis B Core Antigens, Hepatitis B Surface Antigens, Hepatitis B virus, Hepatitis C, Humans, Liver Cirrhosis, Male, Middle Aged, Platelet Count, Veterans, Viremia, Clinical Sciences, Public Health and Health Services, Virology, Clinical sciences, Epidemiology, Public health
Abstract

HIV+/HCV+ persons with isolated HBcAb have a higher prevalence of advanced fibrosis than persons who are non-immune to HBV, who have resolved HBV, or who are HbsAb+ only.

Published
2016

37. Higher dose corticosteroids in patients admitted to hospital with COVID-19 who are hypoxic but not requiring ventilatory support (RECOVERY)

Author

Obbina Abani, Ali Abbas, Fatima Abbas, Joshua Abbas, Kasim Abbas, Mustafa Abbas, Sadia Abbasi, Hakam Abbass, Alfie Abbott, Alison Abbott, Nabeel Abdallah, Ammar Abdelaziz, Ashraf Abdelaziz, Mohamed Abdelfattah, Bushra Abdelqader, Audrey Abdul, Basir Abdul, Siddiqui Abdul, Althaf Abdul Rasheed, Ajibode Abdulakeem, Rezan Abdul-Kadir, Abdullah Abdullah, Abdulfatahi Abdulmumeen, Rasheed Abdul-Raheem, Niyaz Abdulshukkoor, Kula Abdusamad, Yazeed Abed El Khaleq, Mai Abedalla, Abeer Abeer Ul Amna, Lynn Abel, Katrina Abernethy, Movin Abeywickrema, Chandra Abhinaya, Affyarsyah Abidin, Adebanke Aboaba, Abigail Aboagye-Odei, Christopher Aboah, Heba Aboelela, Hani Abo-Leyah, Karim Abouelela, Ahmed Abou-Haggar, Mahmoud Abouibrahim, Ahmed Abousamra, Mona Abouzaid, Miriam Abraham, Tizzy Abraham, Abraheem Abraheem, Judith Abrams, Rebecca Abrams, Hyacinth-John Abu, Ahmed Abu-Arafeh, Syed M Abubacker, Akata Abung, Yousuf Abusamra, Yaa Aceampong, Amaka Achara, Devikumar Acharya, Faustina Acheampong, Prince Acheampong, Sarah Acheampong, Janet Acheson, Shiella Achieng, Andres Acosta, Rebecca Acquah, Catherine Acton, Jacqueline Adabie-Ankrah, Paul Adair, Fiona Adam, Matthew Adam, Huzaifa Adamali, Marta Adamczyk, Carol Adams, Charlotte Adams, Daniel Adams, Kate Adams, Laura Adams, Nikkita Adams, Richard Adams, Tim Adams, Laura Adamu-Ikeme, Krishma Adatia, Kirsty Adcock, Lawrence Addai-Boampong, Afua Addo, Oluwatobi Adeagbo, Ade Adebiyi, Ogunlana Adedeji, Yewande Adegeye, Ken Adegoke, Vicki Adell, Sherna Adenwalla, Femi W Adeoye, Oluwasegun A Adesemoye, Emmanuel O Adewunmi, Adedamola Adeyanju, Joyce Adeyemi, Tenifayo Adeyemo, Binay Adhikari, Shanti A Adhikari, Rina Adhikary, Adhikarla Aditya, Patience Adjepong, Gabrielle Adkins, Adnan Adnan, Marguerite Adriaanse, John Aeron-Thomas, Debbie Affleck, Carmel Afnan, Muhammad Afridi, Patricia Afrim, Felicia Akua Afriyie, Zainab A Aftab, Meenakshi Agarwal, Rachel Agbeko, Chris Agbo, Sunil Aggarwal, Arameh Aghababaie, Laura Aguilar Jimenez, Jacqueline Afrakomah Agyekum, Kwame Agyen, Shafana Ahamed Sadiq, Mohamed H Ahammed Nazeer, Mohammad Ahmad, Syed Ahmad, Afshan Ahmed, Ashar Ahmed, Asim Ahmed, Basheer A R Ahmed, Bilal Ahmed, Forizuddin Ahmed, Hamze Ahmed, Hanad Ahmed, Irshad Ahmed, Khaled Ahmed, Khalil Ahmed, Liban Ahmed, Mahin Ahmed, Maria C Ahmed, Muhammad S Ahmed, Naseer Ahmed, Nausheen Ahmed, Osama Ahmed, Rajia A Ahmed, Rawya Ahmed, Rizwan Ahmed, Saif Ahmed, Sammiya Ahmed, Sana G Ahmed, Syed Ahmed, Syed H Ahmed, Roa Ahmed Ali, Bilal Ahmed Mohamud, Sana Ahmed, Sana Ahmer, Augustine Ahonia, Christine Aiken, Dhiraj Ail, Mark Ainsworth, Myriam Aissa, Lindianne Aitken, Bini Ajay, Abdulakeem Ajibode, Ayesha Ajmi, Nasim Akhtar, Nauman Akhtar, Suha Akili, Bolutito Akinbiyi, Oludoyinsola Akindolie, Yinka Akinfenwa, Olugbenga Akinkugbe, Ibrahim Akinpelu, Mohammad Akram, Olugbenro Aktinade, Uzayr Akudi, Ahmad S A R Al Aaraj, Asma Al Balushi, Majd Al Dakhola, Aladdin Al Swaifi, Eslam Al-Abadi, Adegoke Alabi, Narendra Aladangady, Mohamed Alafifi, Ayaz Alam, Sajid Alam, Abbas Al-Asadi, Kyriaki Alatzoglou, Paul Albert, Albertus Albertus, Lorraine Albon, Angela Alcala, Gemma Alcorn, Stephen Alcorn, Aggie Aldana, David Alderdice, Abdullah Aldesouki, Rayan Aldouri, Jonathan Aldridge, Nicolas Aldridge, Ram Maya Ale, Ana Alegria, Alison Alexander, Courtney Alexander, John Alexander, Peter D G Alexander, Julyan Al-fori, Laith Alghazawi, Osama Alhabsha, Bahij Al-Hakim, Rafil Alhameed, Mohammed Al-Hayali, Shams Al-Hity, Ali Ali, Amanda Ali, Asad Ali, Fawzia R Ali, Jawad Ali, Mariam Ali, Mohamed Ali, Mohammad Ali, Muhammad S Ali, Nayab Ali, Oudai Ali, Ramla Ali, Sakina Ali, Syed Ali, Emilio Aliberti, Jade Alin, Abid Alina, Analyn Alipustain, Bachti Alisjahbana, Fine Aliyuda, Katrin Alizadeh, Maithem Al-Jibury, Saba Al-Juboori, Majid Al-Khalil, Abdullah Alkhudhayri, Moutaz Alkhusheh, Fiona Allan, Nataliya Allan, Alison Allanson, Robert Allcock, Eireann Allen, Jade Allen, Kerry Allen, Louise Allen, Poppy Allen, Rebecca Allen, Sam Allen, Sharon Allen, Simon Allen, Tania Allen, Abiola Alli, Kathryn Allison, Bethan Allman, Helen K Allsop, Lynne Allsop, David Allsup, Amal F T Almahroos, Hassan Al-Moasseb, Magda Al-Obaidi, Lina Alomari, Akram Al-Rabahi, Bahar Al-Ramadhani, Zayneb Al-Saadi, Riyam Al-Sammarraie, Inji Alshaer, Rustam Al-Shahi Salman, Warkaq Al-Shamkhani, Fadia Alsheikh, Bashar Al-Sheklly, Sara Altaf, Amanda Alty, Mary Alvarez, Maria Alvarez Corral, Edward Alveyn, Maysaa Alzetani, Susan Amamou, Noor Amar, Sakkarai Ambalavanan, Robert Ambrogetti, Chris Ambrose, Amir Ameen, Amel Amelia Ganefianty, Katharine Ames, Maria R Amezaga, Allison Amin, Amina Amin, Kanish Amin, Syed Amin, Tara Amin, Badshah Amit, Amjad Amjad, Neelma Amjad, James Amoah-Dankwa, Victoria Amosun, Muhammad Amsal, Khaled Amsha, John Amuasi, Noelia Amutio Martin, Pugh Amy, Ann Anada, Atul Anand, Samantha Anandappa, Satya D Anantapatnaikuni, Ellen Anderson, Julie Anderson, Laura Anderson, Marina Anderson, Michelle 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Souza, Anthony De Soyza, Natasha de Vere, Johannes de Vos, Bethan Deacon, Sharon Dealing, Anna Dean, Julie Dean, Katrina Dean, Stephen Dean, Tessa Dean, Jill Deane, James Dear, Effie Dearden, Catherine Deas, Samuel Debbie, Gabor Debreceni, Vashist Deelchand, Matthew Deeley, Joanne Deery, Emmanuel Defever, Manuela Del Forno, Arnold Dela Rosa, Gonzalo De-La-Cedra, Amanda Dell, Carrie Demetriou, David DeMets, Jane Democratis, Jacqueline Denham, Emmanuelle Denis, Laura Denley, Craig Denmade, Alexandra Dent, Kathy Dent, Martin Dent, Elise Denton, Tom Denwood, Nishigandh Deole, Darshita Depala, Maria Depante, Susan Dermody, Amisha Desai, Asmita Desai, Purav Desai, Sanjeev Deshpande, Vai Deshpande, Sirjana Devkota, Usha Devkota, Debbie Devonport, Matthew Devonport, Prakash Dey, Vishal Dey, Rogin Deylami, Kevin Dhaliwal, Sundip Dhani, Amandeep Dhanoa, Mili Dhar, Ankush Dhariwal, Dawpadee Dharmasena, Devesh Dhasmana, Ekanjali Dhillon, Reiss Dhillon, Syra Dhillon, Meghnath Dhimal, Dipali Dhiru, Trupti Dhorajiwala, Priya Dias, Stephanie Diaz, Kayleigh Diaz-Pratt, Mohammed Dibas, Debbie Dickerson, Pamela Dicks, Matt Dickson, Stuart Dickson, J Digby, Ronneil Digpal, Sean Dillane, Sarah Diment, Paul Dimitri, Georgios Dimitriadis, Sajeel Din, Thai H Dinh, Thi T T Dinh, Alex Dipper, Sabiq Dipro, Laura Dirmantaite, Lorelle Dismore, Lisa Ditchfield, Sarah Diver, Lavanya Diwakar, Preeti Diwan, Caroline Dixon, Giles Dixon, Kate Dixon, Brice Djeugam, Sipho Dlamini, Petr Dlouhy, Andrea D'Mello, Paul Dmitri, Thi Tien Do, Laurence Dobbie, Marinela Dobranszky Oroian, Charlotte Dobson, Lee Dobson, Marie Docherty, David Dockrell, Jacqueline Dodd, James Dodd, Jackie Dodds, Rebecca Dodds, Steve Dodds, Richi Dogra, Conor Doherty, Erin Doherty, Warren Doherty, Yumiko Doi, Iain Doig, Eleanor Doke, Daniel Dolan, Mark Dolman, Rozzie Dolman, Lisa Donald, Katie Donald, Callum Donaldson, Christopher Donaldson, Denise Donaldson, Gillian Donaldson, Kate Donaldson, Phu Khiem Dong, Martha Donkor, Sinead Donlon, Joanne Donnachie, Eilish Donnelly, Ronan Donnelly, Phil Donnison, Aravindhan Donohoe, Gemma Donohoe, Bryan Donohue, Emma Dooks, Reece J Doonan, Rogier Van Doorn, Grainne Doran, Rachael Dore, Kane Dorey, Sharon Dorgan, Kataryna Dos Santos, Moonira Dosani, Davinder Dosanjh, Paula Dospinescu, Isabelle Doss, Theonymfi Doudouliaki, Andrew Dougherty, Jill Doughty, Katie Douglas, Jonathan Douse, Allyn Dow, Lucy Dowden, Michelle Dower, Sud Dowling, Nicola Downer, Charlotte Downes, Rob Downes, Thomas Downes, Damian Downey, Robert Downey, Caroline Downing, Louise Downs, Simon Dowson, Cornel Dragan, Cristina Dragos, Maire Drain, Chelsea Drake, Victoria Drew, Olivia Drewett, Anthony Drexel, Celine Driscoll, Helena Drogan, Odysseas Drosos, Graham Drummond, Katie Drury, Kay Druryk, Ronald Druyeh, Jack Dryburgh-Jones, Simon Drysdale, An Du Thinh, Hazel Dube, Judith Dube, Stephen Duberley, Paige K Duckenfield, Hayley Duckles-Leech, Nicola Duff, Emma Duffield, Heather Duffy, Helen Duffy, Katharine Duffy, Lionel Dufour, Annette Duggan, Parveen Dugh, Rauand Duhoky, Janice Duignan, Jennifer Dulay, Simon Dummer, Alexis Duncan, Andrew Duncan, Christopher Duncan, Fullerton Duncan, Gregory Duncan, Holly Duncan, Robert Duncan, Stephanie Dundas, Do Van Dung, Aileen Dunleavy, Julia Dunleavy, Alessia Dunn, Charlotte Dunn, Damian Dunn, Laura Dunn, Paul Dunn, Charlene Dunne, Karen Dunne, Fiona Dunning, Aidan Dunphy, Tran Thi Hai Duong, Venkat Duraiswamy, Beatriz Duran, Ingrid DuRand, Leanne Durdle, Natalie Duric, Alison Durie, Emily Durie, Samuel Durogbola, Chris Durojaiye, Laura Durrans, Katie Durrant, Hannah Durrington, Iheukwumere Duru, Haris Duvnjak, Akshay Dwarakanath, Laasya Dwarakanath, Dennis Dwomoh Nkrumah, Ellen Dwyer, Zara Dyar, Claudia Dyball, Kristyn Dyer, Harvey Dymond, Tom Dymond, Chris Eades, Lauren Eadie, Rebekah Eadie, Laura Eagles, Beena Eapen, Naomi Earl, Joanne Early, Melissa Earwaker, Nicholas Easom, Clare East, Amy Easthope, Fraser Easton, Jack Easton, Patrick Easton, Ruth Eatough, Oluwadamilola Ebigbola, Martin Ebon, Alison Eccles, Sinan Eccles, Chloe Eddings, Michael Eddleston, Maureen Edgar, Katharine Edgerley, Nicholas Edmond, Mary Edmondson, Tracy Edmunds, Abby Edwards, Alexandra Edwards, Catherine Edwards, Joy Edwards, Kennedy Edwards, Mandy Edwards, Martin Edwards, Sophie Edwards, Jenny Eedle, Aline Eggink, Dawn Egginton, Sam Eggleston, Loveth Ehiorobo, Sarah Eisen, Ugochukwu Ekeowa, Mohamed Ekoi, Ayomide Ekunola, Soha El Behery, Nagla Elashhar, Lisa Elawamy, Mohamed Elbeshy, Kate El-Bouzidi, Jennifer Elder, Mohammed El-Din, Emma Eldridge, Diana Eleanor, Uchenna Elenwa, Ibrahim Eletu, Eman Elfar, Mayy Magdy Elgamal, Amr Elgohary, Mohamed A A Elhadi, Stellios Elia, Jennifer Elias, Tania Elias, Nadia Elkaram, Andrew V Elkins, Julie Ellam, Nikki Ellard, Laura N Ellerton, Lucy Elliot, Amy Elliott, Fiona Elliott, Kerry Elliott, Scott Elliott, Sian Elliott, Annie Ellis, Christine Ellis, Kaytie Ellis, Leila Ellis, Rupert Ellis, Tak-Yan Ellis, Yvette Ellis, Alison C Ellwood, Rahma Elmahdi, Einas Elmahi, Hannah-May Elmasry, Mohammed El-Naggar, Najla Elndari, Omer Elneima, Mohamed Elokl, Ahmed Elradi, Mohamed Elsaadany, Mohammed A S A Elsayed, Sally El-Sayeh, Hana El-Sbahi, Mohammad Elsebaei, Tarek Elsefi, Karim El-Shakankery, Alguili Elsheikh, Hosni El-Taweel, Sarah Elyoussfi, Jonathan Emberey, Jonathan R Emberson, John Emberton, Anna Emery, Julian Emmanuel, Ingrid Emmerson, Michael Emms, Florence Emond, Marieke Emonts, Nicu Enachi, Dickson Enenche, Angila Engden, Katy English, Emma Entwistle, Hene Enyi, Marios Erotocritou, Peter Eskander, Hanif Esmail, Fatheha Essa, Brynach Evans, Chris Evans, Debra Evans, E Evans, Emrys Evans, Gail Evans, Gareth Evans, Isabel Evans, Jack Evans, Jacqueline Evans, Jennifer Evans, John Evans, Jolanta Evans, Lisa Evans, Lynn Evans, Mim Evans, Morgan Evans, Ranoromanana Evans, Sharon Evans, Sian Evans, Teriann Evans, Tomos Evans, Caroline Everden, Serenydd Everden, Lynette Every, Hayley Evison, Lynsey Evison, Chiamaka Ezenduka, Jacqueline Faccenda, Leila Fahel, Youstina Fahmay, Ian Fairbairn, Sara Fairbairn, Terry Fairbairn, Andy Fairclough, Louise Fairlie, Mark Fairweather, Anne Fajardo, Naomi Falcone, Euan Falconer, John Fallon, Andrea Fallow, David Faluyi, Victoria Fancois, Ayaan Farah, Muna Farah, Qayyum Farah, Nowin Z Fard, Leila Fares, Amr Farg, Adam Farmer, Katie Farmer, Toni Farmery, Samantha Farnworth, Faiyaz Farook, Hadia Farooq, Sidrah Farooq, Fiona Farquhar, Holly Farr, Aaron Farrell, Barbara Farrell, Fayed Farrukh, James Farthing, Syeda Farzana, Rahmatu Fasina, Azam Fatemi, Mina Fatemi, Suman Fathima, Nibah Fatimah, Maria Faulkner, Saul N Faust, Clair Favager, Joe Fawke, Sinmidele Fawohunre, Abul Fazal, Aisthath Fazleen, Simon Fearby, Connie Fearnley, Alex Feben, Federico Fedel, Daria Fedorova, Christopher Fegan, Mae Felongo, Lynsey Felton, Tim Felton, Kate Fenlon, Andrea Fenn, Ruth Fennelly, Isabelle Fenner, Ciara Fenton, Melisa Fenton, Gloria Ferenando, Cameron Ferguson, Jenny Ferguson, Kathryn Ferguson, Katie Ferguson, Susan Ferguson, Susie Ferguson, Victoria Ferguson, Denzil Fernandes, Candida Fernandez, Eduardo Fernandez, Maria Fernandez, Sonia Fernandez Lopez, Jaime Fernandez Roman, Callum J Fernando, Jessica Fernando, Ahmed Feroz, Pietro Ferranti, Thais Ferrari, Eleanor Ferrelly, Alexandra Ferrera, Emma Ferriman, Sheldon Ferron, Nicholas Fethers, Ben Field, Janet Field, Rebecca Field, Karen Fielder, Lindsey Fieldhouse, Andra Fielding, Julie Fielding, Sarah Fielding, Asma Fikree, Santos Filipa, Sarah A Filson, Shona Finan, Sarah Finbow, Deborah J Finch, Joanne Finch, Laurie Finch, Simon Finch, Spencer Finch, Natalie Fineman, Jim Finlayson, Lauren Finlayson, Adam Finn, Joanne Finn, Dylan Finnerty, Clare Finney, Deborah Finucane, Sofia Fiouni, Jo Fiquet, Promise Firi, James Fisher, Neil Fisher, Daniel Fishman, Krystofer Fishwick, Carolyn Fitton, Felicity Fitzgerald, Fiona Fitzgerald, Karen Fitzjohn, Jan Flaherty, Michael Flanagan, Charles Flanders, Nikolaos Flaris, Gail Fleming, Julie Fleming, Lucy Fleming, Paul Fleming, William Flesher, Alison Fletcher, Anna Fletcher, Jonathan Fletcher, Lucy Fletcher, Simon Fletcher, Sophie Fletcher, Fiona Flett, Karen Flewitt, Sarah Flockhart, Christopher Flood, Ian Floodgate, Jonathan Flor, Vincent Florence, Mary Flowerdew, Sharon Floyd, Margaret J Flynn, Rachel Flynn, Claire Foden, Adama Fofana, Georgina Fogarty, Paul Foley, Linda Folkes, Tracey Fong, Daniela M Font, Aiwyne Foo, Jane Foo, Andrew Foot, Helen R Foot, Jayne Foot, Jane Forbes, Amber Ford, Jamie Ford, Imogen Fordham, Jennifer Foreman, Matthew Forester, Mohammad Forkan, Caroline Fornolles, Adam Forrest, Ellie Forsey, Miranda Forsey, Thomas Forshall, Elliot Forster, Abigail Forsyth, Julian Forton, Conrad Foster, Emily Foster, Joseph Foster, Rachel A Foster, Tracy Foster, Angela Foulds, Ian Foulds, Folakemi Fowe, Natasha Fowkes, Emily Fowler, Robert Fowler, Stephen Fowler, Amy Fox, Claire Fox, Heather Fox, Jonathan Fox, Laura Fox, Lauren Fox, Natalie Fox, Olivia Fox, Simon Fox, Sarah-Jane Foxton, Eva Fraile, Rebecca Frake, Alex Francioni, Olesya Francis, Rebecca Francis, Sarah Francis, Theodora Francis-Bacon, Helen Frankland, Jessica Franklin, Siobhan Franklin, Catherine Fraser, Andi Fratila, Sharon Frayling, Martyn Fredlund, Anna Freeman, Carol Freeman, Elaine Freeman, Hannah Freeman, Nicola Freeman, Clare Freer, Eleanor French, Thomas French, Karen Freshwater, Matthew Frise, Renate Fromson, Adam Frosh, John Frost, Victoria Frost, Oliver Froud, Rachel Frowd, Arun Fryatt, Andrzej Frygier, Bridget Fuller, Liz Fuller, Lucy Fuller, Tracy Fuller, Duncan Fullerton, Carrie Fung, Gayle Fung, Sarah Funnell, John Furness, Andrew Fyfe, Nytianandan G, Elizabeth Gabbitas, Claire Gabriel, Zoë Gabriel, Hadiza Gachi, Sophie Gaffarena, Sarah Gage, Joshua Gahir, Sarveen Gajebasia, Katarzyna Gajewska-Knapik, Babita Gajmer, Zacharoula Galani, Christopher Gale, Hugo Gale, Linda Gale, Rebecca Gale, Swetha Gali, Bernadette Gallagher, Jude Gallagher, Rosie Gallagher, William Gallagher, Feroze Gallam, Joanne Galliford, Catherine Galloway, Chris Galloway, Emma Galloway, Jacqui Galloway, James Galloway, Anna Galvin, Victoria Galvis, Gareth Gamble, Laura Gamble, Liz Gamble, Brian Gammon, Chien N Gan, Muhammad B Ganaie, Jaikumar Ganapathi, Ramesh Ganapathy, Kaminiben Gandhi, Sarah Gandhi, Usha Ganesh, Thenugan Ganeshanathan, Saibal Ganguly, Abrar Gani, Pauline Ganley, Ukraina Garcia, Emma-James Garden, Antoni D Gardener, Emma Gardiner, Michael Gardiner, Phil Gardiner, Siobhan Gardiner, Caroline Gardiner-Hill, Jonathan Gardner, Louis Gardner, Mark Garfield, Atul Garg, Isha Garg, Nathan Garlick, Daniel Garner, Justin Garner, Lucie Garner, Zoe Garner, Rosaline Garr, Kathryn A Garrero, Manisha Gartaula, Florence Garty, Rachel Gascoyne, Hyeriju Gashau, Aoife Gatenby, Erin Gaughan, Alok Gaurav, Mariana Gavrila, Jane Gaylard, Sophie Gayle, Catherine Geddie, Ian Gedge, Sarah Gee, Fartuun Geele, Kalaichelvi Geerthan, Minnie Gellamucho, Karzan Gelly, Leila Gelmon, Sandra Gelves-Zapata, Gemma Genato, Neal Gent, Susan Gent, Natalie Geoghegan, Aparna George, Bini George, Sam George, Susan George, Tina George, Valerie P George, Simon Georges, Domonique Georgiou, Peter Gerard, Leigh Gerdes, Louise Germain, Helen Gerrish, Abel Getachew, Louise Gethin, Siobhan Gettings, Hisham Ghanayem, Bijan Ghavami Kia, Shaista Ghazal, Anca Gherman, Alison Ghosh, Dipansu Ghosh, Justin Ghosh, Subhamay Ghosh, Sarra Giannopoulou, Malick Gibani, Chris Gibb, Ben Gibbison, Kerry Gibbons, Alex Gibson, Bethan Gibson, Jamie Gibson, Kimberley Gibson, Kirsty Gibson, Sian Gibson, Mary Gigi, Cat Gilbert, Jeanette Gilbert, Kayleigh Gilbert, Benjamin Giles, James Gilham, Mandy Gill, Lynne Gill, Paul Gillen, Annelies Gillesen, Katherine Gillespie, Elizabeth Gillham, Andrew Gillian, Deborah Gilliland, Robert Gillott, Danielle Gilmour, Kate Gilmour, Lesley Gilmour, Louis Ginn, Franciscus Ginting, Theodora Giokanini-Royal, Anna Gipson, Barbie Giri, Joanna Girling, Rhian Gisby, Angelena Gkioni, Aikaterini Gkoritsa, Effrossyni Gkrania-Klotsas, Amy Gladwell, James Glanville, Jessica Glasgow, Susannah Glasgow, Jon Glass, Lynn Glass, Sharon Glaysher, Lisa Gledhill, Eleanor Glenday, Ana Glennon, Jodie Glossop, John Glover, Kyle Glover, Michelle Glover, Jan Glover Bengtsson, Deborah Glowski, Sharon Glynn, Chevanthy Gnanalingam, Julie Goddard, Wendy Goddard, Emily Godden, Jo Godden, Sarah Godlee, Emma Godson, Gillian Godwin, Sukanya Gogoi, Aiky Goh, Manjinder Gohel, Rebeca Goiriz, Sriya Gokaraju, Raphael Goldacre, Arthur Goldsmith, Portia Goldsmith, Darren Gomersall, Lucia Gomez, Raquel Gomez-Marcos, Ali Gondal, Celia Gonzalez, Jack Goodall, Vicky Goodall, Bob Goodenough, Anna Goodfellow, Laura Goodfellow, James Goodlife, Camelia Goodwin, Elizabeth Goodwin, Jayne Goodwin, Paula Goodyear, Rajiv Gooentilleke, Michelle Goonasekara, Sheila Gooseman, Shameer Gopal, Chris Gordon, Sally Gordon, Robin Gore, Hugh Gorick, Caitlin Gorman, Claire Gorman, Stuart Gormely, Maria Gorniok, Diana Gorog, Michelle Gorst, Thomas Gorsuch, Jayshreebahen Gosai, Rebecca Gosling, Sally Gosling, Georgina Gosney, Vanessa Goss, Dzintars Gotham, Naomi Gott, Elizabeth Goudie, Nicole Gould, Susan Gould, Charlotte Goumalatsou, Lysander Gourbault, Abha Govind, Rajesh Govindan, Sharon Gowans, Girish Gowda, Rohit Gowda, Hannah Gower, Pankaj Goyal, Sunil Goyal, Sushant Goyal, Cheryl Graham, Clive Graham, Jonathan Graham, Justin Graham, Libby Graham, Rachel Graham, Sharon Graham, Matthew Graham-Brown, Julia Grahamslaw, Gianluca Grana, Tracyanne Grandison, Louis Grandjean, Alison Grant, Ann Grant, David Grant, Kirstie Grant, Matthew Grant, Pauleen Grant, Rhys Gravell, Jenny Graves, Alasdair Gray, Catherine Gray, Georgina Gray, Glaxy Gray, Jackie Gray, Karen Gray, Nicola Gray, Roxanne Gray, Sebastian Gray, Alan Grayson, Fiona Greaves, Paul Greaves, Alastair Green, Amy Green, Amy S Green, Charlotte Green, Christopher A Green, David Green, Frederick Green, Joel Green, Marie Green, Nicola Green, Stacey Green, Diarra Greene, Philippa Greenfield, Alan Greenhalgh, Daniel Greenwood, Sandra Greer, James Gregory, Jane Gregory, Katie Gregory, Tamsin Gregory, Jill Greig, Julia Greig, Rebecca Grenfell, Teena Grenier, Jack Grenville, Jo Gresty, Susan Grevatt, Glaxy Grey, Samuel Gribben, Andrew Gribbin, Amy Gribble, Natasha Grieg, Douglas Grieve, Ben Griffin, Denise Griffin, Mel Griffin, Sian Griffith, Andrew Griffiths, Daniel Griffiths, David Griffiths, Donna Griffiths, Isabel Griffiths, Mark Griffiths, Nicola Griffiths, Oliver Griffiths, Sandra Griffiths, Sarah Griffiths, Scott Griffiths, Yvonne Griffiths, Sofia Grigoriadou, Steph Grigsby, Paul Grist, Evelina Grobovaite, Dorothy Grogono, Clarissa Grondin, Rachel Groome, Pauline Grose, Liliana Grosu, Jenny Grounds, Margaret Grout, Helen Grover, Jayne Groves, Neil Grubb, Julie Grundy, Francesca Guarino, Sharada Gudur, Jacinta Guerin, Sharazeq Guettari, Shivang Gulati, Vikas Gulia, Harsha Gunasekara, Pumali Gunasekera, Malin Gunawardena, Kirun Gunganah, Jessica Gunn, Emma Gunter, Anup Kumar Gupta, Alok Gupta, Atul Gupta, Rajeev Gupta, Richa Gupta, Rishi Gupta, Tarun Gupta, Vineet Gupta, Ankur Gupta-Wright, Victoria Guratsky, Alvyda Gureviciute, Sambasivarao Gurram, Anju Gurung, Bhawana Gurung, Lilly Gurung, Shraddha Gurung, Sabi Gurung Rai, Hazel Guth, Nick Guthrine, Pradip Gyanwali, Sushma Gyawali, Nam Xuan Ha, Nguyen Thanh Ha, Ruth Habibi, Berkin Hack, James Hackett, Pamela Hackney, Christian Hacon, Aiman Haddad, Denise Hadfield, Nicholas Hadfield, Sally Hadfield, Michalis Hadjiandreou, Nikolaos Hadjisavvas, Anna Haestier, Nauman Hafiz, Rana Hafiz-Ur-Rehman, Javed Hafsa, Samantha Hagan, Jack W Hague, Rosemary Hague, Nafeesah Haider, Kate Haigh, Victoria Haile, Jessica Hailstone, Christina Haines, Scott Hainey, Morton Hair, Brigid Hairsine, Juraj Hajnik, Danielle Hake, Lukman Hakeem, Anne Haldeos, Writaja Halder, Emily Hale, Jennie Hale, Carmel Halevy, Paul Halford, William Halford, Alaina Halim, Alistair Hall, Anthony Hall, Claire Hall, Elizabeth Hall, Fiona Hall, Helen Hall, Jennifer Hall, Kathryn Hall, Laura Hall, Jan Hallas, Kyle Hallas, Charles Hallett, Jackie Halliday, Akmal Hallman, Heather Halls, Maryam Hamdollah-Zadeh, Ifedadepo A Hamed-Adekale, Bilal Hameed, Mohammed Hameed, Raph L Hamers, Imran Hamid, Mohamad Hamie, Raymond Hamill, Bethany Hamilton, Fergus Hamilton, Gus Hamilton, Leigh Hamilton, Melanie Hamilton, Nicola Hamilton, Sara Hamilton, Ruth Hamlin, Eleanor Hamlyn, Beatrice Hammans, Shirley Hammersley, Kate Hammerton, Bev Hammond, Emily Hammond, Leah Hammond, Sally Hammond, Fiona Hammonds, Ibrahim Hamoodi, Karen Hampshire, James A Hampson, Jude Hampson, Lucy Hampson, Lisa Hamzah, Jenny Han, Ozan Hanci, Sadiyah Hand, Lala Handayani, Jasmine Handford, Soran Handrean, Nina K Handzewniak, Sarah Haney, Vu Thi Kim Hang, Sheharyar Hanif, E Hanison, Esther Hanison, Jennifer Hannah, Amy Hannington, Merhej Hannun, Aidan Hanrath, Helena Hanratty, Daniel Hansen, Anita Hanson, Ashley Hanson, Helen Hanson, Jane Hanson, Kathryn Hanson, Steve Hanson, Ala Haqiqi, Monjurul Haque, Henry Harcourt, Lesley Harden, Zoe Harding, Simon Hardman, Marc Hardwick, Gareth Hardy, Joanna Hardy, Yasmine Hardy, Kumar Haresh, Rachel Harford, Beverley Hargadon, James Hargraves, Carolyn Hargreaves, Alice Harin, Mohammed Haris, Edward Harlock, Paula Harman, Tracy Harman, Mark Harmer, Muhammad A Haroon, Charlie Harper, Heather Harper, James Harper, Peter Harper, Rosemary Harper, Sarah Harrhy, Kate Harrington, Sian Harrington, Yasmin Harrington-Davies, Jade Harris, Jess Harris, John Harris, Laura Harris, Marie-Clare Harris, Nichola Harris, Sophie Harris, David Harrison, Laura Harrison, Melanie Harrison, Olakunbi A Harrison, Rachael Harrison, Rowan Harrison, Susie Harrison, Thomas Harrison, Wendy Harrison, Elizabeth Harrod, Ciaran Hart, Dominic Hart, Jessica Hartley, Lisa Hartley, Rosemary Hartley, Ruth Hartley, Tom Hartley, William Hartrey, Phillipa Hartridge, Stuart Hartshorn, Alice Harvey, Angela Harvey, Anna Harvey, Max Harvey, Catherine Harwood, Helen Harwood, Zoe Harzeli, Brigitte Haselden, Kazi Hashem, Mohammed Hashimm, Tadaaki Hashimoto, Imranullah Hashmi, Jack Haslam, Zena Haslam, Grace Hasnip, Adil Hassan, Ali Hassan, Amro Hassan, Awab Hassan, Zeinab Hassan, Sapna Hassasing, Jane Hassell, Philip Hassell, Alex Hastings, Bethany Hastings, Janice Hastings, Sarah Hathaway-Lees, Jonathan Hatton, Jennifer Hau, May Havinden-Williams, Stefan Havlik, Daniel B Hawcutt, Kadean Hawes, Liz Hawes, Nicola Hawes, Lydia Hawker, Annie Hawkins, Joe Hawkins, Nancy Hawkins, W John Hawkins, Dan Hawley, Ed Hawley-Jones, Edward Haworth, Alasdair W Hay, Cathy Hay, Amna Hayat, Jamal Hayat, Mohamed-Riyal Hayathu, Anne Hayes, Jonas Hayes, Kate Hayes, Melony Hayes, Fiona Hayes, Patrick Hayle, Chloe Haylett, Antara Hayman, Melanie Hayman, Matthew Haynes, Richard Haynes, Rachel Hayre, Carole Hays, Sarah Haysom, James Hayward, Patrick Haywood, Hazel Haywood Hasford, Tracy Hazelton, Phoebe Hazenberg, Zhengmai He, Elizabeth Headon, Carrie Heal, Brendan Healy, Jessica L Healy, Amy Hearn, David Heasman, Angela Heath, Debbie Heath, Rowan Heath, Diane Heaton, Adam Heavens, Kerry Hebbron, Catherine Heckman, Gemma Hector, Sadie Heddon, Andy Hedges, Katrine Hedges, Cheryl Heeley, Elaine Heeney, Richard Heinink, Rajdeep Heire, Ingvild Helgesen, Joanne Hemingway, Ulla Hemmila, Beth Hemmings, Scott Hemphill, Deborah Hemsley, Abigail Henderson, Eilidh Henderson, Jennifer Henderson, Steven Henderson, Joanne Henry, Karol Henry, Lavinia Henry, Margo Henry, Natalie Henry, David Henshall, Gillian Herdman, Rosaleen Herdman-Grant, Morag Herkes, Lucas E Hermans, Fe Marie Hernandez, Emma Heron, Lisa Heron, William Herrington, Emilia Heselden, Peta Heslop, Tracey Heslop, Simon Hester, Emily Hetherington, Joseph Hetherington, Chamila Hettiarachchi, Pramodh Hettiarachchi, Hayley Hewer, John Hewertson, Anna Hewetson, Sue Hewins, Nicola Hewitson, Claire Hewitt, Davina Hewitt, Richard Hewitt, Samuel Hey, Robert S Heyderman, Mathis Heydtmann, Joseph Heys, Jonathan Heywood, Meg Hibbert, John Hickey, Naomi Hickey, Peter Hickey, Nicky Hickman, Alex Hicks, Jenny Hicks, Scott R Hicks, Phan Thi Thu Hien, Daniel Higbee, Lucy Higgins, Andrew Higham, Martin Highcock, Judith Highgate, Mondy Hikmat, Amanda Hill, Helen Hill, Joanne Hill, Lisa Hill, Lucy Hill, Phoebe Hill, Uta Hill, Annette Hilldrith, Catherine Hillman-Cooper, Jon Hilton, Zoe Hilton, Sarah Hinch, Andrew Hindle, Esther Hindley, Alice Hindmarsh, Paul Hine, Kim Hinshaw, Clare Hird, Claire Hirst, Lindsay Hirst, Jemma Hives, Htet M Hlaing, Benson Ho, David K K Ho, Rosemary Ho, Michaela Hoare, David Hobden, Gill Hobden, Maria Hobrok, Simon Hobson, Christopher Hodge, Simon Hodge, Lesley Hodgen, George Hodgetts, Holly Hodgkins, Sally Hodgkinson, David Hodgson, Helen Hodgson, Luke Hodgson, Sheila Hodgson, Gemma Hodkinson, Kenneth Hodson, Mike Hodson, Alison Hogan, Matthew Hogben, Lucy Hogg, Lee Hoggett, Abigail Holborow, Catherine Holbrook, Rebecca Holbrook, Catherine Holden, Jill Holden, Melinda Holden, Sophie Holden, Thomas Holder, Niels Holdhof, Hannah Holdsworth, Lisa Holland, Maureen Holland, Nicky Holland, Poppy Holland, Susan Holland, Marie L Hollands, Elizabeth Holliday, Kyra Holliday, Mark Holliday, Nina Holling, Laszlo Hollos, Nora Hollos, Leah Holloway, Simon Holloway, Max Hollowday, Marcus Hollyer, Amy Holman, Ann Holmes, Megan Holmes, Raphael Holmes, Rebecca Holmes, Kelly Holroyd, Beth Holroyd-Hind, Lyndsey Holt, Siobhan Holt, Susie Holt, Alexandra Holyome, Marie Home, Renate Homewood, Kate Hong, Louise Hoole, Clare Hooper, Samantha Hope, Susan Hope, Bridget Hopkins, Peter W Horby, Stephanie Horler, Anil Hormis, Daniel Hornan, Nicola Hornby, Thomas Horne, Zoey Horne, Rebecca Horner, Caroline Horrobin, Latoya Horsford, Megan Horsford, Mark Horsford, Valana Horsham, Alexander Horsley, Ashley Horsley, Elizabeth Horsley, Sarah Horton, Jane Hosea, Toby Hoskins, Muhammad S Hossain, Rashed Hossain, Maxine Hough, Sarah Hough, Catherine Houghton, Kathryn Houghton, Rebecca Houlihan, Kay Housely, Hamish Houston, Roseanna Hovvels, Lee How, Laura Howaniec, Joanne Howard, Kate Howard, Laura Howard, Linda Howard, Lucy Howard, Megan Howard, Sarah Howard, Stuart Howard, Richard Howard-Griffin, Louise Howard-Sandy, Serena Howe, Alice Howell, Mark Howells, Lyn Howie, Kerry Howlett, Sophie Howlett, Ruth Howman, Josh Hrycaiczuk, Hein Htet, Naing Z Htoon, Su Htwe, Ying Hu, Chiang O H Huah, Sylvia Huang, Kelly Hubbard, Abby Huckle, Shahzya Huda, Alison Hudak, Lisa Hudig, Heather Hudson, Suzanne Hudson, Oli Hudson, Alison Hufton, Connor Huggins, Alistair Hughes, Caitlin Hughes, Emma Hughes, Gareth Hughes, Heather Hughes, Luke Hughes, Martin Hughes, Rachel Hughes, Rebecca Hughes, Samantha Hughes, Stephen Hughes, Vikki Hughes, Wesley Hughes, Lukas Huhn, Ching Hui, Ruth Hulbert, Diana Hull, Grace Hull, Robert Hull, Amanda Hulme, Peter Hulme, Wendy Hulse, George Hulston, Ryan Hum, Megan Hume, Charlotte Humphrey, Alasdair Humphries, Amy Humphries, Joanne Humphries, Charlotte Hunt, Fiona Hunt, Jane Hunt, Jonquil Hunt, Kristen Hunt, Luke Hunt, Molly Hunt, Sophie Hunt, Alexandra Hunter, Catherine Hunter, Ewan Hunter, Karl Hunter, Neil Hunter, Ross Hunter, Sophie Hunter, George Huntington, Fuad Huq, Elizabeth Hurditch, Judith Hurdman, Cian Hurley, Katrina Hurley, Mohammed A Husain, Syeda Y Husaini, Coralie Huson, Afreen Hussain, Chreif Hussain, Ibraar Hussain, Ifza Hussain, Mohammad Hussain, Mohammed Hussain, Muhammad Hussain, Reda Hussain, Rizwana Hussain, Samia Hussain, Sanniah Hussain, Yasmin Hussain, Mohammed Hussam El-Din, Samahir F E M Hussein, Ziad Hussein, Rebecca Hussey, Adiel Haqiq Hussien, Anja Hutchinson, Camille Hutchinson, Dorothy Hutchinson, Elizabeth Hutchinson, John Hutchinson, Claire Hutsby, Paula Hutton, Nguyen Quang Huy, Thuong Huyen, Tran Bang Huyen, Nguyen Thi Huyen 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Elizabeth Wasson, Hazel J Watchorn, Holly Waterfall, Abby Waters, Donald Waters, Mark Waterstone, Abigail Watkin, Catherine Watkins, Catrin Watkins, Eleanor Watkins, Karen Watkins, Lynn Watkins, Abigail Watson, Adam J R Watson, Ekaterina Watson, Eleanor Watson, Felicity Watson, J G R Watson, Louisa Watson, Paul Watson, Rebecca Watson, Robert Watson, Kathleen Watson, Malcolm Watters, Donna Watterson, Khairiah Wattimena, Daniel Watts, John Watts, Merlin Watts, Victoria Waugh, Emma Wayman, Matthew Wayman, Akhlaq Wazir, Mark Weatherhead, Nick Weatherly, Chloe Webb, Claire Webb, Hayley Webb, Kathryn Webb, Kylie Webb, Stephen Webb, Cheryl Websdale, Deborah Webster, Ian Webster, Jemma Webster, Tim Webster, Jordan Wedlin, Ling Wee, Rebecca Weerakoon, Thanuja Weerasinghe, Janaka Weeratunga, Maria Weetman, Shuying Wei, Immo Weichert, Emma Welch, Hugh Welch, James Welch, Leanne Welch, Steven Welch, Benjamin Welham, Samantha Weller, Lucy Wellings, Brian Wells, Susan Wellstead, Berni Welsh, Richard Welsh, Ingeborg Welters, Rachael Welton, Victoria Wenn, Lauren Wentworth, Joan Wesonga, Kate Wesseldine, Joe West, Magdelena West, Raha West, Ruth West, Sophie West, Luke Western, Ruth Westhead, Heather Weston, Alice Westwood, Kelly Westwood, Sharon Westwood, Bill Wetherill, Sharon Wheaver, Helen Wheeler, Ben Whelan, Matthew Whelband, Amanda Whileman, Alison Whitcher, Andrew White, Ayesha White, Benjamin White, Catherine White, Christopher White, Duncan White, James White, Jonathan White, Katie White, Marie White, Nick White, Nikki White, Sarah White, Sonia White, Tracey White, Catherine Whitehead, Kelly Whitehorn, Anne Whitehouse, Claire Whitehouse, Tony Whitehouse, Julia Whiteley, Louiza Whiteley, Sophie Whiteley, Rachael Whitham, Gabriel Whitlingum, David Whitmore, Elizabeth Whittaker, Lindsay Whittam, Ashley Whittington, Helen Whittle, Robert Whittle, Eunice Wiafe, Lou Wiblin, Olivia Wickens, John Widdrington, Jason Wieboldt, Hannah Wieringa, Cornelia Wiesender, Laura Wiffen, Andrew Wight, Ashleigh Wignall, Christopher Wignall, Annamaria Wilce, Danielle Wilcock, Emma Wilcock, Louise Wilcox, Ben Wild, Laura Wild, Stephen Wild, Michael Wilde, Laura Wilding, Peter Wilding, Tracey Wildsmith, Joe Wileman, Joy Wiles, Kate Wiles, Elva Wilhelmsen, Thomas Wiliams, Janet Wilkie, David Wilkin, Hannah Wilkins, Joy Wilkins, Suzanne Wilkins, Iain Wilkinson, Lesley Wilkinson, Nicola Wilkinson, Sophia Wilkinson, Susan Wilkinson, Tim Wilkinson, Sylvia Willetts, Aimee Williams, Alexandra Williams, Alison Williams, Angharad Williams, Anna Williams, Ava Williams, Carl Williams, Caroline V Williams, Claire Williams, Dewi Williams, Eleri Williams, Gail Williams, Gemma Williams, Gina Williams, Hannah Williams, Heledd Williams, James Williams, Jennie Williams, Jill Williams, John Williams, Joseph Williams, Karen Williams, Kathryn Williams, Mandy Williams, Marie Williams, Mark Williams, Matthew Williams, Patricia Williams, Penny Williams, Rachel Williams, Robin Williams, Rupert Williams, Samson Williams, Sarah Williams, Sophie Williams, Steffan Williams, Tamanna Williams, Tania Williams, Annie Williamson, Cath Williamson, Catherine Williamson, Dawn Williamson, James D Williamson, Jodie Williamson, Rachel Williamson, Helen Williamson, Elaine Willis, Elizabeth Willis, Emily Willis, Heather Willis, Herika Willis, Joanna Willis, Louise Wills, Lucy Willsher, Catherine Willshire, Francesca Willson, Jayne Willson, Alison Wilson, Andrea Wilson, Anna Wilson, Antoinette Wilson, Billy Wilson, David Wilson, Imogen Wilson, James Wilson, Karen Wilson, Kate Wilson, Kristy-Ann Wilson, Lucinda Wilson, Mark Wilson, Stephen Wilson, Toni Wilson, John Wilson, Khin Lei Yee Win, Marlar Win, Than Win, Tin Tin Win, Wut Yee Win Win, Lucinda Winckworth, Laura Winder, Piers Winder, Stuart Winearl, Helen Winmill, Simon Winn, Carmen Winpenny, Helen Winslow, Helen Winter, Jonathan Winter, Barbara Winter-Goodwin, Joseph Winterton, Hannah Winwood, Jack Wischhusen, Stephen Wisdom, Matthew Wise, Martin Wiselka, Rebecca Wiseman, Sophie Wiseman, Steven Wishart, Tabitha WIshlade, Eric Witele, Nicholas Withers, Janet Wittes, Donna Wixted, Therese Wodehouse, Will Wolf, Nicola Wolff, Kirsten Wolffsohn, Rebecca Wolf-Roberts, Elena Wolodimeroff, Adam Wolstencroft, Alan Wong, Charlotte Wong, Chi-Hung Wong, Chi-Man Wong, Edwin Wong, Jessica S Y Wong, Kit Y Wong, Mei Yin Wong, Nick Wong, Sam Wong, Ting Wong, Aaron B Wongkyezeng, Amanda Wood, Caroline Wood, Dianne Wood, Fiona Wood, Gordon Wood, Hannah Wood, Jennifer Wood, Joe Wood, Lisa Wood, Louise Wood, Madeleine Wood, Stephen Wood, Tracy Wood, Katharine Woodall, Rebecca Woodfield, Christopher Woodford, Elizabeth Woodford, Jill Woodford, Louise Woodhead, Timothy Woodhead, Philip Woodland, Marc Woodman, Myles Woodman, Stephen Woodmansey, Charlotte Woods, Jane Woods, Katherine Woods, Sarah Woods, Zoe Woodward, Megan Woolcock, Gemma Wooldridge, Rebecca Woolf, Chris Woollard, Christopher Woollard, Louisa Woollen, Emma Woolley, Jade Woolley, Daniel Woosey, Dan Wootton, Joanne Wootton, Daniel Worley, Stephy Worton, Jonathan Wraight, Maria Wray, Kim Wren, Lynn Wren, Caroline Wrey Brown, Catherine Wright, Demi Wright, Francesca Wright, Holly Wright, Imogen Wright, Lianne Wright, Rachel Wright, Sarah Wright, Stephanie Wright, Tim Wright, Caroline Wroe, Hannah Wroe, Henry Wu, Peishan Wu, Pensee Wu, Jonathan Wubetu, Fitria Wulandari, Retno Wulandari, Subie Wurie, Craig Wyatt, Frederick Wyn-Griffiths, Inez Wynter, Bindhu Xavier, Arnold Xhikola, Bingru E Xia, Zhongyang Xia, Effua Yacoba, Santosh Yadav, Masseh Yakubi, May Yan, Yuuki Yanagisawa, Freda Yang, Yingjia Yang, Michael Yanney, Woei Lin Yap, Nabil Yaqoob, Salima Yasmin, Bryan Yates, David Yates, Edward Yates, Helen Yates, Thomas Yates, Mark Yates, Jessica Ye, Charlotte Yearwood Martin, Khin Yein, Fiona Yelnoorkar, Lam Minh Yen, Alastair Yeoh, Chun Yu Yeung, Peter Yew, Durgesh Yewatkar, Laura Ylquimiche Melly, Inez Ynter, H Yong, Jemma Yorke, Jasmine Youens, Abdel Younes Ibrahim, Eoin Young, Gail Young, Louise Young, Asfand Yousafzar, Sajeda Youssouf, Ahmed Yousuf, Hartantri Yovita, Chrissie Yu, Jack S J Yuan, Nindya Yufaniaputri, Bernard Yung, Daniel Yusef, Said Yusef, Intekhab Yusuf, Anna-Sophia Zafar, Silvia Zagalo, Su Zaher, Aqsa Zahoor, Mahrukh Zainab, Thornton Zak, Kareem Zaki, Nabhan Zakir, Kasia Zalewska, Ane Zamalloa, Mohsin Zaman, Shakir Zaman, Julie Zamikula, Louise Zammit, Marie Zammit-Mangion, Marcelina Zawadzka, Mohammed Zayed, Esther Zebracki, Daniel Zehnder, Lisa Zeidan, Darius Zeinali, Jing Zhang, Xiaobei Zhao, Dongling Zheng, Doreen Zhu, Madiha Zia, Omar Zibdeh, Rabia Zill-E-Huma, Ei Thankt Zin, Eva Zincone, Garikai Zindoga, Eleanor Zinkin, Vivian Zinyemba, Christos Zipitis, Letizia Zitter, Arkadiusz Zmierczak, Garazi Zubikarai, Azam Zubir, Naz Zuhra, Rasha Zulaikha, Sabrina Zulfikar, Carol Zullo, Ana Zuriaga-Alvaro, University of St Andrews. Infection and Global Health Division, University of St Andrews. School of Medicine, and Group, RECOVERY Collaborative

Subjects
Adult, Male, Hypoxia/etiology, SARS-CoV-2, COVID-19, 3rd-DAS, General Medicine, Adrenal Cortex Hormones/therapeutic use, AC, Dexamethasone/therapeutic use, Hospitals, Oxygen, Treatment Outcome, SDG 3 - Good Health and Well-being, MCP, Humans, Female
Abstract

Background Low-dose corticosteroids have been shown to reduce mortality for patients with COVID-19 requiring oxygen or ventilatory support (non-invasive mechanical ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation). We evaluated the use of a higher dose of corticosteroids in this patient group. Methods This randomised, controlled, open-label platform trial (Randomised Evaluation of COVID-19 Therapy [RECOVERY]) is assessing multiple possible treatments in patients hospitalised for COVID-19. Eligible and consenting adult patients with clinical evidence of hypoxia (ie, receiving oxygen or with oxygen saturation Findings Between May 25, 2021, and May 13, 2022, 1272 patients with COVID-19 and hypoxia receiving no oxygen (eight [1%]) or simple oxygen only (1264 [99%]) were randomly allocated to receive usual care plus higher dose corticosteroids (659 patients) versus usual care alone (613 patients, of whom 87% received low-dose corticosteroids during the follow-up period). Of those randomly assigned, 745 (59%) were in Asia, 512 (40%) in the UK, and 15 (1%) in Africa. 248 (19%) had diabetes and 769 (60%) were male. Overall, 123 (19%) of 659 patients allocated to higher dose corticosteroids versus 75 (12%) of 613 patients allocated to usual care died within 28 days (rate ratio 1·59 [95% CI 1·20–2·10]; p=0·0012). There was also an excess of pneumonia reported to be due to non-COVID infection (64 cases [10%] vs 37 cases [6%]; absolute difference 3·7% [95% CI 0·7–6·6]) and an increase in hyperglycaemia requiring increased insulin dose (142 [22%] vs 87 [14%]; absolute difference 7·4% [95% CI 3·2–11·5]). Interpretation In patients hospitalised for COVID-19 with clinical hypoxia who required either no oxygen or simple oxygen only, higher dose corticosteroids significantly increased the risk of death compared with usual care, which included low-dose corticosteroids. The RECOVERY trial continues to assess the effects of higher dose corticosteroids in patients hospitalised with COVID-19 who require non-invasive ventilation, invasive mechanical ventilation, or extracorporeal membrane oxygenation. Funding UK Research and Innovation (Medical Research Council), National Institute of Health and Care Research, and Wellcome Trust.

Published
2023

38. Association of COPD With Risk for Pulmonary Infections Requiring Hospitalization in HIV-Infected Veterans.

Author

Attia, Engi F, McGinnis, Kathleen A, Feemster, Laura C, Akgün, Kathleen M, Butt, Adeel A, Graber, Christopher J, Fine, Michael J, Goetz, Matthew B, Rodriguez-Barradas, Maria C, Pisani, Margaret A, Tindle, Hilary A, Brown, Sheldon T, Soo Hoo, Guy W, Rimland, David, Gibert, Cynthia L, Huang, Laurence, Freiberg, Matthew S, Hough, Catherine L, and Crothers, Kristina

Subjects
Humans, Tuberculosis, Pulmonary, Pneumonia, Bacterial, Community-Acquired Infections, Pneumonia, Pneumocystis, HIV Infections, Pulmonary Disease, Chronic Obstructive, Hospitalization, Viral Load, Risk Factors, Adult, Middle Aged, Veterans, Female, Male, COPD, pulmonary infection, pneumonia, HIV, comorbidities, Tuberculosis, Pulmonary, Pneumonia, Bacterial, Pneumocystis, Pulmonary Disease, Chronic Obstructive, Pneumonia & Influenza, HIV/AIDS, Chronic Obstructive Pulmonary Disease, Infectious Diseases, Clinical Research, Lung, Infection, Respiratory, Virology, Clinical Sciences, Public Health and Health Services
Abstract

BackgroundPulmonary infections remain more common in HIV-infected (HIV+) compared with uninfected individuals. The increase in chronic lung diseases among aging HIV+ individuals may contribute to this persistent risk. We sought to determine whether chronic obstructive pulmonary disease (COPD) is an independent risk factor for different pulmonary infections requiring hospitalization among HIV+ patients.MethodsWe analyzed data from 41,993 HIV+ Veterans in the nationwide Veterans Aging Cohort Study Virtual Cohort from 1996 to 2009. Using International Classification of Diseases, Ninth Revision codes, we identified baseline comorbid conditions, including COPD, and incident community-acquired pneumonia (CAP), pulmonary tuberculosis (TB), and Pneumocystis jirovecii pneumonia (PCP) requiring hospitalization within 2 years after baseline. We used multivariable Poisson regression to determine incidence rate ratios (IRRs) associated with COPD for each type of pulmonary infection, adjusting for comorbidities, CD4 cell count, HIV viral load, smoking status, substance use, vaccinations, and calendar year at baseline.ResultsUnadjusted incidence rates of CAP, TB, and PCP requiring hospitalization were significantly higher among persons with COPD compared to those without COPD (CAP: 53.9 vs. 19.4 per 1000 person-years; TB: 8.7 vs. 2.8; PCP: 15.5 vs. 9.2; P ≤ 0.001). In multivariable Poisson regression models, COPD was independently associated with increased risk of CAP, TB, and PCP (IRR: 1.94, 95% confidence interval [CI]: 1.64 to 2.30; IRR: 2.60, 95% CI: 1.70 to 3.97; and IRR: 1.48, 95% CI: 1.10 to 2.01, respectively).ConclusionsCOPD is an independent risk factor for CAP, TB, and PCP requiring hospitalization among HIV+ individuals. As the HIV+ population ages, the growing burden of COPD may confer substantial risk for pulmonary infections.

Published
2015

39. Depression and Human Immunodeficiency Virus Infection Are Risk Factors for Incident Heart Failure Among Veterans

Author

White, Jessica R, Chang, Chung-Chou H, So-Armah, Kaku A, Stewart, Jesse C, Gupta, Samir K, Butt, Adeel A, Gibert, Cynthia L, Rimland, David, Rodriguez-Barradas, Maria C, Leaf, David A, Bedimo, Roger J, Gottdiener, John S, Kop, Willem J, Gottlieb, Stephen S, Budoff, Matthew J, Khambaty, Tasneem, Tindle, Hilary A, Justice, Amy C, and Freiberg, Matthew S

Subjects
Biomedical and Clinical Sciences, Public Health, Clinical Sciences, Health Sciences, Medical Microbiology, Prevention, Cardiovascular, Brain Disorders, Serious Mental Illness, Depression, Heart Disease, HIV/AIDS, Mental Health, Clinical Research, Major Depressive Disorder, Aetiology, 2.1 Biological and endogenous factors, Infection, Good Health and Well Being, Adult, Aging, Anti-HIV Agents, Antidepressive Agents, Cardiovascular Diseases, Comorbidity, Depressive Disorder, Major, Diabetes Mellitus, Electronic Health Records, Ethnicity, Female, Follow-Up Studies, HIV Infections, Heart Failure, Humans, Hyperlipidemias, Incidence, Kidney Diseases, Male, Middle Aged, Prospective Studies, Risk Factors, Substance-Related Disorders, United States, Veterans, depression, epidemiology, heart failure, HIV, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences, Sports science and exercise
Abstract

BackgroundBoth HIV and depression are associated with increased heart failure (HF) risk. Depression, a common comorbidity, may further increase the risk of HF among adults with HIV infection (HIV+). We assessed the association between HIV, depression, and incident HF.Methods and resultsVeterans Aging Cohort Study (VACS) participants free from cardiovascular disease at baseline (n=81 427: 26 908 HIV+, 54 519 without HIV [HIV-]) were categorized into 4 groups: HIV- without major depressive disorder (MDD) [reference], HIV- with MDD, HIV+ without MDD, and HIV+ with MDD. International Classification of Diseases, Ninth Revision codes from medical records were used to determine MDD and the primary outcome, HF. After 5.8 years of follow-up, HF rates per 1000 person-years were highest among HIV+ participants with MDD (9.32; 95% confidence interval [CI], 8.20-10.6). In Cox proportional hazards models, HIV+ participants with MDD had a significantly higher risk of HF (adjusted hazard ratio, 1.68; 95% CI, 1.45-1.95) compared with HIV- participants without MDD. MDD was associated with HF in separate fully adjusted models for HIV- and HIV+ participants (adjusted hazard ratio, 1.21; 95% CI, 1.06-1.37; and adjusted hazard ratio, 1.29; 95% CI, 1.11-1.51, respectively). Among those with MDD, baseline antidepressant use was associated with lower risk of incident HF events (adjusted hazard ratio, 0.76; 95% CI, 0.58-0.99).ConclusionsOur study is the first to suggest that MDD is an independent risk factor for HF in HIV+ adults. These results reinforce the importance of identifying and managing MDD among HIV+ patients. Future studies must clarify mechanisms linking HIV, MDD, antidepressants, and HF and identify interventions to reduce HF morbidity and mortality in those with both HIV and MDD.

Published
2015

40. Assessment of stress and self-efficacy for the NIH Toolbox for Neurological and Behavioral Function

Author

Kupst, Mary Jo, Butt, Zeeshan, Stoney, Catherine M, Griffith, James W, Salsman, John M, Folkman, Susan, and Cella, David

Subjects
Mental Health, Basic Behavioral and Social Science, Mind and Body, Neurosciences, Behavioral and Social Science, Good Health and Well Being, Adaptation, Psychological, Adolescent, Adult, Affective Symptoms, Child, Child, Preschool, Cognition, Emotions, Factor Analysis, Statistical, Female, Humans, Male, National Institutes of Health (U.S.), Psychometrics, Psychomotor Performance, Self Efficacy, Stress, Psychological, Surveys and Questionnaires, United States, Young Adult, perceived stress, self-efficacy, psychometrics, NIH Toolbox, Business and Management, Psychology, Clinical Psychology
Abstract

Background and objectivesThe NIH Toolbox for Neurological and Behavioral Function assessment battery contains measures in the domains of cognitive function, motor function, sensory function, and emotional health. It was designed for use in epidemiological and clinical trials health-related research.DesignThis paper describes the first phase of instrument development for the stress and self-efficacy subdomain of emotional health. Based on an extensive literature review and expert consultation, 127 measures were initially considered for inclusion in this subdomain, including measures of stress, self-efficacy, emotion regulation, and coping.ResultsSeveral measures, including emotion regulation and measures of coping strategies, did not meet criteria that were a priori established for inclusion. Psychometric properties of the remaining candidate measures were evaluated using data from five independent samples (combined N = 3175). Confirmatory and exploratory factor analyses indicated the Perceived Stress Scale and the General Self-Efficacy Scale each assessed single dimensions.ConclusionsBased on their psychometric performance, these two instruments were selected for inclusion and subsequent national norming for the NIH Toolbox.

Published
2015

41. HIV Infection, Cardiovascular Disease Risk Factor Profile, and Risk for Acute Myocardial Infarction

Author

Paisible, Anne-Lise, Chang, Chung-Chou H, So-Armah, Kaku A, Butt, Adeel A, Leaf, David A, Budoff, Matthew, Rimland, David, Bedimo, Roger, Goetz, Matthew B, Rodriguez-Barradas, Maria C, Crane, Heidi M, Gibert, Cynthia L, Brown, Sheldon T, Tindle, Hilary A, Warner, Alberta L, Alcorn, Charles, Skanderson, Melissa, Justice, Amy C, and Freiberg, Matthew S

Subjects
Biomedical and Clinical Sciences, Epidemiology, Public Health, Health Sciences, Clinical Sciences, Heart Disease - Coronary Heart Disease, Clinical Research, Aging, Infectious Diseases, HIV/AIDS, Heart Disease, Cardiovascular, Prevention, Good Health and Well Being, Adult, Aged, Cohort Studies, Female, HIV Infections, Humans, Longitudinal Studies, Male, Middle Aged, Myocardial Infarction, Prevalence, Prospective Studies, Risk Factors, Veterans, HIV, optimal cardiovascular health, myocardial infarction, Public Health and Health Services, Virology, Clinical sciences, Public health
Abstract

BackgroundTraditional cardiovascular disease risk factors (CVDRFs) increase the risk of acute myocardial infarction (AMI) among HIV-infected (HIV+) participants. We assessed the association between HIV and incident AMI within CVDRF strata.MethodsCohort-81,322 participants (33% HIV+) without prevalent CVD from the Veterans Aging Cohort Study Virtual Cohort (prospective study of HIV+ and matched HIV- veterans) participated in this study. Veterans were followed from first clinical encounter on/after April 1, 2003, until AMI/death/last follow-up date (December 31, 2009). Predictors-HIV, CVDRFs (total cholesterol, cholesterol-lowering agents, blood pressure, blood pressure medication, smoking, diabetes) used to create 6 mutually exclusive profiles: all CVDRFs optimal, 1+ nonoptimal CVDRFs, 1+ elevated CVDRFs, and 1, 2, 3+ major CVDRFs. Outcome-Incident AMI [defined using enzyme, electrocardiogram (EKG) clinical data, 410 inpatient ICD-9 (Medicare), and/or death certificates]. Statistics-Cox models adjusted for demographics, comorbidity, and substance use.ResultsOf note, 858 AMIs (42% HIV+) occurred over 5.9 years (median). Prevalence of optimal cardiac health was

Published
2015

42. Liver Fibrosis Progression in Hepatitis C Virus Infection After Seroconversion

Author

Butt, Adeel A, Yan, Peng, Re, Vincent Lo, Rimland, David, Goetz, Matthew B, Leaf, David, Freiberg, Matthew S, Klein, Marina B, Justice, Amy C, and Sherman, Kenneth E

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Chronic Liver Disease and Cirrhosis, Hepatitis - C, Hepatitis, Liver Disease, Substance Misuse, Clinical Research, Infectious Diseases, Emerging Infectious Diseases, Digestive Diseases, Infection, Good Health and Well Being, Adult, Case-Control Studies, Cohort Studies, Disease Progression, Female, Hepatic Insufficiency, Hepatitis C, Chronic, Humans, Liver Cirrhosis, Male, Middle Aged, Time Factors, ERCHIVES (Electronically Retrieved Cohort of HCV Infected Veterans) Study Team, Opthalmology and Optometry, Public Health and Health Services, Clinical sciences, Health services and systems
Abstract

ImportanceKnowing the rate of liver fibrosis progression in hepatitis C virus (HCV)-infected persons can help inform patients and providers (clinicians, medical institutions or organizations, and third-party payers) in making treatment decisions.ObjectiveTo determine the rate and factors associated with liver fibrosis progression and hepatic decompensation in persons after acquiring HCV infection.Design, setting, and participantsSecondary data analysis of persons in the Electronically Retrieved Cohort of HCV Infected Veterans (ERCHIVES), a national Veterans Affairs (VA) database, between 2002 and 2012. Among 610 514 persons in ERCHIVES (half were HCV positive), we identified those with an initial negative and subsequent positive test result for HCV antibody and positive HCV RNA test result (HCV+). Controls had 2 negative HCV antibody test results (HCV-) in a comparable time frame and were matched 1:1 on age (in 5-year blocks), race, and sex. We excluded persons with human immunodeficiency virus, hepatitis B, less than 24 months of follow-up, hepatocellular carcinoma, and cirrhosis at baseline.Main outcomes and measuresProgression of liver fibrosis as estimated by the Fibrosis-4 (FIB-4) index; development of cirrhosis, defined by a FIB-4 score greater than 3.5; and development of hepatic decompensation.ResultsThe evaluable data set consisted of 1840 persons who were HCV+ and 1840 HCV- controls. The HCV+ persons were younger and had a lower mean (SD) body mass index (27.39 [5.51] vs 29.49 [6.16]; P

Published
2015

43. Long-term quality of life after liver donation in the adult to adult living donor liver transplantation cohort study (A2ALL)

Author

Ladner, Daniela P, Dew, Mary Amanda, Forney, Sarah, Gillespie, Brenda W, Brown, Robert S, Merion, Robert M, Freise, Chris E, Hayashi, Paul H, Hong, Johnny C, Ashworth, April, Berg, Carl L, Burton, James R, Shaked, Abraham, and Butt, Zeeshan

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, Transplantation, Liver Disease, Digestive Diseases, Organ Transplantation, Comparative Effectiveness Research, Infectious Diseases, Management of diseases and conditions, 7.1 Individual care needs, Good Health and Well Being, Adolescent, Adult, Female, Follow-Up Studies, Forecasting, Humans, Liver Transplantation, Living Donors, Male, Middle Aged, Quality of Life, Retrospective Studies, Surveys and Questionnaires, Time Factors, Tissue and Organ Procurement, Young Adult, Patient reported outcomes, Quality of life, Living donor liver transplantation, Living liver donors, Adult to adult living donor liver transplantation cohort study, Public Health and Health Services, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsThere are few long-term studies of the health-related quality of life (HRQOL) in living liver donors. This study aimed to characterize donor HRQOL in the Adult to Adult Living Donor Liver Transplantation Study (A2ALL) up to 11 years post-donation.MethodsBetween 2004 and 2013, HRQOL was assessed at evaluation, at 3 months, and yearly post-donation in prevalent liver donors using the short-form survey (SF-36), which provides a physical (PCS) and a mental component summary (MCS).ResultsOf the 458 donors enrolled in A2ALL, 374 (82%) had SF-36 data. Mean age at evaluation was 38 (range 18-63), 47% were male, 93% white, and 43% had a bachelor's degree or higher. MCS and PCS means were above the US population at all time points. However, at every time point there were some donors who reported poor scores (>1/2 standard deviation below the age and sex adjusted mean) (PCS: 5.3-26.8%,Mcs10.0-25.0%). Predictors of poor PCS and MCS scores included recipient's death within the two years prior to the survey and education less than a bachelor's degree; poor PCS scores were also predicted by time since donation, Hispanic ethnicity, and at the 3-month post-donation time point.ConclusionsIn summary, most living donors maintain above average HRQOL up to 11 years prospectively, supporting the notion that living donation does not negatively affect HRQOL. However, targeted support for donors at risk for poor HRQOL may improve overall HRQOL outcomes for living liver donors.

Published
2015

44. CD8+ T-cells count in acute myocardial infarction in HIV disease in a predominantly male cohort.

Author

Badejo, Oluwatosin A, Chang, Chung-Chou, So-Armah, Kaku A, Tracy, Russell P, Baker, Jason V, Rimland, David, Butt, Adeel A, Gordon, Adam J, Rinaldo, Charles R, Kraemer, Kevin, Samet, Jeffrey H, Tindle, Hilary A, Goetz, Matthew B, Rodriguez-Barradas, Maria C, Bedimo, Roger, Gibert, Cynthia L, Leaf, David A, Kuller, Lewis H, Deeks, Steven G, Justice, Amy C, and Freiberg, Matthew S

Subjects
CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Humans, HIV Infections, Myocardial Infarction, Lymphocyte Count, Cohort Studies, Adult, Middle Aged, Veterans, Female, Male, Kaplan-Meier Estimate, Biological Sciences, Information and Computing Sciences, Technology
Abstract

Human Immunodeficiency Virus- (HIV-) infected persons have a higher risk for acute myocardial infarction (AMI) than HIV-uninfected persons. Earlier studies suggest that HIV viral load, CD4+ T-cell count, and antiretroviral therapy are associated with cardiovascular disease (CVD) risk. Whether CD8+ T-cell count is associated with CVD risk is not clear. We investigated the association between CD8+ T-cell count and incident AMI in a cohort of 73,398 people (of which 97.3% were men) enrolled in the U.S. Veterans Aging Cohort Study-Virtual Cohort (VACS-VC). Compared to uninfected people, HIV-infected people with high baseline CD8+ T-cell counts (>1065 cells/mm3) had increased AMI risk (adjusted HR=1.82, P

Published
2015

45. Splice-site mutations identified in PDE6A responsible for retinitis pigmentosa in consanguineous Pakistani families.

Author

Khan, Shahid Y, Ali, Shahbaz, Naeem, Muhammad Asif, Khan, Shaheen N, Husnain, Tayyab, Butt, Nadeem H, Qazi, Zaheeruddin A, Akram, Javed, Riazuddin, Sheikh, Ayyagari, Radha, Hejtmancik, J Fielding, and Riazuddin, S Amer

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Rare Diseases, Clinical Research, Eye Disease and Disorders of Vision, Genetics, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Adult, Chromosomes, Human, Pair 5, Consanguinity, Cyclic Nucleotide Phosphodiesterases, Type 6, DNA Mutational Analysis, Eye Proteins, Female, Genes, Recessive, Genetic Markers, Humans, Lod Score, Male, Middle Aged, Mutation, Pakistan, Pedigree, RNA Splice Sites, Retinitis Pigmentosa, Young Adult, Opthalmology and Optometry, Ophthalmology & Optometry, Ophthalmology and optometry
Abstract

PurposeThis study was conducted to localize and identify causal mutations associated with autosomal recessive retinitis pigmentosa (RP) in consanguineous familial cases of Pakistani origin.MethodsOphthalmic examinations that included funduscopy and electroretinography (ERG) were performed to confirm the affectation status. Blood samples were collected from all participating individuals, and genomic DNA was extracted. A genome-wide scan was performed, and two-point logarithm of odds (LOD) scores were calculated. Sanger sequencing was performed to identify the causative variants. Subsequently, we performed whole exome sequencing to rule out the possibility of a second causal variant within the linkage interval. Sequence conservation was performed with alignment analyses of PDE6A orthologs, and in silico splicing analysis was completed with Human Splicing Finder version 2.4.1.ResultsA large multigenerational consanguineous family diagnosed with early-onset RP was ascertained. An ophthalmic clinical examination consisting of fundus photography and electroretinography confirmed the diagnosis of RP. A genome-wide scan was performed, and suggestive two-point LOD scores were observed with markers on chromosome 5q. Haplotype analyses identified the region; however, the region did not segregate with the disease phenotype in the family. Subsequently, we performed a second genome-wide scan that excluded the entire genome except the chromosome 5q region harboring PDE6A. Next-generation whole exome sequencing identified a splice acceptor site mutation in intron 16: c.2028-1G>A, which was completely conserved in PDE6A orthologs and was absent in ethnically matched 350 control chromosomes, the 1000 Genomes database, and the NHLBI Exome Sequencing Project. Subsequently, we investigated our entire cohort of RP familial cases and identified a second family who harbored a splice acceptor site mutation in intron 10: c.1408-2A>G. In silico analysis suggested that these mutations will result in the elimination of wild-type splice acceptor sites that would result in either skipping of the respective exon or the creation of a new cryptic splice acceptor site; both possibilities would result in retinal photoreceptor cells that lack PDE6A wild-type protein.Conclusionswe report two splice acceptor site variations in PDE6A in consanguineous Pakistani families who manifested cardinal symptoms of RP. Taken together with our previously published work, our data suggest that mutations in PDE6A account for about 2% of the total genetic load of RP in our cohort and possibly in the Pakistani population as well.

Published
2015

46. Mutations in GRM6 identified in consanguineous Pakistani families with congenital stationary night blindness.

Author

Naeem, Muhammad Asif, Gottsch, Alexander DH, Ullah, Inayat, Khan, Shaheen N, Husnain, Tayyab, Butt, Nadeem H, Qazi, Zaheeruddin A, Akram, Javed, Riazuddin, Sheikh, Ayyagari, Radha, Hejtmancik, J Fielding, and Riazuddin, S Amer

Subjects
Biomedical and Clinical Sciences, Ophthalmology and Optometry, Clinical Research, Genetics, Aetiology, 2.1 Biological and endogenous factors, Adult, Aged, Amino Acid Sequence, Animals, Base Sequence, Chromosomes, Human, Pair 5, Consanguinity, Electroretinography, Exons, Eye Diseases, Hereditary, Female, Gene Expression, Genes, Recessive, Genetic Diseases, X-Linked, Homozygote, Humans, Male, Molecular Sequence Data, Mutation, Myopia, Night Blindness, Pakistan, Pedigree, Receptors, Glutamate, Sequence Alignment, Sequence Analysis, DNA, Opthalmology and Optometry, Ophthalmology & Optometry, Ophthalmology and optometry
Abstract

PurposeThis study was undertaken to investigate the causal mutations responsible for autosomal recessive congenital stationary night blindness (CSNB) in consanguineous Pakistani families.MethodsTwo consanguineous families with multiple individuals manifesting symptoms of stationary night blindness were recruited. Affected individuals underwent a detailed ophthalmological examination, including fundus examination and electroretinography. Blood samples were collected and genomic DNA was extracted. Exclusion analyses were completed by genotyping closely spaced microsatellite markers, and two-point logarithm of odds (LOD) scores were calculated. All coding exons, along with the exon-intron boundaries of GRM6, were sequenced bidirectionally.ResultsAccording to the medical history available to us, affected individuals in both families had experienced night blindness from the early years of their lives. Fundus photographs of affected individuals in both the families appeared normal, with no signs of attenuated arteries or bone spicule pigmentation. The scotopic electroretinogram (ERG) response were absent in all of the affected individuals, while the photopic measurements show reduced b-waves. During exclusion analyses, both families localized to a region on chromosome 5q that harbors GRM6, a gene previously associated with autosomal recessive CSNB. Bidirectional sequencing of GRM6 identified homozygous single base pair changes, specifically c.1336C>T (p.R446X) and c.2267G>A (p.G756D) in families PKRP170 and PKRP172, respectively.ConclusionsWe identified a novel nonsense and a previously reported missense mutation in GRM6 that were responsible for autosomal recessive CSNB in patients of Pakistani decent.

Published
2015

47. Global mortality associated with 33 bacterial pathogens in 2019

Author

Kevin S Ikuta, Lucien R Swetschinski, Gisela Robles Aguilar, Fablina Sharara, Tomislav Mestrovic, Authia P Gray, Nicole Davis Weaver, Eve E Wool, Chieh Han, Anna Gershberg Hayoon, Amirali Aali, Semagn Mekonnen Abate, Mohsen Abbasi-Kangevari, Zeinab Abbasi-Kangevari, Sherief Abd-Elsalam, Getachew Abebe, Aidin Abedi, Amir Parsa Abhari, Hassan Abidi, Richard Gyan Aboagye, Abdorrahim Absalan, Hiwa Abubaker Ali, Juan Manuel Acuna, Tigist Demssew Adane, Isaac Yeboah Addo, Oyelola A Adegboye, Mohammad Adnan, Qorinah Estiningtyas Sakilah Adnani, Muhammad Sohail Afzal, Saira Afzal, Zahra Babaei Aghdam, Bright Opoku Ahinkorah, Aqeel Ahmad, Araz Ramazan Ahmad, Rizwan Ahmad, Sajjad Ahmad, Sohail Ahmad, Sepideh Ahmadi, Ali Ahmed, Haroon Ahmed, Jivan Qasim Ahmed, Tarik Ahmed Rashid, Marjan Ajami, Budi Aji, Mostafa Akbarzadeh-Khiavi, Chisom Joyqueenet Akunna, Hanadi Al Hamad, Fares Alahdab, Ziyad Al-Aly, Mamoon A Aldeyab, Alicia V Aleman, Fadwa Alhalaiqa Naji Alhalaiqa, Robert Kaba Alhassan, Beriwan Abdulqadir Ali, Liaqat Ali, Syed Shujait Ali, Yousef Alimohamadi, Vahid Alipour, Atiyeh Alizadeh, Syed Mohamed Aljunid, Kasim Allel, Sami Almustanyir, Edward Kwabena Ameyaw, Arianna Maever L Amit, Nivedita Anandavelane, Robert Ancuceanu, Catalina Liliana Andrei, Tudorel Andrei, Dewi Anggraini, Adnan Ansar, Anayochukwu Edward Anyasodor, Jalal Arabloo, Aleksandr Y Aravkin, Demelash Areda, Timur Aripov, Anton A Artamonov, Judie Arulappan, Raphael Taiwo Aruleba, Muhammad Asaduzzaman, Tahira Ashraf, Seyyed Shamsadin Athari, Daniel Atlaw, Sameh Attia, Marcel Ausloos, Tewachew Awoke, Beatriz Paulina Ayala Quintanilla, Tegegn Mulatu Ayana, Sina Azadnajafabad, Amirhossein Azari Jafari, Darshan B B, Muhammad Badar, Ashish D Badiye, Nayereh Baghcheghi, Sara Bagherieh, Atif Amin Baig, Indrajit Banerjee, Aleksandra Barac, Mainak Bardhan, Francesco Barone-Adesi, Hiba Jawdat Barqawi, Amadou Barrow, Pritish Baskaran, Saurav Basu, Abdul-Monim Mohammad Batiha, Neeraj Bedi, Melaku Ashagrie Belete, Uzma Iqbal Belgaumi, Rose G Bender, Bharti Bhandari, Dinesh Bhandari, Pankaj Bhardwaj, Sonu Bhaskar, Krittika Bhattacharyya, Suraj Bhattarai, Saeid Bitaraf, Danilo Buonsenso, Zahid A Butt, Florentino Luciano Caetano dos Santos, Jiao Cai, Daniela Calina, Paulo Camargos, Luis Alberto Cámera, Rosario Cárdenas, Muge Cevik, Joshua Chadwick, Jaykaran Charan, Akhilanand Chaurasia, Patrick R Ching, Sonali Gajanan Choudhari, Enayet Karim Chowdhury, Fazle Rabbi Chowdhury, Dinh-Toi Chu, Isaac Sunday Chukwu, Omid Dadras, Fentaw Teshome Dagnaw, Xiaochen Dai, Saswati Das, Anna Dastiridou, Sisay Abebe Debela, Fitsum Wolde Demisse, Solomon Demissie, Diriba Dereje, Msganaw Derese, Hardik Dineshbhai Desai, Fikadu Nugusu Dessalegn, Samuel Abebe A Dessalegni, Belay Desye, Kartik Dhaduk, Meghnath Dhimal, Sameer Dhingra, Nancy Diao, Daniel Diaz, Shirin Djalalinia, Milad Dodangeh, Deepa Dongarwar, Bezabih Terefe Dora, Fariba Dorostkar, Haneil Larson Dsouza, Eleonora Dubljanin, Susanna J Dunachie, Oyewole Christopher Durojaiye, Hisham Atan Edinur, Habtamu Bekele Ejigu, Michael Ekholuenetale, Temitope Cyrus Ekundayo, Hassan El-Abid, Muhammed Elhadi, Mohamed A Elmonem, Amir Emami, Luchuo Engelbert Bain, Daniel Berhanie Enyew, Ryenchindorj Erkhembayar, Babak Eshrati, Farshid Etaee, Adeniyi Francis Fagbamigbe, Shahab Falahi, Aida Fallahzadeh, Emerito Jose A Faraon, Ali Fatehizadeh, Ginenus Fekadu, João C Fernandes, Allegra Ferrari, Getahun Fetensa, Irina Filip, Florian Fischer, Masoud Foroutan, Peter Andras Gaal, Muktar A Gadanya, Abhay Motiramji Gaidhane, Balasankar Ganesan, Mesfin Gebrehiwot, Reza Ghanbari, Mohammad Ghasemi Nour, Ahmad Ghashghaee, Ali Gholamrezanezhad, Abdolmajid Gholizadeh, Mahaveer Golechha, Pouya Goleij, Davide Golinelli, Amador Goodridge, Damitha Asanga Gunawardane, Yuming Guo, Rajat Das Gupta, Sapna Gupta, Veer Bala Gupta, Vivek Kumar Gupta, Alemu Guta, Parham Habibzadeh, Atlas Haddadi Avval, Rabih Halwani, Asif Hanif, Md. 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Mamo, Galana Ayana, Manla, Yosef, Martorell, Miquel, Matei, Clara N, McManigal, Barney, Mehrabi Nasab, Entezar, Mehrotra, Ravi, Melese, Addisu, Mendoza-Cano, Oliver, Menezes, Ritesh G, Mentis, Alexios-Fotios A, Micha, Georgia, Michalek, Irmina Maria, Micheletti Gomide Nogueira de Sá, Ana Carolina, Milevska Kostova, Neda, Mir, Shabir Ahmad, Mirghafourvand, Mojgan, Mirmoeeni, Seyyedmohammadsadeq, Mirrakhimov, Erkin M, Mirza-Aghazadeh-Attari, Mohammad, Misganaw, Abay Sisay, Misganaw, Awoke, Misra, Sanjeev, Mohammadi, Esmaeil, Mohammadi, Mokhtar, Mohammadian-Hafshejani, Abdollah, Mohammed, Shafiu, Mohan, Syam, Mohseni, Mohammad, Mokdad, Ali H, Momtazmanesh, Sara, Monasta, Lorenzo, Moore, Catrin E, Moradi, Maryam, Moradi Sarabi, Mostafa, Morrison, Shane Dougla, Motaghinejad, Majid, Mousavi Isfahani, Haleh, Mousavi Khaneghah, Amin, Mousavi-Aghdas, Seyed Ali, Mubarik, Sumaira, Mulita, Francesk, Mulu, Getaneh Baye B, Munro, Sandra B, Muthupandian, Saravanan, Nair, Tapas Sadasivan, Naqvi, Atta Abba, Narang, Himanshi, Natto, Zuhair S, Naveed, Muhammad, Nayak, Biswa Prakash, Naz, Shumaila, Negoi, Ionut, Nejadghaderi, Seyed Aria, Neupane Kandel, Sandhya, Ngwa, Che Henry, Niazi, Robina Khan, Nogueira de Sá, Antonio Tolentino, Noroozi, Nafise, Nouraei, Hasti, Nowroozi, Ali, Nuñez-Samudio, Virginia, Nutor, Jerry John, Nzoputam, Chimezie Igwegbe, Nzoputam, Ogochukwu Janet, Oancea, Bogdan, Obaidur, Rahman Md, Ojha, Vivek Anand, Okekunle, Akinkunmi Paul, Okonji, Osaretin Christabel, Olagunju, Andrew T, Olusanya, Bolajoko Olubukunola, Omar Bali, Ahmed, Omer, Emad, Otstavnov, Nikita, Oumer, Bilcha, P A, Mahesh, Padubidri, Jagadish Rao, Pakshir, Keyvan, Palicz, Tamá, Pana, Adrian, Pardhan, Shahina, Paredes, Jose L, Parekh, Utsav, Park, Eun-Cheol, Park, Seoyeon, Pathak, Ashish, Paudel, Rajan, Paudel, Uttam, Pawar, Shrikant, Pazoki Toroudi, Hamidreza, Peng, Minjin, Pensato, Umberto, Pepito, Veincent Christian Filipino, Pereira, Marco, Peres, Mario F P, Perico, Norberto, Petcu, Ionela-Roxana, Piracha, Zahra Zahid, Podder, Indrashi, Pokhrel, Nayanum, Poluru, Ramesh, Postma, Maarten J, Pourtaheri, Naeimeh, Prashant, Akila, Qattea, Ibrahim, Rabiee, Mohammad, Rabiee, Navid, Radfar, Amir, Raeghi, Saber, Rafiei, Sima, Raghav, Pankaja Raghav, Rahbarnia, Leila, Rahimi-Movaghar, Vafa, Rahman, Mosiur, Rahman, Muhammad Aziz, Rahmani, Amir Masoud, Rahmanian, Vahid, Ram, Pradhum, Ranjha, Muhammad Modassar Ali Nawaz, Rao, Sowmya J, Rashidi, Mohammad-Mahdi, Rasul, Azad, Ratan, Zubair Ahmed, Rawaf, Salman, Rawassizadeh, Reza, Razeghinia, Mohammad Sadegh, Redwan, Elrashdy Moustafa Mohamed, Regasa, Misganu Teshoma, Remuzzi, Giuseppe, Reta, Melese Abate, Rezaei, Nazila, Rezapour, Aziz, Riad, Abanoub, Ripon, Rezaul Karim, Rudd, Kristina E, Saddik, Basema, Sadeghian, Saeid, Saeed, Umar, Safaei, Mohsen, Safary, Azam, Safi, Sher Zaman, Sahebazzamani, Maryam, Sahebkar, Amirhossein, Sahoo, Harihar, Salahi, Saina, Salahi, Sarvenaz, Salari, Hedayat, Salehi, Sana, Samadi Kafil, Hossein, Samy, Abdallah M, Sanadgol, Nima, Sankararaman, Senthilkumar, Sanmarchi, Francesco, Sathian, Brijesh, Sawhney, Monika, Saya, Ganesh Kumar, Senthilkumaran, Subramanian, Seylani, Allen, Shah, Pritik A, Shaikh, Masood Ali, Shaker, Elaheh, Shakhmardanov, Murad Ziyaudinovich, Sharew, Mequannent Melaku, Sharifi-Razavi, Athena, Sharma, Purva, Sheikhi, Rahim Ali, Sheikhy, Ali, Shetty, Pavanchand H, Shigematsu, Mika, Shin, Jae Il, Shirzad-Aski, Hesamaddin, Shivakumar, K M, Shobeiri, Parnian, Shorofi, Seyed Afshin, Shrestha, Sunil, Sibhat, Migbar Mekonnen, Sidemo, Negussie Boti, Sikder, Mustafa Kamal, Silva, Luís Manuel Lopes Rodrigue, Singh, Jasvinder A, Singh, Paramdeep, Singh, Surjit, Siraj, Md Shahjahan, Siwal, Samarjeet Singh, Skryabin, Valentin Yurievich, Skryabina, Anna Aleksandrovna, Socea, Bogdan, Solomon, Damtew Damtew, Song, Yimeng, Sreeramareddy, Chandrashekhar T, Suleman, Muhammad, Suliankatchi Abdulkader, Rizwan, Sultana, Saima, Szócska, Mikló, Tabatabaeizadeh, Seyed-Amir, Tabish, Mohammad, Taheri, Majid, Taki, Elahe, Tan, Ker-Kan, Tandukar, Sarmila, Tat, Nathan Y, Tat, Vivian Y, Tefera, Belay Negash, Tefera, Yibekal Manaye, Temesgen, Gebremaryam, Temsah, Mohamad-Hani, Tharwat, Samar, Thiyagarajan, Arulmani, Tleyjeh, Imad I, Troeger, Christopher E, Umapathi, Krishna Kishore, Upadhyay, Era, Valadan Tahbaz, Sahel, Valdez, Pascual R, Van den Eynde, Jef, van Doorn, H. Rogier, Vaziri, Siavash, Verras, Georgios-Ioanni, Viswanathan, Harimadhav, Vo, Bay, Waris, Abdul, Wassie, Gizachew Tadesse, Wickramasinghe, Nuwan Darshana, Yaghoubi, Sajad, Yahya, Gahin Abdulraheem Tayib Yahya, Yahyazadeh Jabbari, Seyed Hossein, Yigit, Arzu, Yiğit, Vahit, Yon, Dong Keon, Yonemoto, Naohiro, Zahir, Mazyar, Zaman, Burhan Abdullah, Zaman, Sojib Bin, Zangiabadian, Moein, Zare, Iman, Zastrozhin, Mikhail Sergeevich, Zhang, Zhi-Jiang, Zheng, Peng, Zhong, Chenwen, Zoladl, Mohammad, Zumla, Alimuddin, Hay, Simon I, Dolecek, Christiane, Sartorius, Benn, Murray, Christopher J L, and Naghavi, Mohsen

Subjects
Male, Bacteria, Syndrome, Bacterial Infections, General Medicine, Global Health, Global Burden of Disease, Risk Factors, Sepsis, Humans, Female, Mortality, Child, Africa South of the Sahara
Abstract

Background: Reducing the burden of death due to infection is an urgent global public health priority. Previous studies have estimated the number of deaths associated with drug-resistant infections and sepsis and found that infections remain a leading cause of death globally. Understanding the global burden of common bacterial pathogens (both susceptible and resistant to antimicrobials) is essential to identify the greatest threats to public health. To our knowledge, this is the first study to present global comprehensive estimates of deaths associated with 33 bacterial pathogens across 11 major infectious syndromes. Methods: We estimated deaths associated with 33 bacterial genera or species across 11 infectious syndromes in 2019 using methods from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2019, in addition to a subset of the input data described in the Global Burden of Antimicrobial Resistance 2019 study. This study included 343 million individual records or isolates covering 11 361 study-location-years. We used three modelling steps to estimate the number of deaths associated with each pathogen: deaths in which infection had a role, the fraction of deaths due to infection that are attributable to a given infectious syndrome, and the fraction of deaths due to an infectious syndrome that are attributable to a given pathogen. Estimates were produced for all ages and for males and females across 204 countries and territories in 2019. 95% uncertainty intervals (UIs) were calculated for final estimates of deaths and infections associated with the 33 bacterial pathogens following standard GBD methods by taking the 2·5th and 97·5th percentiles across 1000 posterior draws for each quantity of interest. Findings: From an estimated 13·7 million (95% UI 10·9–17·1) infection-related deaths in 2019, there were 7·7 million deaths (5·7–10·2) associated with the 33 bacterial pathogens (both resistant and susceptible to antimicrobials) across the 11 infectious syndromes estimated in this study. We estimated deaths associated with the 33 bacterial pathogens to comprise 13·6% (10·2–18·1) of all global deaths and 56·2% (52·1–60·1) of all sepsis-related deaths in 2019. Five leading pathogens—Staphylococcus aureus, Escherichia coli, Streptococcus pneumoniae, Klebsiella pneumoniae, and Pseudomonas aeruginosa—were responsible for 54·9% (52·9–56·9) of deaths among the investigated bacteria. The deadliest infectious syndromes and pathogens varied by location and age. The age-standardised mortality rate associated with these bacterial pathogens was highest in the sub-Saharan Africa super-region, with 230 deaths (185–285) per 100 000 population, and lowest in the high-income super-region, with 52·2 deaths (37·4–71·5) per 100 000 population. S aureus was the leading bacterial cause of death in 135 countries and was also associated with the most deaths in individuals older than 15 years, globally. Among children younger than 5 years, S pneumoniae was the pathogen associated with the most deaths. In 2019, more than 6 million deaths occurred as a result of three bacterial infectious syndromes, with lower respiratory infections and bloodstream infections each causing more than 2 million deaths and peritoneal and intra-abdominal infections causing more than 1 million deaths. Interpretation: The 33 bacterial pathogens that we investigated in this study are a substantial source of health loss globally, with considerable variation in their distribution across infectious syndromes and locations. Compared with GBD Level 3 underlying causes of death, deaths associated with these bacteria would rank as the second leading cause of death globally in 2019; hence, they should be considered an urgent priority for intervention within the global health community. Strategies to address the burden of bacterial infections include infection prevention, optimised use of antibiotics, improved capacity for microbiological analysis, vaccine development, and improved and more pervasive use of available vaccines. These estimates can be used to help set priorities for vaccine need, demand, and development. Funding: Bill & Melinda Gates Foundation, Wellcome Trust, and Department of Health and Social Care, using UK aid funding managed by the Fleming Fund.

Published
2022

48. HIV infection and cardiovascular disease in women.

Author

Womack, Julie, Chang, Chung-Chou, So-Armah, Kaku, Alcorn, Charles, Baker, Jason, Brown, Sheldon, Gottdiener, John, Gottlieb, Stephen, Justice, Amy, Leaf, David, McGinnis, Kathleen, Rimland, David, Rodriguez-Barradas, Maria, Sico, Jason, Skanderson, Melissa, Tindle, Hilary, Tracy, Russell, Warner, Alberta, Freiberg, Matthew, Butt, Adeel, Gibert, Cynthia, Goetz, Matthew, and Budoff, Matthew

Subjects
AIDS, CVD risk factors, Women, Adult, Age Distribution, Aged, Cardiovascular Diseases, Case-Control Studies, Comorbidity, Confidence Intervals, Female, HIV Infections, Humans, Longitudinal Studies, Middle Aged, Prevalence, Proportional Hazards Models, Prospective Studies, Risk Assessment, Severity of Illness Index, Survival Analysis, United States, User-Computer Interface, Veterans
Abstract

BACKGROUND: HIV infection is associated with increased risk of cardiovascular disease (CVD) in men. Whether HIV is an independent risk factor for CVD in women has not yet been established. METHODS AND RESULTS: We analyzed data from the Veterans Aging Cohort Study on 2187 women (32% HIV infected [HIV(+)]) who were free of CVD at baseline. Participants were followed from their first clinical encounter on or after April 01, 2003 until a CVD event, death, or the last follow-up date (December 31, 2009). The primary outcome was CVD (acute myocardial infarction [AMI], unstable angina, ischemic stroke, and heart failure). CVD events were defined using clinical data, International Classification of Diseases, Ninth Revision, Clinical Modification codes, and/or death certificate data. We used Cox proportional hazards models to assess the association between HIV and incident CVD, adjusting for age, race/ethnicity, lipids, smoking, blood pressure, diabetes, renal disease, obesity, hepatitis C, and substance use/abuse. Median follow-up time was 6.0 years. Mean age at baseline of HIV(+) and HIV uninfected (HIV(-)) women was 44.0 versus 43.2 years (P

Published
2014

49. Hepatic decompensation in antiretroviral-treated patients co-infected with HIV and hepatitis C virus compared with hepatitis C virus-monoinfected patients: a cohort study.

Author

Lo Re, Vincent, Kallan, Michael J, Tate, Janet P, Localio, A Russell, Lim, Joseph K, Goetz, Matthew Bidwell, Klein, Marina B, Rimland, David, Rodriguez-Barradas, Maria C, Butt, Adeel A, Gibert, Cynthia L, Brown, Sheldon T, Park, Lesley, Dubrow, Robert, Reddy, K Rajender, Kostman, Jay R, Strom, Brian L, and Justice, Amy C

Subjects
Hepatitis - C, Digestive Diseases, Clinical Research, Chronic Liver Disease and Cirrhosis, HIV/AIDS, Emerging Infectious Diseases, Infectious Diseases, Liver Disease, Hepatitis, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Infection, Good Health and Well Being, Adult, Anti-Retroviral Agents, Ascites, Bacterial Infections, Carcinoma, Hepatocellular, Coinfection, Esophageal and Gastric Varices, Female, Gastrointestinal Hemorrhage, HIV, HIV Infections, Hepatitis C, Chronic, Humans, Incidence, Liver Neoplasms, Male, Medication Adherence, Middle Aged, Peritonitis, RNA, Viral, Retrospective Studies, Treatment Outcome, Viral Load, Clinical Sciences, Public Health and Health Services
Abstract

BackgroundThe incidence and determinants of hepatic decompensation have been incompletely examined among patients co-infected with HIV and hepatitis C virus (HCV) in the antiretroviral therapy (ART) era, and few studies have compared outcome rates with those of patients with chronic HCV alone.ObjectiveTo compare the incidence of hepatic decompensation between antiretroviral-treated patients co-infected with HIV and HCV and HCV-monoinfected patients and to evaluate factors associated with decompensation among co-infected patients receiving ART.DesignRetrospective cohort study.SettingVeterans Health Administration.Patients4280 co-infected patients who initiated ART and 6079 HCV-monoinfected patients receiving care between 1997 and 2010. All patients had detectable HCV RNA and were HCV treatment-naive.MeasurementsIncident hepatic decompensation, determined by diagnoses of ascites, spontaneous bacterial peritonitis, or esophageal variceal hemorrhage.ResultsThe incidence of hepatic decompensation was greater among co-infected than monoinfected patients (7.4% vs. 4.8% at 10 years; P < 0.001). Compared with HCV-monoinfected patients, co-infected patients had a higher rate of hepatic decompensation (hazard ratio [HR] accounting for competing risks, 1.56 [95% CI, 1.31 to 1.86]). Co-infected patients who maintained HIV RNA levels less than 1000 copies/mL still had higher rates of decompensation than HCV-monoinfected patients (HR, 1.44 [CI, 1.05 to 1.99]). Baseline advanced hepatic fibrosis (FIB-4 score >3.25) (HR, 5.45 [CI, 3.79 to 7.84]), baseline hemoglobin level less than 100 g/L (HR, 2.24 [CI, 1.20 to 4.20]), diabetes mellitus (HR, 1.88 [CI, 1.38 to 2.56]), and nonblack race (HR, 2.12 [CI, 1.65 to 2.72]) were each associated with higher rates of decompensation among co-infected patients.LimitationObservational study of predominantly male patients.ConclusionDespite receiving ART, patients co-infected with HIV and HCV had higher rates of hepatic decompensation than HCV-monoinfected patients. Rates of decompensation were higher for co-infected patients with advanced liver fibrosis, severe anemia, diabetes, and nonblack race.Primary funding sourceNational Institutes of Health.

Published
2014

50. AIPL1 implicated in the pathogenesis of two cases of autosomal recessive retinal degeneration.

Author

Li, David, Jin, Chongfei, Jiao, Xiaodong, Li, Lin, Bushra, Tahmina, Naeem, Muhammad Asif, Butt, Nadeem H, Husnain, Tayyab, Sieving, Paul A, Riazuddin, Sheikh, Riazuddin, S Amer, and Hejtmancik, J Fielding

Subjects
Fundus Oculi, Chromosomes, Human, Pair 17, Humans, Retinal Degeneration, Adaptor Proteins, Signal Transducing, Carrier Proteins, Eye Proteins, RNA Splice Sites, Electroretinography, Pedigree, Family, Amino Acid Sequence, Protein Structure, Tertiary, Haplotypes, Genes, Recessive, Lod Score, Mutation, Molecular Sequence Data, Adult, Middle Aged, Pakistan, Female, Male, Chromosomes, Human, Pair 17, Adaptor Proteins, Signal Transducing, Protein Structure, Tertiary, Genes, Recessive, Opthalmology and Optometry, Ophthalmology & Optometry
Abstract

PurposeTo localize and identify the gene and mutations causing autosomal recessive retinal dystrophy in two consanguineous Pakistani families.MethodsConsanguineous families from Pakistan were ascertained to be affected with autosomal recessive retinal degeneration. All affected individuals underwent thorough ophthalmologic examinations. Blood samples were collected, and genomic DNA was extracted using a salting out procedure. Genotyping was performed using microsatellite markers spaced at approximately 10 cM intervals. Two-point linkage analysis was performed with the lod score method. Direct DNA sequencing of amplified genomic DNA was performed for mutation screening of candidate genes.ResultsGenome-wide linkage scans yielded a lod score of 3.05 at θ=0 for D17S1832 and 3.82 at θ=0 for D17S938, localizing the disease gene to a 12.22 cM (6.64 Mb) region flanked by D17S1828 and D17S1852 for family 61032 and family 61227, which contains aryl hydrocarbon receptor interacting protein-like 1 (AIPL1), a gene previously implicated in recessive Leber congenital amaurosis and autosomal dominant cone-rod dystrophy. Sequencing of AIPL1 showed a homozygous c.773G>C (p.Arg258Pro) sequence change in all affected individuals of family 61032 and a homozygous c.465G>T (p.(H93_Q155del)) change in all affected members of family 61227.ConclusionsThe results strongly suggest that the c.773G>C (p.R258P) and c.465G>T (p.(H93_Q155del)) mutations in AIPL1 cause autosomal recessive retinal degeneration in these consanguineous Pakistani families.

Published
2014

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