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3. Intake of B vitamins and the risk of developing islet autoimmunity and type 1 diabetes in the TEDDY study

Author

Hakola, Leena, Mramba, Lazarus K., Uusitalo, Ulla, Andrén Aronsson, Carin, Hummel, Sandra, Niinistö, Sari, Erlund, Iris, Yang, Jimin, Rewers, Marian J., Akolkar, Beena, McIndoe, Richard A., Rich, Stephen S., Hagopian, William A., Ziegler, Anette, Lernmark, Åke, Toppari, Jorma, Krischer, Jeffrey P., Norris, Jill M., and Virtanen, Suvi M.

Published
2024
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6. Abatacept for Delay of Type 1 Diabetes Progression in Stage 1 Relatives at Risk: A Randomized, Double-Masked, Controlled Trial

Author

Russell, William E, Bundy, Brian N, Anderson, Mark S, Cooney, Laura A, Gitelman, Stephen E, Goland, Robin S, Gottlieb, Peter A, Greenbaum, Carla J, Haller, Michael J, Krischer, Jeffrey P, Libman, Ingrid M, Linsley, Peter S, Long, S Alice, Lord, Sandra M, Moore, Daniel J, Moore, Wayne V, Moran, Antoinette M, Muir, Andrew B, Raskin, Philip, Skyler, Jay S, Wentworth, John M, Wherrett, Diane K, Wilson, Darrell M, Ziegler, Anette-Gabriele, Herold, Kevan C, and Group, Type 1 Diabetes TrialNet Study

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Immunology, Clinical Research, Clinical Trials and Supportive Activities, Nutrition, Prevention, Diabetes, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Metabolic and endocrine, Humans, Abatacept, Diabetes Mellitus, Type 1, Immunosuppressive Agents, T-Lymphocytes, Regulatory, Glucose, Type 1 Diabetes TrialNet Study Group
Abstract

ObjectivePrevious studies showed that inhibiting lymphocyte costimulation reduces declining β-cell function in individuals newly diagnosed with type 1 diabetes. We tested whether abatacept would delay or prevent progression of type 1 diabetes from normal glucose tolerance (NGT) to abnormal glucose tolerance (AGT) or to diabetes and the effects of treatment on immune and metabolic responses.Research design and methodsWe conducted a phase 2, randomized, placebo-controlled, double-masked trial of abatacept in antibody-positive participants with NGT who received monthly abatacept/placebo infusions for 12 months. The end point was AGT or diabetes, assessed by oral glucose tolerance tests.ResultsA total of 101 participants received abatacept and 111 placebo. Of these, 81 (35 abatacept and 46 placebo) met the end point of AGT or type 1 diabetes diagnosis (hazard ratio 0.702; 95% CI 0.452, 1.09; P = 0.11) The C-peptide responses to oral glucose tolerance tests were higher in the abatacept arm (P < 0.03). Abatacept reduced the frequency of inducible T-cell costimulatory (ICOS)+ PD1+ T-follicular helper (Tfh) cells during treatment (P < 0.0001), increased naive CD4+ T cells, and also reduced the frequency of CD4+ regulatory T cells (Tregs) from the baseline (P = 0.0067). Twelve months after treatment, the frequency of ICOS+ Tfh, naive CD4+ T cells, and Tregs returned to baseline.ConclusionsAlthough abatacept treatment for 1 year did not significantly delay progression to glucose intolerance in at-risk individuals, it impacted immune cell subsets and preserved insulin secretion, suggesting that costimulation blockade may modify progression of type 1 diabetes.

Published
2023

8. High Concentrations of Immunoglobulin G Against Cow Milk Proteins and Frequency of Cow Milk Consumption Are Associated With the Development of Islet Autoimmunity and Type 1 Diabetes—The Trial to Reduce Insulin-dependent Diabetes Mellitus (IDDM) in the Genetically at Risk (TRIGR) Study

Author

Niinistö, Sari, Cuthbertson, David, Miettinen, Maija E, Hakola, Leena, Nucci, Anita, Korhonen, Tuuli E, Hyöty, Heikki, Krischer, Jeffrey P, Vaarala, Outi, Knip, Mikael, Savilahti, Erkki, and Virtanen, Suvi M

Published
2024
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9. A toxicology study of Csf2ra complementation and pulmonary macrophage transplantation therapy of hereditary PAP in mice

Author

Arumugam, Paritha, Carey, Brenna C., Wikenheiser-Brokamp, Kathryn A., Krischer, Jeffrey, Wessendarp, Matthew, Shima, Kenjiro, Chalk, Claudia, Stock, Jennifer, Ma, Yan, Black, Diane, Imbrogno, Michelle, Collins, Margaret, Kalenda Yombo, Dan Justin, Sakthivel, Haripriya, Suzuki, Takuji, Lutzko, Carolyn, Cancelas, Jose A., Adams, Michelle, Hoskins, Elizabeth, Lowe-Daniels, Dawn, Reeves, Lilith, Kaiser, Anne, and Trapnell, Bruce C.

Published
2024
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10. Distinct transcriptomic profiles in children prior to the appearance of type 1 diabetes-linked islet autoantibodies and following enterovirus infection

Author

Lin, Jake, Moradi, Elaheh, Salenius, Karoliina, Lehtipuro, Suvi, Häkkinen, Tomi, Laiho, Jutta E., Oikarinen, Sami, Randelin, Sofia, Parikh, Hemang M., Krischer, Jeffrey P., Toppari, Jorma, Lernmark, Åke, Petrosino, Joseph F., Ajami, Nadim J., She, Jin-Xiong, Hagopian, William A., Rewers, Marian J., Lloyd, Richard E., Rautajoki, Kirsi J., Hyöty, Heikki, and Nykter, Matti

Published
2023
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14. Imatinib therapy for patients with recent-onset type 1 diabetes: a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial

Author

Gitelman, Stephen E, Bundy, Brian N, Ferrannini, Ele, Lim, Noha, Blanchfield, J Lori, DiMeglio, Linda A, Felner, Eric I, Gaglia, Jason L, Gottlieb, Peter A, Long, S Alice, Mari, Andrea, Mirmira, Raghavendra G, Raskin, Philip, Sanda, Srinath, Tsalikian, Eva, Wentworth, John M, Willi, Steven M, Krischer, Jeffrey P, Bluestone, Jeffrey A, Group, Gleevec Trial Study, Barr, Mayalin, Buchanan, Jeanne, Cabbage, Joanne, Coleman, Peter, De La Vega, Monica, Evans-Molina, Carmella, Ferrara, Christine, Healy, Felicity, Higgins, Laurie, Hildinger, Megan, Jenkins, Margaret, Bryant, Nora Kayton, Kinderman, Amanda, Koshy, Nisha, Kost, Brianne, Krishfield, Suzanne, Kucheruk, Olena, Lindsley, Karen, Mantravadi, Manasa, Mesfin, Shelley, Michels, Aaron, Migre, Mary Ellen, Minnock, Pantea, Mohammed-Nur, Elham, Nelson, Jennifer, Nursing, Ashvin, O'Donnell, Ryan, Olivos, Diana, Parker, Melissa, Redl, Leanne, Reed, Nicole, Resnick, Brittany, Sayre, Peter, Serti, Elisavet, Sims, Emily, Smith, Karen, Soppe, Carol, Stuart, Fiona, Szubowicz, Sarah, Tansey, Michel, Terrell, Jennifer, Tersey, Sarah, Torok, Christine, Watson, Kelly, Wesch, Rebecca, Willi, Steven, and Woerner, Stephanie

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Trials and Supportive Activities, Prevention, Autoimmune Disease, Clinical Research, Diabetes, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Adolescent, Adult, Biomarkers, Blood Glucose, Diabetes Mellitus, Type 1, Double-Blind Method, Female, Follow-Up Studies, Humans, Imatinib Mesylate, Male, Middle Aged, Prognosis, Protein Kinase Inhibitors, Young Adult, Gleevec Trial Study Group, Medical Biochemistry and Metabolomics, Public Health and Health Services, Clinical sciences, Medical biochemistry and metabolomics
Abstract

BackgroundType 1 diabetes results from autoimmune-mediated destruction of β cells. The tyrosine kinase inhibitor imatinib might affect relevant immunological and metabolic pathways, and preclinical studies show that it reverses and prevents diabetes. Our aim was to evaluate the safety and efficacy of imatinib in preserving β-cell function in patients with recent-onset type 1 diabetes.MethodsWe did a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial. Patients with recent-onset type 1 diabetes (

Published
2021

15. Pregnancy in women with osteogenesis imperfecta: pregnancy characteristics, maternal, and neonatal outcomes

Author

Rao, Rashmi, Cuthbertson, David, Nagamani, Sandesh CS, Sutton, Vernon Reid, Lee, Brendan H, Krischer, Jeffrey, and Krakow, Deborah

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Preterm, Low Birth Weight and Health of the Newborn, Osteogenesis Imperfecta, Perinatal Period - Conditions Originating in Perinatal Period, Pediatric, Clinical Research, Rare Diseases, Infant Mortality, Contraception/Reproduction, Reproductive health and childbirth, Good Health and Well Being, Cesarean Section, Cross-Sectional Studies, Female, Humans, Infant, Infant, Newborn, Intensive Care Units, Neonatal, Pregnancy, fractures, maternal, neonatal outcomes, osteogenesis imperfecta, pregnancy, Reproductive medicine
Abstract

BackgroundWomen with rare diseases, such as osteogenesis imperfecta, may consider pregnancy, although data regarding outcomes, specific risks, and management strategies are lacking.ObjectiveThe Brittle Bone Disorders Consortium of the National Institute of Health Rare Diseases Clinical Research Network established an Osteogenesis Imperfecta Pregnancy Registry to collect and evaluate pregnancy, maternal, and neonatal outcomes in women with osteogenesis imperfecta.Study designThis was a cross-sectional, survey-based study. Appropriate participants of the Brittle Bone Disorders Consortium Contact Registry were invited to participate in the study. Self-reported information regarding pregnancy characteristics and maternal and neonatal outcomes of women with osteogenesis imperfecta was compared with that of the general population, referenced by literature-based standards. Furthermore, compared with the general population, cohorts of women and fetuses with osteogenesis imperfecta were evaluated to determine whether the presence of osteogenesis imperfecta conveyed an increase in antepartum, intrapartum, and postpartum complications and an increase in adverse neonatal outcomes.ResultsHere, a total 132 participants completed the survey. Compared with the general population, women with osteogenesis imperfecta had higher rates of diabetes in pregnancy (13.3% vs 7%; 95% confidence interval, 7.0-19.6; P=.049), cesarean delivery (68.5% vs 32.7%; 95% confidence interval, 59.9-77.1; P

Published
2021

16. Associations of dietary patterns between age 9 and 24 months with risk of celiac disease autoimmunity and celiac disease among children at increased risk

Author

Hård af Segerstad, Elin M., Mramba, Lazarus K., Liu, Xiang, Uusitalo, Ulla, Yang, Jimin, Norris, Jill, Virtanen, Suvi M., Liu, Edwin, Kurppa, Kalle, Koletzko, Sibylle, Ziegler, Annette G., Toppari, Jorma, Rewers, Marian, Akolkar, Beena, Krischer, Jeffrey P., Aronsson, Carin Andrén, and Agardh, Daniel

Published
2023
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17. One-food versus six-food elimination diet therapy for the treatment of eosinophilic oesophagitis: a multicentre, randomised, open-label trial

Author

Kliewer, Kara L, Gonsalves, Nirmala, Dellon, Evan S, Katzka, David A, Abonia, Juan P, Aceves, Seema S, Arva, Nicoleta C, Besse, John A, Bonis, Peter A, Caldwell, Julie M, Capocelli, Kelley E, Chehade, Mirna, Cianferoni, Antonella, Collins, Margaret H, Falk, Gary W, Gupta, Sandeep K, Hirano, Ikuo, Krischer, Jeffrey P, Leung, John, Martin, Lisa J, Menard-Katcher, Paul, Mukkada, Vincent A, Peterson, Kathryn A, Shoda, Tetsuo, Rudman Spergel, Amanda K, Spergel, Jonathan M, Yang, Guang-Yu, Zhang, Xue, Furuta, Glenn T, and Rothenberg, Marc E

Published
2023
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18. Longitudinal Metabolome-Wide Signals Prior to the Appearance of a First Islet Autoantibody in Children Participating in the TEDDY Study

Author

Li, Qian, Parikh, Hemang, Butterworth, Martha D, Lernmark, Åke, Hagopian, William, Rewers, Marian, She, Jin-Xiong, Toppari, Jorma, Ziegler, Anette-G, Akolkar, Beena, Fiehn, Oliver, Fan, Sili, Krischer, Jeffrey P, Barbour, Aaron, Bautista, Kimberly, Baxter, Judith, Felipe-Morales, Daniel, Driscoll, Kimberly, Frohnert, Brigitte I, Stahl, Marisa, Gesualdo, Patricia, Hoffman, Michelle, Karban, Rachel, Liu, Edwin, Norris, Jill, Peacock, Stesha, Shorrosh, Hanan, Steck, Andrea, Stern, Megan, Villegas, Erica, Waugh, Kathleen, Simell, Olli G, Adamsson, Annika, Ahonen, Suvi, Åkerlund, Mari, Hakola, Leena, Hekkala, Anne, Holappa, Henna, Hyöty, Heikki, Ikonen, Anni, Ilonen, Jorma, Jäminki, Sinikka, Jokipuu, Sanna, Karlsson, Leena, Kero, Jukka, Kähönen, Miia, Knip, Mikael, Koivikko, Minna-Liisa, Koskinen, Merja, Koreasalo, Mirva, Kurppa, Kalle, Kytölä, Jarita, Latva-aho, Tiina, Lindfors, Katri, Lönnrot, Maria, Mäntymäki, Elina, Mattila, Markus, Miettinen, Maija, Multasuo, Katja, Mykkänen, Teija, Niininen, Tiina, Niinistö, Sari, Nyblom, Mia, Oikarinen, Sami, Ollikainen, Paula, Othmani, Zhian, Pohjola, Sirpa, Rajala, Petra, Rautanen, Jenna, Riikonen, Anne, Riski, Eija, Pekkola, Miia, Romo, Minna, Ruohonen, Satu, Simell, Satu, Sjöberg, Maija, Stenius, Aino, Tossavainen, Päivi, Vähä-Mäkilä, Mari, Vainionpää, Sini, Varjonen, Eeva, Veijola, Riitta, Viinikangas, Irene, Virtanen, Suvi M, Schatz, Desmond, Hopkins, Diane, Steed, Leigh, Bryant, Jennifer, Silvis, Katherine, Haller, Michael, Gardiner, Melissa, McIndoe, Richard, Sharma, Ashok, Anderson, Stephen W, Jacobsen, Laura, Marks, John, and Towe, PD

Subjects
Pediatric, Autoimmune Disease, Diabetes, Prevention, Nutrition, Metabolic and endocrine, Alanine, Amino Acids, Branched-Chain, Autoantibodies, Child, Preschool, Dehydroascorbic Acid, Diabetes Mellitus, Type 1, Fatty Acids, Female, Genetic Predisposition to Disease, Glutamate Decarboxylase, Humans, Infant, Infant, Newborn, Insulin Antibodies, Longitudinal Studies, Male, Metabolome, Methionine, Phosphatidylethanolamines, Prodromal Symptoms, Proline, Risk, Triglycerides, gamma-Aminobutyric Acid, TEDDY Study Group, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

Children at increased genetic risk for type 1 diabetes (T1D) after environmental exposures may develop pancreatic islet autoantibodies (IA) at a very young age. Metabolic profile changes over time may imply responses to exposures and signal development of the first IA. Our present research in The Environmental Determinants of Diabetes in the Young (TEDDY) study aimed to identify metabolome-wide signals preceding the first IA against GAD (GADA-first) or against insulin (IAA-first). We profiled metabolomes by mass spectrometry from children's plasma at 3-month intervals after birth until appearance of the first IA. A trajectory analysis discovered each first IA preceded by reduced amino acid proline and branched-chain amino acids (BCAAs), respectively. With independent time point analysis following birth, we discovered dehydroascorbic acid (DHAA) contributing to the risk of each first IA, and γ-aminobutyric acid (GABAs) associated with the first autoantibody against insulin (IAA-first). Methionine and alanine, compounds produced in BCAA metabolism and fatty acids, also preceded IA at different time points. Unsaturated triglycerides and phosphatidylethanolamines decreased in abundance before appearance of either autoantibody. Our findings suggest that IAA-first and GADA-first are heralded by different patterns of DHAA, GABA, multiple amino acids, and fatty acids, which may be important to primary prevention of T1D.

Published
2020

19. Introducing the Endotype Concept to Address the Challenge of Disease Heterogeneity in Type 1 Diabetes.

Author

Battaglia, Manuela, Ahmed, Simi, Anderson, Mark S, Atkinson, Mark A, Becker, Dorothy, Bingley, Polly J, Bosi, Emanuele, Brusko, Todd M, DiMeglio, Linda A, Evans-Molina, Carmella, Gitelman, Stephen E, Greenbaum, Carla J, Gottlieb, Peter A, Herold, Kevan C, Hessner, Martin J, Knip, Mikael, Jacobsen, Laura, Krischer, Jeffrey P, Long, S Alice, Lundgren, Markus, McKinney, Eoin F, Morgan, Noel G, Oram, Richard A, Pastinen, Tomi, Peters, Michael C, Petrelli, Alessandra, Qian, Xiaoning, Redondo, Maria J, Roep, Bart O, Schatz, Desmond, Skibinski, David, and Peakman, Mark

Subjects
Humans, Diabetes Mellitus, Type 1, Disease Progression, Insulin, Blood Glucose, Phenotype, Precision Medicine, Biological Variation, Population, Clinical Trials and Supportive Activities, Autoimmune Disease, Diabetes, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Good Health and Well Being, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

The clinical diagnosis of new-onset type 1 diabetes has, for many years, been considered relatively straightforward. Recently, however, there is increasing awareness that within this single clinical phenotype exists considerable heterogeneity: disease onset spans the complete age range; genetic susceptibility is complex; rates of progression differ markedly, as does insulin secretory capacity; and complication rates, glycemic control, and therapeutic intervention efficacy vary widely. Mechanistic and immunopathological studies typically show considerable patchiness across subjects, undermining conclusions regarding disease pathways. Without better understanding, type 1 diabetes heterogeneity represents a major barrier both to deciphering pathogenesis and to the translational effort of designing, conducting, and interpreting clinical trials of disease-modifying agents. This realization comes during a period of unprecedented change in clinical medicine, with increasing emphasis on greater individualization and precision. For complex disorders such as type 1 diabetes, the option of maintaining the "single disease" approach appears untenable, as does the notion of individualizing each single patient's care, obliging us to conceptualize type 1 diabetes less in terms of phenotypes (observable characteristics) and more in terms of disease endotypes (underlying biological mechanisms). Here, we provide our view on an approach to dissect heterogeneity in type 1 diabetes. Using lessons from other diseases and the data gathered to date, we aim to delineate a roadmap through which the field can incorporate the endotype concept into laboratory and clinical practice. We predict that such an effort will accelerate the implementation of precision medicine and has the potential for impact on our approach to translational research, trial design, and clinical management.

Published
2020

20. Advancing patient care through the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR)

Author

Aceves, Seema, Collins, Margaret H, Rothenberg, Marc E, Furuta, Glenn T, Gonsalves, Nirmala, Researchers, Consortium of Eosinophilic Gastrointestinal Disease, Abonia, J Pablo, Almonte, Samuel, Andrews, Rachel, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, MurrayPetzold, Cristin, Newbury, Robert, Nhu, Quan, Oyibo, Oghenekpaobor, Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Rudman-Spergel, Amanda, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, MaryJo, and Sun, Kiki

Subjects
Biomedical and Clinical Sciences, Immunology, Clinical Research, Digestive Diseases, Clinical Trials and Supportive Activities, Evaluation of treatments and therapeutic interventions, Detection, screening and diagnosis, 6.9 Resources and infrastructure (treatment evaluation), 4.5 Resources and infrastructure (detection), Good Health and Well Being, Biomedical Research, Clinical Trials as Topic, Enteritis, Eosinophilia, Eosinophilic Esophagitis, Gastritis, National Institutes of Health (U.S.), United States, Eosinophils, gastrointestinal, consortium, allergy, esophagitis, advocacy, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Allergy
Abstract

Recent advances in rare disease research are accelerated by the work of consortia that have been supported by the National Institutes of Health. Development of such consortia rely on multidisciplinary relationships and engagement with patient advocacy groups, as well as the National Institutes of Health and industry and academic partners. In this rostrum we present the development of such a process that focuses on eosinophilic gastrointestinal diseases. Principal investigators, patient advocacy groups, research assistants, and trainees work together to perform natural history studies that promote clinical trial readiness tools, conduct clinical trials, train a new generation of investigators, and perform innovative pilot studies.

Published
2020

21. Metabolite-related dietary patterns and the development of islet autoimmunity.

Author

Johnson, Randi K, Vanderlinden, Lauren, DeFelice, Brian C, Kechris, Katerina, Uusitalo, Ulla, Fiehn, Oliver, Sontag, Marci, Crume, Tessa, Beyerlein, Andreas, Lernmark, Åke, Toppari, Jorma, Ziegler, Anette-G, She, Jin-Xiong, Hagopian, William, Rewers, Marian, Akolkar, Beena, Krischer, Jeffrey, Virtanen, Suvi M, Norris, Jill M, and TEDDY Study Group

Subjects
TEDDY Study Group
Abstract

The role of diet in type 1 diabetes development is poorly understood. Metabolites, which reflect dietary response, may help elucidate this role. We explored metabolomics and lipidomics differences between 352 cases of islet autoimmunity (IA) and controls in the TEDDY (The Environmental Determinants of Diabetes in the Young) study. We created dietary patterns reflecting pre-IA metabolite differences between groups and examined their association with IA. Secondary outcomes included IA cases positive for multiple autoantibodies (mAb+). The association of 853 plasma metabolites with outcomes was tested at seroconversion to IA, just prior to seroconversion, and during infancy. Key compounds in enriched metabolite sets were used to create dietary patterns reflecting metabolite composition, which were then tested for association with outcomes in the nested case-control subset and the full TEDDY cohort. Unsaturated phosphatidylcholines, sphingomyelins, phosphatidylethanolamines, glucosylceramides, and phospholipid ethers in infancy were inversely associated with mAb+ risk, while dicarboxylic acids were associated with an increased risk. An infancy dietary pattern representing higher levels of unsaturated phosphatidylcholines and phospholipid ethers, and lower sphingomyelins was protective for mAb+ in the nested case-control study only. Characterization of this high-risk infant metabolomics profile may help shape the future of early diagnosis or prevention efforts.

Published
2019

22. The influence of pubertal development on autoantibody appearance and progression to type 1 diabetes in the TEDDY study

Author

Warncke, Katharina, primary, Tamura, Roy, additional, Schatz, Desmond A, additional, Veijola, Riitta, additional, Steck, Andrea K, additional, Akolkar, Beena, additional, Hagopian, William, additional, Krischer, Jeffrey P, additional, Lernmark, Åke, additional, Rewers, Marian J, additional, Toppari, Jorma, additional, McIndoe, Richard, additional, Ziegler, Anette-G, additional, Vehik, Kendra, additional, Haller, Michael J, additional, and Elding Larsson, Helena, additional

Published
2024
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25. An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes

Author

Herold, Kevan C, Bundy, Brian N, Long, S Alice, Bluestone, Jeffrey A, DiMeglio, Linda A, Dufort, Matthew J, Gitelman, Stephen E, Gottlieb, Peter A, Krischer, Jeffrey P, Linsley, Peter S, Marks, Jennifer B, Moore, Wayne, Moran, Antoinette, Rodriguez, Henry, Russell, William E, Schatz, Desmond, Skyler, Jay S, Tsalikian, Eva, Wherrett, Diane K, Ziegler, Anette-Gabriele, and Greenbaum, Carla J

Subjects
Clinical Research, Clinical Trials and Supportive Activities, Diabetes, Autoimmune Disease, Prevention, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Adolescent, Adult, Antibodies, Monoclonal, Humanized, CD3 Complex, Child, Diabetes Mellitus, Type 1, Disease Progression, Double-Blind Method, Exanthema, Female, Glucose Tolerance Test, HLA-DR3 Antigen, HLA-DR4 Antigen, Humans, Lymphocyte Count, Lymphopenia, Male, Middle Aged, Proportional Hazards Models, T-Lymphocytes, Young Adult, Type 1 Diabetes TrialNet Study Group, Medical and Health Sciences, General & Internal Medicine
Abstract

BackgroundType 1 diabetes is a chronic autoimmune disease that leads to destruction of insulin-producing beta cells and dependence on exogenous insulin for survival. Some interventions have delayed the loss of insulin production in patients with type 1 diabetes, but interventions that might affect clinical progression before diagnosis are needed.MethodsWe conducted a phase 2, randomized, placebo-controlled, double-blind trial of teplizumab (an Fc receptor-nonbinding anti-CD3 monoclonal antibody) involving relatives of patients with type 1 diabetes who did not have diabetes but were at high risk for development of clinical disease. Patients were randomly assigned to a single 14-day course of teplizumab or placebo, and follow-up for progression to clinical type 1 diabetes was performed with the use of oral glucose-tolerance tests at 6-month intervals.ResultsA total of 76 participants (55 [72%] of whom were ≤18 years of age) underwent randomization - 44 to the teplizumab group and 32 to the placebo group. The median time to the diagnosis of type 1 diabetes was 48.4 months in the teplizumab group and 24.4 months in the placebo group; the disease was diagnosed in 19 (43%) of the participants who received teplizumab and in 23 (72%) of those who received placebo. The hazard ratio for the diagnosis of type 1 diabetes (teplizumab vs. placebo) was 0.41 (95% confidence interval, 0.22 to 0.78; P = 0.006 by adjusted Cox proportional-hazards model). The annualized rates of diagnosis of diabetes were 14.9% per year in the teplizumab group and 35.9% per year in the placebo group. There were expected adverse events of rash and transient lymphopenia. KLRG1+TIGIT+CD8+ T cells were more common in the teplizumab group than in the placebo group. Among the participants who were HLA-DR3-negative, HLA-DR4-positive, or anti-zinc transporter 8 antibody-negative, fewer participants in the teplizumab group than in the placebo group had diabetes diagnosed.ConclusionsTeplizumab delayed progression to clinical type 1 diabetes in high-risk participants. (Funded by the National Institutes of Health and others; ClinicalTrials.gov number, NCT01030861.).

Published
2019

26. Low-Dose Anti-Thymocyte Globulin Preserves C-Peptide, Reduces HbA1c, and Increases Regulatory to Conventional T-Cell Ratios in New-Onset Type 1 Diabetes: Two-Year Clinical Trial Data

Author

Haller, Michael J, Long, S Alice, Blanchfield, J Lori, Schatz, Desmond A, Skyler, Jay S, Krischer, Jeffrey P, Bundy, Brian N, Geyer, Susan M, Warnock, Megan V, Miller, Jessica L, Atkinson, Mark A, Becker, Dorothy J, Baidal, David A, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Gottlieb, Peter A, Herold, Kevan C, Marks, Jennifer B, Moran, Antoinette, Rodriguez, Henry, Russell, William E, Wilson, Darrell M, Greenbaum, Carla J, Battaglia, Manuela, Becker, Dorothy, Bingley, Penelope, Bosi, Emanuele, Buckner, Jane, Clements, Mark, Colman, Peter G, DiMeglio, Linda, Evans-Molina, Carmella, Gottlieb, Peter, Herold, Kevan, Knip, Mikael, Lernmark, Ake, Moore, Wayne, Muir, Andrew, Palmer, Jerry, Peakman, Mark, Philipson, Louis, Raskin, Philip, Redondo, Maria, Russell, William, Sosenko, Jay M, Spain, Lisa, Wentworth, John, Wherrett, Diane, Winter, William, Ziegler, Anette, Anderson, Mark, Antinozzi, Peter, Insel, Richard, Kay, Thomas, Pugliese, Alberto, Roep, Bart, Toppari, Jorma, Leschek, Ellen, Bourcier, Katarzyna, Ridge, John, Rafkin, Lisa, Santiago, Irene, Bundy, Brian, Abbondondolo, Michael, Adams, Timothy, Asif, Ilma, Bjellquist, Jenna, Boonstra, Matthew, Burroughs, Cristina, Cleves, Mario, Cuthbertson, David, DeSalvatore, Meagan, Eberhard, Christopher, Fiske, Steve, Ford, Julie, Garmeson, Jennifer, Geyer, Susan, and Hays, Brian

Subjects
Prevention, Diabetes, Clinical Trials and Supportive Activities, Clinical Research, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Adolescent, Adult, Antilymphocyte Serum, C-Peptide, CD4-CD8 Ratio, Child, Diabetes Mellitus, Type 1, Double-Blind Method, Female, Flow Cytometry, Glycated Hemoglobin, Granulocyte Colony-Stimulating Factor, Humans, Immunologic Factors, Male, T-Lymphocytes, Regulatory, Young Adult, Type 1 Diabetes TrialNet ATG-GCSF Study Group, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

A three-arm, randomized, double-masked, placebo-controlled phase 2b trial performed by the Type 1 Diabetes TrialNet Study Group previously demonstrated that low-dose anti-thymocyte globulin (ATG) (2.5 mg/kg) preserved β-cell function and reduced HbA1c for 1 year in new-onset type 1 diabetes. Subjects (N = 89) were randomized to 1) ATG and pegylated granulocyte colony-stimulating factor (GCSF), 2) ATG alone, or 3) placebo. Herein, we report 2-year area under the curve (AUC) C-peptide and HbA1c, prespecified secondary end points, and potential immunologic correlates. The 2-year mean mixed-meal tolerance test-stimulated AUC C-peptide, analyzed by ANCOVA adjusting for baseline C-peptide, age, and sex (n = 82) with significance defined as one-sided P < 0.025, was significantly higher in subjects treated with ATG versus placebo (P = 0.00005) but not ATG/GCSF versus placebo (P = 0.032). HbA1c was significantly reduced at 2 years in subjects treated with ATG (P = 0.011) and ATG/GCSF (P = 0.022) versus placebo. Flow cytometry analyses demonstrated reduced circulating CD4:CD8 ratio, increased regulatory T-cell:conventional CD4 T-cell ratios, and increased PD-1+CD4+ T cells following low-dose ATG and ATG/GCSF. Low-dose ATG partially preserved β-cell function and reduced HbA1c 2 years after therapy in new-onset type 1 diabetes. Future studies should determine whether low-dose ATG might prevent or delay the onset of type 1 diabetes.

Published
2019

27. Randomized Trial of Lisinopril Versus Carvedilol to Prevent Trastuzumab Cardiotoxicity in Patients With Breast Cancer

Author

Guglin, Maya, Krischer, Jeffrey, Tamura, Roy, Fink, Angelina, Bello-Matricaria, Lauren, McCaskill-Stevens, Worta, and Munster, Pamela N

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Cardiovascular, Cancer, Clinical Trials and Supportive Activities, Clinical Research, Breast Cancer, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Adult, Aged, Antineoplastic Agents, Breast Neoplasms, Cardiotonic Agents, Carvedilol, Female, Heart, Humans, Lisinopril, Middle Aged, Stroke Volume, Trastuzumab, breast cancer, cardiotoxicity, ejection fraction, heart failure, trastuzumab, Cardiorespiratory Medicine and Haematology, Public Health and Health Services, Cardiovascular System & Hematology, Cardiovascular medicine and haematology
Abstract

BackgroundTrastuzumab is highly effective for human epidermal growth factor receptor type 2 (HER2)-positive breast cancer but is associated with a decline in left ventricular ejection fraction.ObjectivesThe purpose of this study was to determine whether angiotensin-converting enzyme inhibitors or beta-blockers reduce the rate of trastuzumab-induced cardiotoxicity (left ventricular ejection fraction decrease >10%, or >5% if below 50%) and limit treatment interruptions.MethodsIn this double-blind, multicenter, placebo-controlled trial, cardiotoxicity and treatment interruptions in patients with HER2-positive breast cancer treated with trastuzumab for 12 months were evaluated over a 2-year period. Patients were stratified by anthracycline use and then randomized to receive lisinopril, carvedilol, or placebo.ResultsThe study included 468 women, age 51 ± 10.7 years. For the entire cohort, cardiotoxicity was comparable in the 3 arms and occurred in 32% of patients on placebo, 29% on carvedilol, and 30% on lisinopril. For patients receiving anthracyclines, the event rates were higher in the placebo group (47%) than in the lisinopril (37%) and the carvedilol (31%) groups. Cardiotoxicity-free survival was longer on both carvedilol (hazard ratio: 0.49; 95% confidence interval: 0.27 to 0.89; p = 0.009) and lisinopril (hazard ratio: 0.53; 95% confidence interval: 0.30 to 0.94; p = 0.015) than on placebo. In the whole cohort, as well as in the anthracycline arm, patients on active therapy with either angiotensin-converting enzyme inhibitor or beta-blockers experienced fewer interruptions in trastuzumab than those on placebo.ConclusionsIn patients with HER2-positive breast cancer treated with trastuzumab, both lisinopril and carvedilol prevented cardiotoxicity in patients receiving anthracyclines. For such patients, lisinopril or carvedilol should be considered to minimize interruptions of trastuzumab. (Lisinopril or Coreg CR in Reducing Side Effects in Women With Breast Cancer Receiving Trastuzumab; NCT01009918).

Published
2019

28. Challenges in IBD Research: Environmental Triggers

Author

Ho, Shuk-Mei, Lewis, James D, Mayer, Emeran A, Bernstein, Charles N, Plevy, Scott E, Chuang, Emil, Rappaport, Stephen M, Croitoru, Kenneth, Korzenik, Joshua R, Krischer, Jeffrey, Hyams, Jeffrey S, Judson, Richard, Kellis, Manolis, Jerrett, Michael, Miller, Gary W, Grant, Melanie L, Shtraizent, Nataly, Honig, Gerard, Hurtado-Lorenzo, Andrés, and Wu, Gary D

Subjects
Crohn's Disease, Clinical Research, Digestive Diseases, Autoimmune Disease, Inflammatory Bowel Disease, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Diet, Environmental Exposure, Gastrointestinal Microbiome, Gene-Environment Interaction, Humans, Inflammatory Bowel Diseases, Life Style, Risk Factors, Crohn's disease, ulcerative colitis, environment, exposome, smoking, antibiotic, virus, pollutant, diet, epidemiology, in silico modeling, Crohn’s disease, Clinical Sciences, Gastroenterology & Hepatology
Abstract

Environmental triggers is part of five focus areas of the Challenges in IBD research document, which also includes preclinical human IBD mechanisms, novel technologies, precision medicine and pragmatic clinical research. The Challenges in IBD research document provides a comprehensive overview of current gaps in inflammatory bowel diseases (IBD) research and delivers actionable approaches to address them. It is the result of a multidisciplinary input from scientists, clinicians, patients, and funders, and represents a valuable resource for patient centric research prioritization. In particular, the environmental triggers section is focused on the main research gaps in elucidating causality of environmental factors in IBD. Research gaps were identified in: 1) epidemiology of exposures; 2) identification of signatures of biological response to exposures; and 3) mechanisms of how environmental exposures drive IBD. To address these gaps, the implementation of longitudinal prospective studies to determine disease evolution and identify sub-clinical changes in response to exposures is proposed. This can help define critical windows of vulnerability and risk prediction. In addition, systems biology analysis and in silico modeling were proposed as approaches to integrate the IBD exposome for the identification of biological signatures of response to exposures, and to develop prediction models of the effects of environmental factors in driving disease activity and response to therapy. This research could lead to identification of biomarkers of exposures and new modalities for therapeutic intervention. Finally, hypothesis-driven mechanistic studies to understand gene-environment interactions and to validate causality of priority factors should be performed to determine how environment influences clinical outcomes.

Published
2019

29. A multicenter study to evaluate pulmonary function in osteogenesis imperfecta

Author

Tam, Allison, Chen, Shan, Schauer, Evan, Grafe, Ingo, Bandi, Venkata, Shapiro, Jay R, Steiner, Robert D, Smith, Peter A, Bober, Michael B, Hart, Tracy, Cuthbertson, David, Krischer, Jeffrey, Mullins, Mary, Byers, Peter H, Sandhaus, Robert A, Durigova, Michaela, Glorieux, Francis H, Rauch, Frank, Sutton, Vernon Reid, Lee, Brendan, Consortium, Members of the Brittle Bone Disorders, Rush, Eric T, and Nagamani, Sandesh CS

Subjects
Congenital Structural Anomalies, Lung, Osteogenesis Imperfecta, Rare Diseases, Pediatric, Clinical Research, Good Health and Well Being, Adolescent, Adult, Aged, Child, Female, Forced Expiratory Volume, Humans, Male, Middle Aged, Respiratory Function Tests, Severity of Illness Index, Spirometry, Vital Capacity, Young Adult, lung disease, osteogenesis imperfecta, pulmonary function, spirometry, Members of the Brittle Bone Disorders Consortium, Genetics, Clinical Sciences, Genetics & Heredity
Abstract

Pulmonary complications are a significant cause for morbidity and mortality in osteogenesis imperfecta (OI). However, to date, there have been few studies that have systematically evaluated pulmonary function in individuals with OI. We analyzed spirometry measurements, including forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1 ), in a large cohort of individuals with OI (n = 217) enrolled in a multicenter, observational study. We show that individuals with the more severe form of the disease, OI type III, have significantly reduced FVC and FEV1 which do not follow the expected trends of the normal population. We also show that "normalization" of FVC and FEV1 using general population data to generate percent predicted values underestimates the pulmonary involvement in OI. Within each subtype of OI, we used linear mixed models to find potential correlations between FEV1 and FVC with the clinical variables including mobility, bisphosphonate use, and scoliosis. Our results are an important step in understanding the extent of pulmonary involvement in individuals with OI and for developing pulmonary endpoints for use in the routine patient care as well as in the investigation of new therapies.

Published
2018

30. Evaluating Eosinophilic Colitis as a Unique Disease Using Colonic Molecular Profiles: A Multi-Site Study

Author

Pablo Abonia, J., Aceves, Seema, Almonte, Samuel, Andrews, Rachel, Anvari, Sara, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Chiou, Eric, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Gonsalves, Nirmala, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, Murray-Petzold, Cristin, Newbury, Robert, Nhu, Quan, Olive, Anthony, Oyibo, Oghenekpaobor (Joel), Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Spergel, Amanda Rudman, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, Mary Jo, Sun, Kiki, Tasco, Amy, Tholen, Crystal, Thompson, Katherine, Tomkinson, Tiffany, Tran, Daisy, Tylicki, Alexandra, Urv, Tiina, Wang, Mei-Lun, Wechsler, Joshua, Wershil, Barry, Wheatley, Lisa, Wilkey, Leah, Yang, Guang-Yu, Zalewski, Angelika, Zicarelli, Amy, Shoda, Tetsuo, Collins, Margaret H., Rochman, Mark, Wen, Ting, Caldwell, Julie M., Mack, Lydia E., Osswald, Garrett A., Besse, John A., Haberman, Yael, Aceves, Seema S., Arva, Nicoleta C., Capocelli, Kelley E., Davis, Carla M., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Mukkada, Vincent A., Putnam, Philip E., Spergel, Jonathan M., Wechsler, Joshua B., Furuta, Glenn T., Denson, Lee A., and Rothenberg, Marc E.

Published
2022
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33. Telomere length is not a main factor for the development of islet autoimmunity and type 1 diabetes in the TEDDY study

Author

Törn, Carina, Liu, Xiang, Onengut-Gumuscu, Suna, Counts, Kevin M., Moreno, Jose Leonardo, Remedios, Cassandra L., Chen, Wei-Min, LeFaive, Jonathon, Butterworth, Martha D., Akolkar, Beena, Krischer, Jeffrey P., Lernmark, Åke, Rewers, Marian, She, Jin-Xiong, Toppari, Jorma, Ziegler, Anette-Gabriele, Ratan, Aakrosh, Smith, Albert V., Hagopian, William A., Rich, Stephen S., and Parikh, Hemang M.

Published
2022
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34. Loss of Endothelial TSPAN12 Promotes Fibrostenotic Eosinophilic Esophagitis via Endothelial Cell–Fibroblast Crosstalk

Author

Abonia, J. Pablo, Aceves, Seema, Almonte, Samuel, Andrews, Rachel, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Gonsalves, Nirmala, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, MurrayPetzold, Cristin, Newbury, Robert, Nhu, Quan, Oyibo, Oghenekpaobor (Joel), Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Spergel, Amanda Rudman, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, MaryJo, Sun, Kiki, Tasco, Amy, Tholen, Crystal, Thompson, Katherine, Tomkinson, Tiffany, Tran, Daisy, Tylicki, Alexandra, Urv, Tiina, Wang, Mei-Lun, Wechsler, Joshua, Wershil, Barry, Wheatley, Lisa, Wilkey, Leah, Yang, Guang-Yu, Zalewski, Angelika, Zicarelli, Amy, Shoda, Tetsuo, Wen, Ting, Caldwell, Julie M., Ben-Baruch Morgenstern, Netali, Osswald, Garrett A., Rochman, Mark, Mack, Lydia E., Felton, Jennifer M., Arva, Nicoleta C., Atkins, Dan, Bonis, Peter A., Capocelli, Kelley E., Collins, Margaret H., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Menard-Katcher, Paul A., Mukkada, Vincent A., Putnam, Philip E., Rudman Spergel, Amanda K., Spergel, Jonathan M., Wechsler, Joshua B., Aceves, Seema S., Furuta, Glenn T., and Rothenberg, Marc E.

Published
2022
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35. Low-Dose Anti-Thymocyte Globulin (ATG) Preserves β-Cell Function and Improves HbA1c in New-Onset Type 1 Diabetes

Author

Haller, Michael J, Schatz, Desmond A, Skyler, Jay S, Krischer, Jeffrey P, Bundy, Brian N, Miller, Jessica L, Atkinson, Mark A, Becker, Dorothy J, Baidal, David, DiMeglio, Linda A, Gitelman, Stephen E, Goland, Robin, Gottlieb, Peter A, Herold, Kevan C, Marks, Jennifer B, Moran, Antoinette, Rodriguez, Henry, Russell, William, Wilson, Darrell M, Greenbaum, Carla J, Greenbaum, C, Atkinson, M, Baidal, D, Battaglia, M, Becker, D, Bingley, P, Bosi, E, Buckner, J, Clements, M, Colman, P, DiMeglio, L, Evans-Molina, C, Gitelman, S, Goland, R, Gottlieb, P, Herold, K, Knip, M, Krischer, J, Lernmark, A, Moore, W, Moran, A, Muir, A, Palmer, J, Peakman, M, Philipson, L, Raskin, P, Redondo, M, Rodriguez, H, Russell, W, Spain, L, Schatz, DA, Sosenko, J, Wherrett, D, Wilson, D, Winter, W, Ziegler, A, Anderson, M, Antinozzi, P, Benoist, C, Blum, J, Bourcier, K, Chase, P, Clare-Salzler, M, Clynes, R, Cowie, C, Eisenbarth, G, Fathman, CG, Grave, G, Harrison, L, Hering, B, Insel, R, Jordan, S, Kaufman, F, Kay, T, Kenyon, N, Klines, R, Lachin, J, Leschek, E, Mahon, J, Marks, JB, Monzavi, R, Nanto-Salonen, K, Nepom, G, Orban, T, Parkman, R, Pescovitz, M, Peyman, J, Pugliese, A, Ridge, J, Roep, B, Roncarolo, M, Savage, P, Simell, O, Sherwin, R, Siegelman, M, Skyler, JS, Steck, A, Thomas, J, Trucco, M, and Wagner, J

Subjects
Pediatric, Diabetes, Clinical Trials and Supportive Activities, Clinical Research, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Metabolic and endocrine, Adolescent, Adult, Antilymphocyte Serum, C-Peptide, Child, Cytoprotection, Diabetes Mellitus, Type 1, Dose-Response Relationship, Drug, Double-Blind Method, Drug Therapy, Combination, Female, Glycated Hemoglobin, Granulocyte Colony-Stimulating Factor, Humans, Insulin-Secreting Cells, Male, Pilot Projects, Polyethylene Glycols, Recombinant Proteins, Young Adult, Type 1 Diabetes TrialNet ATG-GCSF Study Group
Abstract

ObjectiveA pilot study suggested that combination therapy with low-dose anti-thymocyte globulin (ATG) and pegylated granulocyte colony-stimulating factor (GCSF) preserves C-peptide in established type 1 diabetes (T1D) (duration 4 months to 2 years). We hypothesized that 1) low-dose ATG/GCSF or 2) low-dose ATG alone would slow the decline of β-cell function in patients with new-onset T1D (duration

Published
2018

36. Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study.

Author

Abonia, J, Atkins, Dan, Bonis, Peter, Caldwell, Julie, Capocelli, Kelley, Carpenter, Christina, Collins, Margaret, Dellon, Evan, Eby, Michael, Gonsalves, Nirmala, Gupta, Sandeep, Falk, Gary, Hirano, Ikuo, Menard-Katcher, Paul, Kuhl, Jonathan, Krischer, Jeffrey, Leung, John, Mukkada, Vincent, Spergel, Jonathan, Trimarchi, Michael, Yang, Guang-Yu, Zimmermann, Nives, Furuta, Glenn, Rothenberg, Marc, Shoda, Tetsuo, Wen, Ting, and Aceves, Seema

Subjects
Adolescent, Adult, Aged, Biopsy, Child, Child, Preschool, Cross-Sectional Studies, Eosinophilic Esophagitis, Esophagoscopy, Female, Gene Expression Profiling, Humans, Hyperplasia, Leukocyte Count, Machine Learning, Male, Middle Aged, Phenotype, Prospective Studies, Severity of Illness Index, Young Adult
Abstract

BACKGROUND: Eosinophilic oesophagitis is understood in terms of quantifiable histological, endoscopic, and molecular features. Data are scant for inter-relations of these features and their potential to identify distinct disease endotypes. We aimed to identify clinical-pathological correlations between endoscopic and histological disease variables by transcription profiling of the oesophagus of patients with eosinophilic oesophagitis of varying severity and disease activity states. METHODS: We did a cross-sectional study across ten hospital sites in the USA associated with the Consortium of Eosinophilic Gastrointestinal Disease Researchers. We analysed oesophageal biopsy specimens taken from paediatric and adult patients with eosinophilic oesophagitis (discovery cohort), using the eosinophilic oesophagitis diagnostic panel (EDP), a set of 96 informative transcripts. Histological and endoscopic features were assessed by quantification of oesophageal eosinophils and use of the eosinophilic oesophagitis histology scoring system (HSS) and the eosinophilic oesophagitis endoscopic reference score (EREFS). Associations among the various histological, endoscopic, and molecular features were analysed by Spearman correlation. Results were replicated in a biologically independent, single-centre, validation cohort of patients with active eosinophilic oesophagitis. FINDINGS: The discovery cohort contained 185 samples and the validation cohort comprised 100 specimens. In the discovery cohort, EDP showed intersite consistency, significant correlation with oesophageal eosinophils (p

Published
2018

37. Alignment of parent- and child-reported outcomes and histology in eosinophilic esophagitis across multiple CEGIR sites.

Author

King, Eileen, Collins, Margaret, Yang, Guang-Yu, Capocelli, Kelley, Abonia, J, Atkins, Dan, Bonis, Peter, Carpenter, Christina, Dellon, Evan, Eby, Michael, Falk, Gary, Gonsalves, Nirmala, Gupta, Sandeep, Hirano, Ikuo, Kocher, Kendra, Krischer, Jeffrey, Leung, John, Lipscomb, Jessi, Menard-Katcher, Paul, Mukkada, Vincent, Pan, Zhaoxing, Spergel, Jonathan, Sun, Qin, Wershil, Barry, Rothenberg, Marc, Furuta, Glenn, and Aceves, Seema

Subjects
Consortium of Eosinophilic Gastrointestinal Disease Researchers, Eosinophil, eosinophilic esophagitis, eosinophilic oesophagitis, patient-reported outcomes, pediatric QOL EoE module, pediatric eosinophilic esophagitis symptom score, quality of life, symptoms, version 2, Adolescent, Child, Child, Preschool, Eosinophilic Esophagitis, Female, Humans, Male, Parents, Patient Reported Outcome Measures, Quality of Life, Self Report, Surveys and Questionnaires
Abstract

BACKGROUND: Patient-reported outcome metrics for eosinophilic esophagitis (EoE) have been developed and validated but not used in a multicenter pediatric population or systematically aligned with histology. OBJECTIVE: We sought to understand (1) the potential of caregiver report to predict patient self-reported symptoms and (2) the correlation of patient-reported outcome domains with histology. METHODS: Patients with EoE (n = 310) and their parents participating in the Consortium of Gastrointestinal Eosinophilic Disease Researchers (CEGIR) observational clinical trial were queried for baseline patient symptoms and quality of life (QOL) by using the Pediatric Eosinophilic Esophagitis Symptom Score, version 2 (PEESSv2.0), and the Pediatric QOL EoE module (PedsQL-EoE), and biopsy specimens were analyzed by using the EoE Histology Scoring System. RESULTS: PEESSv2.0 parental and child reports aligned across all domains (r = 0.68-0.73, P

Published
2018

38. Eosinophilic oesophagitis endotype classification by molecular, clinical, and histopathological analyses: a cross-sectional study

Author

Shoda, Tetsuo, Wen, Ting, Aceves, Seema S, Abonia, J Pablo, Atkins, Dan, Bonis, Peter A, Caldwell, Julie M, Capocelli, Kelley E, Carpenter, Christina L, Collins, Margaret H, Dellon, Evan S, Eby, Michael D, Gonsalves, Nirmala, Gupta, Sandeep K, Falk, Gary W, Hirano, Ikuo, Menard-Katcher, Paul, Kuhl, Jonathan T, Krischer, Jeffrey P, Leung, John, Mukkada, Vincent A, Spergel, Jonathan M, Trimarchi, Michael P, Yang, Guang-Yu, Zimmermann, Nives, Furuta, Glenn T, Rothenberg, Marc E, and Researchers, Consortium of Eosinophilic Gastrointestinal Disease

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Research, 2.1 Biological and endogenous factors, 4.2 Evaluation of markers and technologies, Detection, screening and diagnosis, Aetiology, Adolescent, Adult, Aged, Biopsy, Child, Child, Preschool, Cross-Sectional Studies, Eosinophilic Esophagitis, Esophagoscopy, Female, Gene Expression Profiling, Humans, Hyperplasia, Leukocyte Count, Machine Learning, Male, Middle Aged, Phenotype, Prospective Studies, Severity of Illness Index, Young Adult, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Clinical sciences
Abstract

BackgroundEosinophilic oesophagitis is understood in terms of quantifiable histological, endoscopic, and molecular features. Data are scant for inter-relations of these features and their potential to identify distinct disease endotypes. We aimed to identify clinical-pathological correlations between endoscopic and histological disease variables by transcription profiling of the oesophagus of patients with eosinophilic oesophagitis of varying severity and disease activity states.MethodsWe did a cross-sectional study across ten hospital sites in the USA associated with the Consortium of Eosinophilic Gastrointestinal Disease Researchers. We analysed oesophageal biopsy specimens taken from paediatric and adult patients with eosinophilic oesophagitis (discovery cohort), using the eosinophilic oesophagitis diagnostic panel (EDP), a set of 96 informative transcripts. Histological and endoscopic features were assessed by quantification of oesophageal eosinophils and use of the eosinophilic oesophagitis histology scoring system (HSS) and the eosinophilic oesophagitis endoscopic reference score (EREFS). Associations among the various histological, endoscopic, and molecular features were analysed by Spearman correlation. Results were replicated in a biologically independent, single-centre, validation cohort of patients with active eosinophilic oesophagitis.FindingsThe discovery cohort contained 185 samples and the validation cohort comprised 100 specimens. In the discovery cohort, EDP showed intersite consistency, significant correlation with oesophageal eosinophils (p

Published
2018

39. Alignment of parent- and child-reported outcomes and histology in eosinophilic esophagitis across multiple CEGIR sites

Author

Aceves, Seema S, King, Eileen, Collins, Margaret H, Yang, Guang-Yu, Capocelli, Kelley E, Abonia, J Pablo, Atkins, Dan, Bonis, Peter A, Carpenter, Christina L, Dellon, Evan S, Eby, Michael D, Falk, Gary W, Gonsalves, Nirmala, Gupta, Sandeep K, Hirano, Ikuo, Kocher, Kendra, Krischer, Jeffrey P, Leung, John, Lipscomb, Jessi, Menard-Katcher, Paul, Mukkada, Vincent A, Pan, Zhaoxing, Spergel, Jonathan M, Sun, Qin, Wershil, Barry K, Rothenberg, Marc E, Furuta, Glenn T, Researchers, Consortium of Eosinophilic Gastrointestinal Disease, Arrington, Ashley, Bailey, Jeanie, Besse, John, Book, Wendy M, Burke, Deirdre, Covington, Jacquelyn, DeMarschall, Maureen, Dohil, Ranjan, Dubner, Allison, Foote, Heather, Guan, Shaobo, Hurnton, Alicia, Kodroff, Ellyn, Kuhl, Jonathan, Kyle, Shay, Lewis, Megan, Mack, Denise, McGee, Sarah, Mingler, Melissa, Moist, Susan, Muir, Amanda, Poppendeck, Heidi, Putnam, Philip, Reidy, Cathy, Rudman-Spergel, Amanda K, Sable, Kathleen, Scott, Melissa, Strobel, Mary Jo, Thompson, Katherine, and Wechsler, Joshua

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Food Allergies, Clinical Trials and Supportive Activities, Clinical Research, Digestive Diseases, Pediatric, Adolescent, Child, Child, Preschool, Eosinophilic Esophagitis, Female, Humans, Male, Parents, Patient Reported Outcome Measures, Quality of Life, Self Report, Surveys and Questionnaires, Eosinophil, eosinophilic esophagitis, eosinophilic oesophagitis, Consortium of Eosinophilic Gastrointestinal Disease Researchers, patient-reported outcomes, pediatric eosinophilic esophagitis symptom score, version 2, pediatric QOL EoE module, symptoms, quality of life, Immunology, Allergy
Abstract

BACKGROUND:Patient-reported outcome metrics for eosinophilic esophagitis (EoE) have been developed and validated but not used in a multicenter pediatric population or systematically aligned with histology. OBJECTIVE:We sought to understand (1) the potential of caregiver report to predict patient self-reported symptoms and (2) the correlation of patient-reported outcome domains with histology. METHODS:Patients with EoE (n = 310) and their parents participating in the Consortium of Gastrointestinal Eosinophilic Disease Researchers (CEGIR) observational clinical trial were queried for baseline patient symptoms and quality of life (QOL) by using the Pediatric Eosinophilic Esophagitis Symptom Score, version 2 (PEESSv2.0), and the Pediatric QOL EoE module (PedsQL-EoE), and biopsy specimens were analyzed by using the EoE Histology Scoring System. RESULTS:PEESSv2.0 parental and child reports aligned across all domains (r = 0.68-0.73, P

Published
2018

40. Creating a multi-center rare disease consortium - the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR).

Author

Cheng, Katherine, Gupta, Sandeep K, Kantor, Susanna, Kuhl, Jonathan T, Aceves, Seema S, Bonis, Peter A, Capocelli, Kelley E, Carpenter, Christina, Chehade, Mirna, Collins, Margaret H, Dellon, Evan S, Falk, Gary W, Gopal-Srivastava, Rashmi, Gonsalves, Nirmala, Hirano, Ikuo, King, Eileen C, Leung, John, Krischer, Jeffrey P, Mukkada, Vincent A, Schoepfer, Alain, Spergel, Jonathan M, Straumann, Alex, Yang, Guang-Yu, Furuta, Glenn T, and Rothenberg, Marc E

Subjects
Eosinophilic diseases, collaborations, multicenter consortium, rare diseases
Abstract

Eosinophilic gastrointestinal disorders (EGIDs) affect various segments of the gastrointestinal tract. Since these disorders are rare, collaboration is essential to enroll subjects in clinical studies and study the broader population. The Rare Diseases Clinical Research Network (RDCRN), a program of the National Center for Advancing Translational Sciences (NCATS), funded the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR) in 2014 to advance the field of EGIDs. CEGIR facilitates collaboration among various centers, subspecialties, patients, professional organizations and patient-advocacy groups and includes 14 clinical sites. It has successfully initiated two large multi-center clinical studies looking to refine EGID diagnoses and management. Several pilot studies are underway that focus on various aspects of EGIDs including novel therapeutic interventions, diagnostic and monitoring methods, and the role of the microbiome in pathogenesis. CEGIR currently nurtures five physician-scholars through a career training development program and has published more than 40 manuscripts since its inception. This review focuses on CEGIR's operating model and progress and how it facilitates a framework for exchange of ideas and stimulates research and innovation. This consortium provides a model for progress on other potential clinical areas.

Published
2017

42. A Sunnier Forecast But Still Some Clouds: Trends in Pediatric Cancer Care in Florida from 1981-2020

Author

Shaw, Peter, primary, Metts, Jonathan, additional, Amankwah, Ernest, additional, Eslin, Don, additional, Bradfield, Scott, additional, Slayton, William, additional, Hays, Brian, additional, Calkins, Brian, additional, MacArthur, Craig, additional, Rico, Juan, additional, Barredo, Julio, additional, Smith, Amy, additional, Hanif, Iftikhar, additional, Rodriguez-Cortes, Hector, additional, Nagasubramanian, Ramamoorthy, additional, and Krischer, Jeffrey, additional

Published
2024
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43. Imatinib therapy for patients with recent-onset type 1 diabetes: a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial

Author

Barr, Mayalin, Blanchfield, J Lori, Bluestone, Jeffrey A, Buchanan, Jeanne, Bundy, Brian N, Cabbage, Joanne, Coleman, Peter, De La Vega, Monica, DiMeglio, Linda A, Evans-Molina, Carmella, Felner, Eric I, Ferrannini, Ele, Ferrara, Christine, Gaglia, Jason L, Gitelman, Stephen E, Gottlieb, Peter A, Healy, Felicity, Higgins, Laurie, Hildinger, Megan, Jenkins, Margaret, Kayton Bryant, Nora, Kinderman, Amanda, Koshy, Nisha, Kost, Brianne, Krischer, Jeffrey P, Krishfield, Suzanne, Kucheruk, Olena, Lim, Noha, Lindsley, Karen, Long, S Alice, Mantravadi, Manasa, Mari, Andrea, Mesfin, Shelley, Michels, Aaron, Migre, Mary Ellen, Minnock, Pantea, Mirmira, Raghavendra G, Mohammed-Nur, Elham, Nelson, Jennifer, Nursing, Ashvin, O'Donnell, Ryan, Olivos, Diana, Parker, Melissa, Raskin, Philip, Redl, Leanne, Reed, Nicole, Resnick, Brittany, Sanda, Srinath, Sayre, Peter, Serti, Elisavet, Sims, Emily, Smith, Karen, Soppe, Carol, Stuart, Fiona, Szubowicz, Sarah, Tansey, Michel, Terrell, Jennifer, Tersey, Sarah, Torok, Christine, Tsalikian, Eva, Watson, Kelly, Wentworth, John M, Wesch, Rebecca, Willi, Steven, Woerner, Stephanie, and Willi, Steven M

Published
2021
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46. Osteogenesis imperfecta tooth level phenotype analysis: Cross-sectional study

Author

Lee, Brendan, Sutton, V. Reid, Nagamani, Sandesh C.S., Glorieux, Francis, Lee, Janice, Esposito, Paul, Wallace, Maegen, Bober, Michael, Eyre, David, Gomez, Danielle, Harris, Gerald, Hart, Tracy, Jain, Mahim, Krakow, Deborah, Krischer, Jeffrey, Orwoll, Eric, Nicol, Lindsey, Raggio, Cathleen, Smith, Peter, Tosi, Laura, Taqi, Doaa, Moussa, Hanan, Schwinghamer, Timothy, Ducret, Maxime, Dagdeviren, Didem, Retrouvey, Jean-Marc, Rauch, Frank, and Tamimi, Faleh

Published
2021
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48. Cranio‐cervical abnormalities in moderate‐to‐severe osteogenesis imperfecta – Genotypic and phenotypic determinants.

Author

Marulanda, Juliana, Retrouvey, Jean‐Marc, Lee, Brendan, Sutton, V. Reid, Nagamani, Sandesh C. S., Rauch, Frank, Glorieux, Francis, Lee, Janice, Esposito, Paul, Wallace, Maegen, Bober, Michael, Eyre, David, Gomez, Danielle, Harris, Gerald, Hart, Tracy, Jain, Mahim, Krakow, Deborah, Krischer, Jeffrey, Orwoll, Eric, and Nicol, Lindsey

Subjects
OSTEOGENESIS imperfecta, EHLERS-Danlos syndrome, CONE beam computed tomography, SKULL base, GENOTYPES, BASILAR invagination
Abstract

Introduction: Cranio‐cervical anomalies are significant complications of osteogenesis imperfecta (OI), a rare bone fragility disorder that is usually caused by mutations in collagen type I encoding genes. Objective: To assess cranio‐cervical anomalies and associated clinical findings in patients with moderate‐to‐severe OI using 3D cone beam computed tomography (CBCT) scans. Methods: Cross‐sectional analysis of CBCT scans in 52 individuals with OI (age 10–37 years; 32 females) and 40 healthy controls (age 10–32 years; 26 females). Individuals with a diagnosis of OI type III (severe, n = 11), type IV (moderate, n = 33) and non‐collagen OI (n = 8) were recruited through the Brittle Bone Disorders Consortium. Controls were recruited through the orthodontic clinic of the University of Missouri‐Kansas City (UMKC). Results: OI and control groups were similar in mean age (OI: 18.4 [SD: 7.2] years, controls: 18.1 [SD: 6.3] years). The cranial base angle was increased in the OI group (OI: mean 148.6° [SD: 19.3], controls: mean 130.4° [SD: 5.7], P =.001), indicating a flatter cranial base. Protrusion of the odontoid process into the foramen magnum (n = 7, 14%) and abnormally located odontoid process (n = 19, 37%) were observed in the OI group but not in controls. Low stature, expressed as height z‐score (P =.01), presence of DI (P =.04) and being male (P =.04) were strong predictors of platybasia, whereas height z‐score (P =.049) alone was found as positive predictor for basilar impression as per the Chamberlain measurement. Conclusion: The severity of the phenotype in OI, as expressed by the height z‐score, correlates with the severity of cranial base anomalies such as platybasia and basilar impression in moderate‐to‐severe OI. Screening for cranial base anomalies is advisable in individuals with moderate‐to‐severe OI, with special regards to the individuals with a shorter stature and DI. [ABSTRACT FROM AUTHOR]

Published
2024
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49. Advancing patient care through the Consortium of Eosinophilic Gastrointestinal Disease Researchers (CEGIR)

Author

Abonia, J. Pablo, Aceves, Seema, Almonte, Samuel, Andrews, Rachel, Arrington, Ashley, Arva, Nicoleta, Atkins, Fred, Bailey, Dominique, Berry, Alexis, Besl, Bridget, Bolton, Scott, Bonis, Peter, Book, Wendy, Bray, Kimberly, Brown, Teresa, Burger, Cassandra, Burke, Deirdre, Cahoon, Jonathon, Capocelli, Kelley, Chehade, Mirna, Collins, Margaret, Davis, Carla, Dellon, Evan, DeMarshall, Maureen, DiTommaso, Lauren, Dohil, Ranjan, Eby, Michael, Falk, Gary, Fleischer, David, Foote, Heather, Foss, Kelci, Friedlander, Joel, Fulkerson, Patricia, Furuta, Glenn, Geno, Debra, Gonsalves, Nirmala, Greuter, Thomas, Gupta, Sandeep, Hamilton, Frank, Harris, Kirk, Harris, Jennifer, Hirano, Ikuo, Hiremath, Girish, Holland-Thomas, Nicole, Jacinto, Lea, Kagalwalla, Amir, Kaseta, Timothy, Katzka, David, Keeley, Kaitlin, Khosh-Hemmat, Emad, Khoury, Paneez, King, Eileen, Kliewer, Kara, Klion, Amy, Knowles, Jennifer, Kocher, Kendra, Kodroff, Ellyn, Krischer, Jeffrey, Kyle, Shay, Leung, John, Levy, Meredith, Liacouras, Chris, Mack, Denise, Martin, Lisa, Martin, Ellen, McCright-Gill, Talaya, Menard-Katcher, Paul, Menard-Katcher, Calies, Mendoza, Gabriela, Mingler, Melissa, Minnicozzi, Mike, Muir, Amanda, Mukkada, Vincent, MurrayPetzold, Cristin, Newbury, Robert, Nhu, Quan, Oyibo, Oghenekpaobor (Joel), Paliana, Allisa, Pan, Zhaoxing, Pesek, Robbie, Peterson, Kathryn, Poppendeck, Heidi, Putnam, Philip, Rivera, Fabian, Rothenberg, Marc, Rudman-Spergel, Amanda, Sable, Kathleen, Schoepfer, Alain, Scott, Melissa, Sheridan, Rachel, Sinanovic, Selma, Spergel, Jonathan, Strobel, MaryJo, Sun, Kiki, Tasco, Amy, Tholen, Crystal, Thompson, Katherine, Tomkinson, Tiffany, Tran, Daisy, Tylicki, Alexandra, Urv, Tiina, Wang, Mei-Lun, Wechsler, Joshua, Wershil, Barry, Wheatley, Lisa, Wilkey, Leah, Yang, Guang-Yu, Zalewski, Angelika, Zicarelli, Amy, Collins, Margaret H., Rothenberg, Marc E., and Furuta, Glenn T.

Published
2020
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