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BACKGROUND AND AIM Patients with HIV-hepatitis C virus (HCV) coinfection progress towards liver fibrosis and cirrhosis more rapidly compared with HCV mono-infected individuals. This necessitates an accurate assessment of liver stiffness with transient elastography to guide treatment. METHODS Searches of PubMed, EMBASE, Web of Science, and the Cochrane Library databases were performed through January 2016 to assess the diagnostic accuracy of transient elastography for liver stiffness in the HIV-HCV population. Included studies were analyzed according to the Cochrane DTA Working Group methodology. Bivariate and hierarchical models were used to compute pooled sensitivity and specificity. Positive and negative likelihood ratios were also determined. A Fagan nomogram was constructed. Meta-regression analysis was performed with assessment of publication bias using Deeks' funnel plot asymmetry testing. RESULTS A total of six studies (n = 756) met the inclusion criteria. The diagnostic accuracy of elastography for the diagnosis of moderate (≥F2) fibrosis was 88% (95% confidence interval [CI], 0.85-0.90). The pooled sensitivity and specificity of moderate fibrosis was 97% (95% CI, 0.82-0.91) and 64% (95% CI, 0.45-0.79), respectively. The diagnostic accuracy of elastography for the assessment of cirrhosis was 94% (95% CI, 0.91-0.95). The pooled sensitivity and specificity for cirrhosis was 90% (95% CI, 0.74-0.97) and 87% (95% CI, 0.80-0.92), respectively. Meta-regression analysis demonstrated that CD4 cell count did not impact diagnostic accuracy of elastography. CONCLUSIONS Transient elastography is a noninvasive imaging modality with excellent ability to assess for cirrhosis in patients with HIV-HCV coinfection.

Chronic hepatitis B virus (CHB) chronically infects over 350 million people worldwide (1). CHB can lead to end stage liver disease and hepatocellular cancer with significant morbidity and mortality (2). Infants born to mothers who are positive for both hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) have a 70–90% chance of acquiring perinatal hepatitis B virus (HBV) infection (3). Postnatal hepatitis B immunization (HBIG) plus HBV vaccine administered within 24 h of birth reduces vertical transmission in about 85–95% of recipients (3). The main causes of prophylaxis failure include high maternal viral load, HBeAg positivity, in utero infection, escape mutants and the immune status of the mother (4). Of these, high maternal serum viral load (HBV DNA level >106 copies/ml) appears to be the major cause of prophylaxis failure, with up to 3–9% of perinatal transmissions reported despite both active and passive immunizations (2, 5). Antiviral drugs are safe and effective in the third trimester to prevent intrauterine transmission of hepatitis B virus and are recommended for CHB-infected gravid mothers (between weeks 28 and 32) with high viral load, followed by postnatal HBIG in the newborn (2, 5–9). Although all major liver society guidelines recommend third trimester antiviral therapy for women at higher risk of mother-to-child transmission of HBV, several areas of controversy remain, including the preferred antiviral drug, the optimal HBV viral load that warrants treatment, the gestational week at which to initiate therapy, and when to stop treatment after delivery (2, 5, 9). Antiviral therapies which have been used to decrease the HBV DNA levels during late pregnancy include nucleotide/nucleoside analogue polymerase inhibitors such as lamivudine (LAM), telbivudine (TBV), entecavir (ETV) and tenofovir (TDV) (1, 2, 4–18). Despite the benefits of adding an anitiviral agent to standard immunoprophylaxis, it is unknown whether one of these antiviral agents is superior to the other. Although clinical trials have evaluated each of these antiviral agents, no head-to-head comparison studies have been performed. In this study, we use a network meta-analysis design to compare the efficacy of the various antiviral drugs used in the prevention of vertical transmission of HBV.

Background & Aims In light of the dramatically changing hepatitis C therapeutic landscape, knowledge of the current burden of HCV infection in the general population of the United States is critical. Methods The National Health and Nutrition Examination survey collects nationally representative data on HCV infection in the civilian population of the United States. Data from 2001 to 2010 were combined for this study. HCV testing was completed in 38,025 participants. Results The prevalence of anti-HCV in the United Sates decreased from 1.9% (95% CI 1.5%–2.5%) in 2001–2002 to 1.3% (95% CI 0.9%–1.8%) in 2005–2006, and remained stable up to 2010. About 67% of all infected persons were positive for HCV RNA, indicating 2.3 million people with chronic HCV infection, of whom 68% have genotype 1. Seventy percent of infected persons were born between 1945 and 1965, with prevalence of 3.5% (95% CI 2.2%–4.8%). The stable rate since 2006 is mostly related to prevalent cases and foreign born persons migrating into US. Other important risk factors include less education and low economic status. Race, HIV status, number of sexual partners, and blood transfusions are no longer associated with HCV infection. Conclusions As of 2010, approximately 2.3 million persons were chronically infected with Hepatitis C in the US. Most of those infected are prevalent, rather than incident cases. The prevalence of HCV was on the decline, but has stabilized since 2006. Future studies should explore reasons for no decline in HCV prevalence since 2006.

Background This paper examines socio-economic and geographic differences in payment and payment coping mechanisms for health services in southeast Nigeria. It shows the extent to which the poor and rural dwellers disproportionally bear the burden of health care costs and offers policy recommendations for improvements. Methods Questionnaires were used to collect data from 3071 randomly selected households in six communities in southeast Nigeria using a four week recall. The sample was divided into quintiles (Q1-Q5) using a socio-economic status (SES) index as well as into geographic groups (rural, peri-urban and urban). Tabulations and logistic regression were used to determine the relationships between payment and payment coping mechanisms and key independent variables. Q1/Q5 and rural/urban ratios were the measures of equity. Results Most of the respondents used out-of-pocket spending (OOPS) and own money to pay for healthcare. There was statistically significant geographic differences in the use of own money to pay for health services indicating more use among rural dwellers. Logistic regression showed statistically significant geographic differences in the use of both OOPS and own money when controlling for the effects of potential cofounders. Conclusions This study shows statistically significant geographic differences in the use of OOPS and own money to pay for health services. Though the SES differences were not statistically significant, they showed high equity ratios indicating more use among poor and rural dwellers. The high expenditure incurred on drugs alone highlights the need for expediting pro-poor interventions like exemptions and waivers aimed at improving access to health care for the vulnerable poor and rural dwellers.

Background & Aims We investigated the prevalence of and trends and risk factors for fecal incontinence (FI) in the United States among non-institutionalized adults from 2005 to 2010. Methods We analyzed data from 14,759 participants in the U.S. National Health and Nutrition Examination Survey (49% women, 20 years or older) from 2005 to 2010 (the FI Severity Index was added in 2005–2006). FI was defined as accidental leakage of solid or liquid stool or mucus at least once in preceding month. Sampling weights were used to obtain estimates for the national population. Logistic regression was used to identify risk factors for FI. Results The prevalence of FI among non-institutionalized U.S. adults was 8.39% (95% confidence interval, 7.76–9.05). It was stable throughout the study period: 8.26% in 2005–2006, 8.48% in 2007–2008, and 8.41% in 2009–2010. FI resulted in release of liquid stool in most cases (6.16%). Prevalence increased with age from 2.91% among 20- to 29-year-old participants to 16.16% (14.15%–18.39%) among participants 70 years and older. Independent risk factors for FI included older age, diabetes mellitus, urinary incontinence, frequent and loose stools, and multiple chronic illnesses. FI was more common among women only when they had urinary incontinence. Conclusions FI is a common problem among non-institutionalized U.S. adults. Its prevalence remained stable from 2005–2010. Diabetes mellitus and chronic diarrhea are modifiable risk factors. Future studies on risk factors for FI should assess for presence of urinary incontinence.

Background: Indomethacin (INDO) is a non-steroidal anti-inflammatory drug (NSAID) used for the treatment of patent ductus arteriosus in preterm infants and as a tocolytic agent in pregnant women. The exposure of preterm infants to INDO is associated with an increased risk of developing enteropathies such as necrotizing enterocolitis. Despite increasing progress in establishing the pathways involved in NSAID-induced damage, understanding the pathogenesis of gastrointestinal injury by NSAIDs in neonates relies on a limited number of studies carried out in animal models. Aims: In the present study, we combined our method for maintaining the mid-gestation human intestine in serum-free organ culture with highthroughput genomic studies and bioinformatic pathway analysis to investigate the specific intestinal effects of INDO on the overall physiology of both the small and large intestine at mid-gestation. Methods: After determining the optimal concentration of INDO to be 1μM (.90% inhibition of intestinal prostaglandin E2 production), a dose that corresponds to the range of circulating levels in treated preterm babies, we used Illumina microarrays to establish global gene expression profiles in human intestinal explants (ileums and colons) in response to an INDO treatment of 48 h. Differentially expressed genes between control and INDO-treated explants were determined using the Mann-Whitney test (p , 0.05), and further analyzed with Ingenuity Pathway Analysis software (IPA 8.8) to identify biological functions and canonical pathways modulated by INDO. Results: The gene expression profiles identified revealed that a large proportion of statistically significant biological, physiological and metabolic functions were modulated by INDO in the immature intestine. As expected, a number of these significantly modulated functions were inflammation-related such as "Inflammatory diseases", "Inflammatory response", and "Acute phase response". Noteworthily, we have identified a series of metabolic-related gene clusters that were found to be significantly modulated, namely "Glycolysis/gluconeogenesis", "Oxidative phosphorylation" and "Free radical scavenging/oxidoreductase activity". Further analysis by qPCR confirmed that the expression of representative genes involved in these metabolic functions, such as ALDOA, LDHA, NDUFA9, DUOX2, SOD2, and TFF1, was inhibited by INDO in both intestinal segments, indicating that this adverse metabolic effect could be a component of the pathogenesis of intestinal damage induced by INDO. Conclusion: This study identified several different metabolic pathways that are modulated by INDO in the immature human intestine and suggests a mechanistic basis for better understanding the contributing effects of INDO and other NSAIDs on neonatal intestinal pathologies.

the anal verge (P,0.01), whilst gender and anastomotic height were not associated with constipation. Neither age nor radiotherapy were associated with constipation or FI. Conclusions: Bowel dysfunction, consisting of FI and constipation (characterised by evacuatory dysfunction), appears to be prevalent after anterior resection surgery and persists up to a decade after surgery. Low anastomotic height, reflecting loss of more rectum, is associated with FI, but not constipation.