Search

Your search keyword '"Furuta, Glenn T."' showing total 1,281 results
Start Over Author "Furuta, Glenn T."
1,281 results on '"Furuta, Glenn T."'

1. HIF-2α-dependent induction of miR-29a restrains TH1 activity during T cell dependent colitis

Author

Czopik, Agnieszka K., McNamee, Eóin N., Vaughn, Victoria, Huang, Xiangsheng, Bang, In Hyuk, Clark, Trent, Wang, Yanyu, Ruan, Wei, Nguyen, Tom, Masterson, Joanne C., Tak, Eunyoung, Frank, Sandra, Collins, Colm B., Li, Howard, Rodriguez-Aguayo, Cristian, Lopez-Berestein, Gabriel, Gerich, Mark E., Furuta, Glenn T., Yuan, Xiaoyi, Sood, Anil K., de Zoeten, Edwin F., and Eltzschig, Holger K.

Published
2024
Full Text
View/download PDF

4. Long-term durability between parent and child patient-reported outcomes in eosinophilic esophagitis

Author

Martin, Lisa J., Zhang, Xue, Chehade, Mirna, Davis, Carla M., Dellon, Evan S., Falk, Gary W., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish S., Katzka, David A., Khoury, Paneez, Leung, John, Menard-Katcher, Paul, Gonsalves, Nirmala, Pesek, Robert D., Spergel, Jonathan M., Wechsler, Joshua B., Kliewer, Kara, Arva, Nicoleta C., Collins, Margaret H., Pletneva, Maria, Yang, Guang-Yu, Furuta, Glenn T., Rothenberg, Marc E., and Aceves, Seema S.

Published
2024
Full Text
View/download PDF

5. Clinical and molecular correlates of the Index of Severity for Eosinophilic Esophagitis

Author

Sato, Hiroki, Dellon, Evan S., Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Davis, Carla M., Falk, Gary W., Furuta, Glenn T., Gonsalves, Nirmala P., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish, Katzka, David A., Khoury, Paneez, Leung, John, Menard-Katcher, Paul, Pesek, Robbie, Peterson, Kathryn A., Pletneva, Maria A., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Rothenberg, Marc E., and Shoda, Tetsuo

Published
2024
Full Text
View/download PDF

8. A Multicenter Long-Term Cohort Study of Eosinophilic Esophagitis Variants and Their Progression to Eosinophilic Esophagitis Over Time

Author

Greuter, Thomas, Straumann, Alex, Fernandez-Marrero, Yuniel, Germic, Nina, Hosseini, Aref, Chanwangpong, Apinya, Yousefi, Shida, Simon, Dagmar, Collins, Margaret H., Bussmann, Christian, Chehade, Mirna, Dellon, Evan S., Furuta, Glenn T., Gonsalves, Nirmala, Hirano, Ikuo, Moawad, Fouad J., Biedermann, Luc, Safroneeva, Ekaterina, Schoepfer, Alain M., and Simon, Hans-Uwe

Published
2024
Full Text
View/download PDF

9. A MULTICENTER LONG-TERM COHORT STUDY OF EOSINOPHILIC ESOPHAGITIS VARIANTS AND THEIR PROGRESSION TO EOE OVER TIME

Author

Greuter, Thomas, Straumann, Alex, Fernandez-Marrero, Yuniel, Germic, Nina, Hosseini, Aref, Chanwangpong, Apinya, Yousefi, Shida, Simon, Dagmar, Collins, Margaret H., Bussmann, Christian, Chehade, Mirna, Dellon, Evan S., Furuta, Glenn T., Gonsalves, Nirmala, Hirano, Ikuo, Moawad, Fouad J., Biedermann, Luc, Safroneeva, Ekaterina, Schoepfer, Alain M., and Simon, Hans-Uwe

Published
2024
Full Text
View/download PDF

11. CSF1-dependent macrophage support matrisome and epithelial stress-induced keratin remodeling in Eosinophilic esophagitis

Author

Benson, Taylor M., Markey, Gary E., Hammer, Juliet A., Simerly, Luke, Dzieciatkowska, Monika, Jordan, Kimberly R., Capocelli, Kelley E., Scullion, Kathleen M., Crowe, Louise, Ryan, Sinéad, Black, Jennifer O., Crue, Taylor, Andrews, Rachel, Burger, Cassandra, McNamee, Eóin N., Furuta, Glenn T., Menard-Katcher, Calies, and Masterson, Joanne C.

Published
2024
Full Text
View/download PDF

12. One-food versus 4-food elimination diet for pediatric eosinophilic esophagitis: A multisite randomized trial

Author

Kliewer, Kara L., Abonia, J. Pablo, Aceves, Seema S., Atkins, Dan, Bonis, Peter A., Capocelli, Kelley E., Chehade, Mirna, Collins, Margaret H., Dellon, Evan S., Fei, Lin, Furuta, Glenn T., Gupta, Sandeep K., Kagalwalla, Amir, Leung, John, Mir, Sabina, Mukkada, Vincent A., Pesek, Robbie, Rosenberg, Chen, Shoda, Tetsuo, Spergel, Jonathan M., Sun, Qin, Wechsler, Joshua B., Yang, Guang-Yu, and Rothenberg, Marc E.

Published
2024
Full Text
View/download PDF

13. Metabolic dysfunction mediated by HIF-1α contributes to epithelial differentiation defects in eosinophilic esophagitis

Author

Ryan, Sinéad, Crowe, Louise, Almeida Cruz, Sofía N., Galbraith, Matthew D., O’Brien, Carol, Hammer, Juliet A., Bergin, Ronan, Kellett, Shauna K., Markey, Gary E., Benson, Taylor M., Fagan, Olga, Espinosa, Joaquin M., Conlon, Niall, Donohoe, Claire L., McKiernan, Susan, Hogan, Andrew E., McNamee, Eóin N., Furuta, Glenn T., Menard-Katcher, Calies, and Masterson, Joanne C.

Published
2024
Full Text
View/download PDF

14. Nonepithelial Gene Expression Correlates With Symptom Severity in Adults With Eosinophilic Esophagitis

Author

Kim, Seung, Ben-Baruch Morgenstern, Netali, Osonoi, Kasumi, Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Dellon, Evan S., Falk, Gary W., Furuta, Glenn T., Gonsalves, Nirmala P., Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish, Katzka, David A., Khoury, Paneez, Leung, John, Pesek, Robbie, Peterson, Kathryn A., Pletneva, Maria A., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Rothenberg, Marc E., and Shoda, Tetsuo

Published
2024
Full Text
View/download PDF

15. Breakthroughs in understanding and treating eosinophilic gastrointestinal diseases presented at the CEGIR/TIGERs Symposium at the 2022 American Academy of Allergy, Asthma & Immunology Meeting

Author

Chehade, Mirna, Wright, Benjamin L., Atkins, Dan, Aceves, Seema S., Ackerman, Steven J., Assa’ad, Amal H., Bauer, Maureen, Collins, Margaret H., Commins, Scott P., Davis, Carla M., Dellon, Evan S., Doerfler, Bethan, Gleich, Gerald J., Gupta, Sandeep K., Hill, David A., Jensen, Elizabeth T., Katzka, David, Kliewer, Kara, Kodroff, Ellyn, Kottyan, Leah C., Kyle, Shay, Muir, Amanda B., Pesek, Robert D., Peterson, Kathryn, Shreffler, Wayne G., Spergel, Jonathan M., Strobel, Mary Jo, Wechsler, Joshua, Zimmermann, Nives, Furuta, Glenn T., and Rothenberg, Marc E.

Published
2023
Full Text
View/download PDF

16. Esophageal Epithelium and Lamina Propria Are Unevenly Involved in Eosinophilic Esophagitis

Author

Hiremath, Girish, Sun, Lili, Collins, Margaret H., Bonis, Peter A., Arva, Nicoleta C., Capocelli, Kelley E., Chehade, Mirna, Davis, Carla M., Falk, Gary W., Gonsalves, Nirmala, Gupta, Sandeep K., Hirano, Ikuo, Leung, John, Khoury, Paneez, Mukkada, Vincent A., Martin, Lisa J., Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Aceves, Seema S., Furuta, Glenn T., Rothenberg, Marc.E., Koyama, Tatsuki, and Dellon, Evan S.

Published
2023
Full Text
View/download PDF

20. Monitoring Patients With Eosinophilic Esophagitis in Routine Clinical Practice - International Expert Recommendations

Author

Arnim, Ulrike von, Biedermann, Luc, Aceves, Seema S., Bonis, Peter A., Collins, Margaret H., Dellon, Evan S., Furuta, Glenn T., Gonsalves, Nirmala, Gupta, Sandeep, Hirano, Ikuo, Lucendo, Alfredo J., Miehlke, Stephan, Oliva, Salvatore, Schlag, Christoph, Schoepfer, Alain, Straumann, Alex, Vieth, Michael, and Bredenoord, Albert J.

Published
2023
Full Text
View/download PDF

22. Development of a Practical Guide to Implement and Monitor Diet Therapy for Eosinophilic Esophagitis

Author

Aceves, Seema S., Abonia, Pablo, Atkins, Dan, Bonis, Peter A., Chehade, Mirna, Falk, Gary W., Furuta, Glenn T., Gupta, Sandeep K., Kagalwalla, Amir F., Kodroff, Ellyn, Kyle, Scholeigh, Leung, John, Menard-Katcher, Paul, Mir, Sabina, Mukkada, Vincent A., Pesek, Robert, Rothenberg, Marc E., Spergel, Jonathan M., Strobel, Mary Jo, Wechsler, Joshua B., Chang, Joy W., Kliewer, Kara, Haller, Emily, Lynett, Amanda, Doerfler, Bethany, Katzka, David A., Peterson, Kathryn A., Dellon, Evan S., and Gonsalves, Nirmala

Published
2023
Full Text
View/download PDF

23. Technical review on the management of eosinophilic esophagitis: a report from the AGA institute and the joint task force on allergy-immunology practice parameters

Author

Rank, Matthew A, Sharaf, Rajiv N, Furuta, Glenn T, Aceves, Seema S, Greenhawt, Matthew, Spergel, Jonathan M, Falck-Ytter, Yngve T, Dellon, Evan S, Institute, AGA, Chachu, Karen A, Day, Lukejohn, Lebwohl, Benjamin, Muniraj, Thiruvengadam, Patel, Amit, Peery, Anne F, Shah, Raj, Singh, Harminder, Singh, Siddharth, Spechler, Stuart J, Sultan, Shahnaz, Su, Grace L, Thrift, Aaron P, Weiss, Jennifer M, Weizman, Adam V, collaborators, Joint Task Force on Allergy-Immunology Practice Parameters, Bernstein, Jonathan A, Dinakar, Chitra, Golden, David BK, Khan, David A, Lieberman, Jay, Oppenheimer, John, Shaker, Marcus, Stukus, David R, Wallace, Dana V, and Wang, Julie

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Food Allergies, Digestive Diseases, Clinical Research, Nutrition, Advisory Committees, Allergens, Allergy and Immunology, Diet, Eosinophilic Esophagitis, Expert Testimony, Glucocorticoids, Humans, Immunotherapy, Interdisciplinary Communication, Practice Guidelines as Topic, Proton Pump Inhibitors, AGA Institute. Electronic address: clinicalpractice@gastro.org, Joint Task Force on Allergy-Immunology Practice Parameters collaborators. Electronic address: drdanawallace@gmail.com, AGA Institute, Joint Task Force on Allergy-Immunology Practice Parameters collaborators, Immunology, Allergy
Abstract

Eosinophilic esophagitis (EoE) is a chronic inflammatory condition of the esophagus. Many new studies have been reported recently that describe EoE management. An expert panel was convened by the American Gastroenterological Association Institute and the Joint Task Force on Allergy-Immunology Practice Parameters to provide a technical review to be used as the basis for an updated clinical guideline. This technical review was developed using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) framework. Eighteen focused EoE management questions were considered, with 15 answered using the GRADE framework and 3 with a narrative summary. There is moderate certainty in the evidence that topical glucocorticosteroids effectively reduce esophageal eosinophil counts to

Published
2020

24. Molecular, endoscopic, histologic, and circulating biomarker-based diagnosis of eosinophilic gastritis: Multi-site study

Author

Shoda, Tetsuo, Wen, Ting, Caldwell, Julie M, Collins, Margaret H, Besse, John A, Osswald, Garrett A, Abonia, J Pablo, Arva, Nicoleta C, Atkins, Dan, Capocelli, Kelley E, Dellon, Evan S, Falk, Gary W, Gonsalves, Nirmala, Gupta, Sandeep K, Hirano, Ikuo, Mukkada, Vincent A, Putnam, Philip E, Sheridan, Rachel M, Spergel, Amanda K Rudman, Spergel, Jonathan M, Wechsler, Joshua B, Yang, Guang-Yu, Aceves, Seema S, Furuta, Glenn T, Rothenberg, Marc E, and Researchers, Consortium of Eosinophilic Gastrointestinal Disease

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Clinical Research, Detection, screening and diagnosis, 4.1 Discovery and preclinical testing of markers and technologies, Adolescent, Adult, Biomarkers, Child, Cytokines, Endoscopy, Gastrointestinal, Enteritis, Eosinophilia, Female, Gastritis, Humans, Male, Biomarker, diagnostic panel, eosinophil, eosinophilic gastritis, transcriptome, Consortium of Eosinophilic Gastrointestinal Disease Researchers, Immunology, Allergy
Abstract

BackgroundEosinophilic gastritis (EG) is a clinicopathologic disorder with marked gastric eosinophilia and clinical symptoms. There is an unmet need among patients with EG for more precise diagnostic tools.ObjectiveWe aimed to develop tissue- and blood-based diagnostic platforms for EG.MethodsPatients with EG and control subjects without EG were enrolled across 9 Consortium of Eosinophilic Gastrointestinal Disease Researchers-associated sites. An EG Diagnostic Panel (EGDP; gastric transcript subset) and EG blood biomarker panel (protein multiplex array) were analyzed. EGDP18 scores were derived from the expression of 18 highly dysregulated genes, and blood EG scores were derived from dysregulated cytokine/chemokine levels.ResultsGastric biopsy specimens and blood samples from 185 subjects (patients with EG, n = 74; control subjects without EG, n = 111) were analyzed. The EGDP (1) identified patients with active EG (P < .0001, area under the curve ≥ 0.95), (2) effectively monitored disease activity in longitudinal samples (P = .0078), (3) highly correlated in same-patient samples (antrum vs body, r = 0.85, P < .0001), and (4) inversely correlated with gastric peak eosinophil levels (r = -0.83, P < .0001), periglandular circumferential collars (r = -0.73, P < .0001), and endoscopic nodularity (r = -0.45, P < .0001). For blood-based platforms, eotaxin-3, thymus and activation-regulated chemokine, IL-5, and thymic stromal lymphopoietin levels were significantly increased. Blood EG scores (1) distinguished patients with EG from control subjects without EG (P < .0001, area under the curve ≥ 0.91), (2) correlated with gastric eosinophil levels (plasma: r = 0.72, P = .0002; serum: r = 0.54, P = .0015), and (3) inversely correlated with EGDP18 scores (plasma: r = -0.64, P = .0015; serum: r = -0.46, P = .0084). Plasma eotaxin-3 levels strongly associated with gastric CCL26 expression (r = 0.81, P < .0001).ConclusionWe developed tissue- and blood-based platforms for assessment of EG and uncovered robust associations between specific gastric molecular profiles and histologic and endoscopic features, providing insight and clinical readiness tools for this emerging rare disease.

Published
2020

25. 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

26. 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
Full Text
View/download PDF

29. Overestimation of the diagnosis of eosinophilic colitis with reliance on billing codes

Author

Muir, Amanda B, Jensen, Elizabeth T, Wechsler, Joshua B, Menard-Katcher, Paul, Falk, Gary W, Aceves, Seema S, Furuta, Glenn T, Dellon, Evan S, Rothenberg, Mark E, and Spergel, Jonathan M

Subjects
Biomedical and Clinical Sciences, Immunology, Adult, Child, Colitis, Colon, Diagnosis, Differential, Diagnostic Errors, Eosinophilia, Eosinophils, Humans, International Classification of Diseases, Retrospective Studies, United States
Published
2019

30. Variation in Endoscopic Activity Assessment and Endoscopy Score Validation in Adults With Eosinophilic Esophagitis

Author

Schoepfer, Alain M, Hirano, Ikuo, Coslovsky, Michael, Roumet, Marie C, Zwahlen, Marcel, Kuehni, Claudia E, Hafner, David, Alexander, Jeffrey A, Dellon, Evan S, Gonsalves, Nirmala, Leung, John, Bussmann, Christian, Collins, Margaret H, Newbury, Robert O, Smyrk, Thomas C, Woosley, John T, Yang, Guang-Yu, Romero, Yvonne, Katzka, David A, Furuta, Glenn T, Gupta, Sandeep K, Aceves, Seema S, Chehade, Mirna, Spergel, Jonathan M, Falk, Gary W, Meltzer, Brian A, Comer, Gail M, Straumann, Alex, Safroneeva, Ekaterina, Group, International EEsAI Study, Achem, Sami R, Arora, Amindra S, Alpan, Oral, Armstrong, David, Attwood, Stephen E, Butterfield, Joseph H, Crowell, Michael D, DeVault, Kenneth R, Drouin, Eric, Enav, Benjamin, Enders, Felicity T, Fleischer, David E, Foxx-Orenstein, Amy, Francis, Dawn L, Guyatt, Gordon H, Harris, Lucinda A, Kagalwalla, Amir F, Kita, Hirohito, Krishna, Murli, Lee, James J, Lewis, John C, Lim, Kaiser, Locke, G Richard, Murray, Joseph A, Nguyen, Cuong C, Orbelo, Diana M, Pasha, Shabana F, Ramirez, Francisco C, Sheikh, Javed, Umar, Sarah B, Weiler, Catherine R, Wo, John M, Wu, Tsung-Teh, and Yost, Kathleen J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Digestive Diseases, Clinical Research, Clinical Trials and Supportive Activities, Prevention, Adolescent, Adult, Aged, Anti-Inflammatory Agents, Dose-Response Relationship, Drug, Eosinophilic Esophagitis, Esophagoscopy, Esophagus, Female, Fluticasone, Humans, Male, Middle Aged, Prognosis, Severity of Illness Index, Young Adult, Index, Variability in Endoscopic Assessment, Instrument, International EEsAI Study Group, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsEosinophilic esophagitis (EoE) is assessed endoscopically (endoscopic activity), based on grades of edema, rings, exudates, furrows, and strictures (EREFS). We examined variations in endoscopic assessments of severity, developed and validated 3 EREFS-based scoring systems, and assessed responsiveness of these systems using data from a randomized placebo-controlled trial of patients with EoE.MethodsFor the development set, 5 gastroenterologists reviewed EREFS findings from 266 adults with EoE and provided endoscopist global assessment scores (EndoGA, scale of 0 to 10); variation (ΔEndoGA) was assessed using linear regression. We evaluated simple scores (features given arbitrary values from 0 to 3) and developed 2 scoring systems (adjusted score range, 0-100). We then fitted our linear regression model with mean EndoGA to data from 146 adults recruited in centers in Switzerland and the United States between April 2011 and December 2012. For the validation set, we collected data from 120 separate adults (recruited in centers in Switzerland and the United States between May 2013 and July 2014), assessing regression coefficient-based scores using Bland-Altman method. We assessed the responsiveness of our scoring systems using data from a randomized trial of patients with EoE given fluticasone (n=16) or placebo (n=8).ResultsThe distribution of EndoGA values differed among endoscopists (mean ΔEndoGA, 2.6±1.8; range 0-6.6). We developed 2 regression-based scoring systems to assess overall and proximal and distal esophageal findings; variation in endoscopic features accounted for more than 90% of the mean EndoGA variation. In the validation group, differences between mean EndoGA and regression-based scores were small (ranging from -4.70 to 2.03), indicating good agreement. In analyses of data from the randomized trial, the baseline to end of study change in patients given fluticasone was a reduction of 24.3 in simple score (reduction of 4.6 in patients given placebo, P=.052); a reduction of 23.5 in regression-based overall score (reduction of 6.56 in patients given placebo, P=.12), and a reduction of 23.8 (reduction of 8.44 in patients given placebo, P=.11).ConclusionAssessments of endoscopic activity in patients with EoE vary among endoscopists. In an analysis of data from a randomized controlled trial, we found that newly developed scoring systems are no better than simple scoring system in detecting changes in endoscopic activity. These results support the use of a simple scoring system in evaluation of endoscopic activity in patients with EoE. clinicaltrials.gov no: NCT00939263 and NCT01386112.

Published
2019

31. International Consensus Recommendations for Eosinophilic Gastrointestinal Disease Nomenclature

Author

Dellon, Evan S., Gonsalves, Nirmala, Abonia, J. Pablo, Alexander, Jeffrey A., Arva, Nicoleta C., Atkins, Dan, Attwood, Stephen E., Auth, Marcus K.H., Bailey, Dominique D., Biederman, Luc, Blanchard, Carine, Bonis, Peter A., Bose, Paroma, Bredenoord, Albert J., Chang, Joy W., Chehade, Mirna, Collins, Margaret H., Di Lorenzo, Carlo, Dias, Jorge Amil, Dohil, Ranjan, Dupont, Christophe, Falk, Gary W., Ferreira, Cristina T., Fox, Adam T., Genta, Robert M., Greuter, Thomas, Gupta, Sandeep K., Hirano, Ikuo, Hiremath, Girish S., Horsley-Silva, Jennifer L., Ishihara, Shunji, Ishimura, Norihisa, Jensen, Elizabeth T., Gutiérrez-Junquera, Carolina, Katzka, David A., Khoury, Paneez, Kinoshita, Yoshikazu, Kliewer, Kara L., Koletzko, Sibylle, Leung, John, Liacouras, Chris A., Lucendo, Alfredo J., Martin, Lisa J., McGowan, Emily C., Menard-Katcher, Calies, Metz, David C., Miller, Talya L., Moawad, Fouad J., Muir, Amanda B., Mukkada, Vincent A., Murch, Simon, Nhu, Quan M., Nomura, Ichiro, Nurko, Samuel, Ohtsuka, Yoshikazu, Oliva, Salvatore, Orel, Rok, Papadopoulou, Alexandra, Patel, Dhyanesh A., Pesek, Robert D., Peterson, Kathryn A., Philpott, Hamish, Putnam, Philip E., Richter, Joel E., Rosen, Rachel, Ruffner, Melanie A., Safroneeva, Ekaterina, Schreiner, Philipp, Schoepfer, Alain, Schroeder, Shauna R., Shah, Neil, Souza, Rhonda F., Spechler, Stuart J., Spergel, Jonathan M., Straumann, Alex, Talley, Nicholas J., Thapar, Nikhil, Vandenplas, Yvan, Venkatesh, Rajitha D., Vieira, Mario C., von Arnim, Ulrike, Walker, Marjorie M., Wechsler, Joshua B., Wershil, Barry K., Wright, Benjamin L., Yamada, Yoshiyuki, Yang, Guang-Yu, Zevit, Noam, Rothenberg, Marc E., Furuta, Glenn T., and Aceves, Seema S.

Published
2022
Full Text
View/download PDF

32. 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
Full Text
View/download PDF

33. Long-Lasting Dissociation of Esophageal Eosinophilia and Symptoms After Dilation in Adults With Eosinophilic Esophagitis

Author

Safroneeva, Ekaterina, Pan, Zhaoxing, King, Eileen, Martin, Lisa J., Collins, Margaret H., Yang, Guang-Yu, Capocelli, Kelley E., Arva, Nicoleta C., Abonia, J. Pablo, Atkins, Dan, Bonis, Peter A., Dellon, Evan S., Falk, Gary W., Gonsalves, Nirmala, Gupta, Sandeep K., Hirano, Ikuo, Leung, John, Menard-Katcher, Paul A., Mukkada, Vincent A., Schoepfer, Alain M., Spergel, Jonathan M., Wershil, Barry K., Rothenberg, Marc E., Aceves, Seema S., and Furuta, Glenn T.

Published
2022
Full Text
View/download PDF

34. Human Epidemiology and Response to SARS-CoV-2 (HEROS): objectives, design, and enrollment results of a 12-city remote observational surveillance study of households with children, using direct-to-participant methods.

Author

Fulkerson, Patricia C, Lussier, Stephanie J, Bendixsen, Casper G, Castina, Sharon M, Gebretsadik, Tebeb, Marlin, Jessica S, Russell, Patty B, Seibold, Max A, Everman, Jamie L, Moore, Camille M, Snyder, Brittney M, Thompson, Kathy, Tregoning, George S, Wellford, Stephanie, Arbes, Samuel J, Bacharier, Leonard B, Calatroni, Agustin, Camargo Jr, Carlos A, Dupont, William D, and Furuta, Glenn T

Subjects
PUBLIC health surveillance, RISK assessment, RESEARCH funding, FAMILIES, ALLERGIES, LONGITUDINAL method, TELEMEDICINE, GENE expression profiling, COVID-19, SARS-CoV-2, ASTHMA, MEDICAL referrals
Abstract

The Human Epidemiology and Response to SARS-CoV-2 (HEROS) Study is a prospective, multicity, 6-month incidence study conducted from May 2020 to February 2021. The objectives were to identify risk factors for SARS-CoV-2 infection and household transmission among children and people with asthma and allergic diseases, and to use the host nasal transcriptome sampled longitudinally to understand infection risk and sequelae at the molecular level. To overcome challenges of clinical study implementation due to the coronavirus pandemic, this surveillance study used direct-to-participant methods to remotely enroll and prospectively follow eligible children who are participants in other National Institutes of Health–funded pediatric research studies and their household members. Households participated in weekly surveys and biweekly nasal sampling regardless of symptoms. The aim of this report is to widely share the methods and study instruments and to describe the rationale, design, execution, logistics, and characteristics of a large, observational, household-based, remote cohort study of SARS-CoV-2 infection and transmission in households with children. The study enrolled a total of 5598 individuals, including 1913 principal participants (children), 1913 primary caregivers, 729 secondary caregivers, and 1043 other household children. This study was successfully implemented without necessitating any in-person research visits and provides an approach for rapid execution of clinical research. Trial registration: ClinicalTrials.gov. Identifier: NCT04375761 [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

35. HIF-2α-dependent induction of miR-29a restrains TH1 activity during T cell dependent colitis.

Author

Czopik, Agnieszka K., McNamee, Eóin N., Vaughn, Victoria, Huang, Xiangsheng, Bang, In Hyuk, Clark, Trent, Wang, Yanyu, Ruan, Wei, Nguyen, Tom, Masterson, Joanne C., Tak, Eunyoung, Frank, Sandra, Collins, Colm B., Li, Howard, Rodriguez-Aguayo, Cristian, Lopez-Berestein, Gabriel, Gerich, Mark E., Furuta, Glenn T., Yuan, Xiaoyi, and Sood, Anil K.

Subjects
INFLAMMATORY bowel diseases, HYPOXIA-inducible factors, CELLULAR control mechanisms, CELL physiology, TRANSCRIPTION factors, T cells
Abstract

Metabolic imbalance leading to inflammatory hypoxia and stabilization of hypoxia-inducible transcription factors (HIFs) is a hallmark of inflammatory bowel diseases. We hypothesize that HIF could be stabilized in CD4+ T cells during intestinal inflammation and alter the functional responses of T cells via regulation of microRNAs. Our assays reveal markedly increased T cell-intrinsic hypoxia and stabilization of HIF protein during experimental colitis. microRNA screen in primary CD4+ T cells points us towards miR-29a and our subsequent studies identify a selective role for HIF-2α in CD4-cell-intrinsic induction of miR-29a during hypoxia. Mice with T cell-intrinsic HIF-2α deletion display elevated T-bet (target of miR-29a) levels and exacerbated intestinal inflammation. Mice with miR-29a deficiency in T cells show enhanced intestinal inflammation. T cell-intrinsic overexpression of HIF-2α or delivery of miR-29a mimetic dampen TH1-driven colitis. In this work, we show a previously unrecognized function for hypoxia-dependent induction of miR-29a in attenuating TH1-mediated inflammation. Inflammatory intestinal lesions are often hypoxic, which results in the stabilization and activation of hypoxia-inducible-factors (HIF). Here authors show that in a mouse model of colitis, HIF-2α is specifically stabilized in CD4+ type 1T helper (TH1) cells, leading to the upregulation of miR-29a expression and suppression of TH1 cell function, which pathway is potentially targetable for therapeutic purposes. [ABSTRACT FROM AUTHOR]

Published
2024
Full Text
View/download PDF

37. 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
Full Text
View/download PDF

38. Mucosal Microbiota Associated With Eosinophilic Esophagitis and Eosinophilic Gastritis

Author

Furuta, Glenn T., Fillon, Sophie A., Williamson, Kayla M., Robertson, Charles E., Stevens, Mark J., Aceves, Seema S., Arva, Nicoleta C., Chehade, Mirna, Collins, Margaret H., Davis, Carla M., Dellon, Evan S., Falk, Gary W., Gonsalves, Nirmala, Gupta, Sandeep K., Hirano, Ikuo, Khoury, Paneez, Leung, John, Martin, Lisa J., Menard-Katcher, Paul, Mukkada, Vincent A., Peterson, Kathryn, Spergel, Jonathan M., Wechsler, Joshua B., Yang, Guang-Yu, Rothenberg, Marc E., and Harris, J. Kirk

Published
2023
Full Text
View/download PDF

39. Heterogeneity in Clinical, Endoscopic, and Histologic Outcome Measures and Placebo Response Rates in Clinical Trials of Eosinophilic Esophagitis: A Systematic Review

Author

Ma, Christopher, van Rhijn, Bram D, Jairath, Vipul, Nguyen, Tran M, Parker, Claire E, Aceves, Seema S, Furuta, Glenn T, Gupta, Sandeep K, Katzka, David A, Safroneeva, Ekaterina, Schoepfer, Alain M, Straumann, Alex, Spergel, Jonathan M, Pai, Rish K, Feagan, Brian G, Hirano, Ikuo, Dellon, Evan S, and Bredenoord, Albert J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Clinical Trials and Supportive Activities, Clinical Research, Cancer, Digestive Diseases, Evaluation of treatments and therapeutic interventions, 6.1 Pharmaceuticals, Adolescent, Adult, Anti-Inflammatory Agents, Child, Eosinophilic Esophagitis, Esophagus, Female, Humans, Male, Outcome Assessment, Health Care, Placebos, Randomized Controlled Trials as Topic, Treatment Outcome, Young Adult, Inflammation, Drug, Endoscopy, Histology, Patient-Reported Outcomes, Placebo, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background & aimsAgents are being developed for treatment of eosinophilic esophagitis (EoE). However, it is not clear what outcome measures would best determine the efficacy and safety of these agents in clinical trials. We performed a systematic review of outcomes used in randomized placebo-controlled trials of EoE and we estimate the placebo response and rates of remission.MethodsWe searched MEDLINE, Embase, CENTRAL, ClinicalTrials.gov, and the EU Clinical Trials Register from inception through February 20, 2018 for randomized controlled trials of pharmacologic therapies for EoE. Efficacy outcome definitions, measurement tools, and the proportion of patients responding to placebo were collected and stratified by based on histologic, endoscopic, and patient-reported outcomes.ResultsWe analyzed data from 22 placebo-controlled trials, comprising 1112 patients with EoE. Ten additional active registered trials were identified. Most published trials evaluated topical corticosteroid therapy (13/22, 59.1%). Histologic outcomes measuring eosinophil density and patient-reported outcomes were reported in 21/22 published trials (95.5%). No consistently applied definitions of histologic or patient-reported response or remission were identified. Endoscopic outcomes were described in 60% (12/20) of published trials. The EoE Endoscopic Reference Score is the most commonly applied tool for describing changes in endoscopic appearance. The median histologic response to placebo was 3.7% (range, 0%-31.6%) and the median rate of remission in patients given placebo was 0.0% (range, 0%-11.0%). The median patient-reported response to placebo was 14.4% (range, 8.6%-77.8%) and rate of remission in patients given placebo was 26.2% (range, 13.2%-35.7%).ConclusionsIn a systematic review of the literature, we found that no standardized definitions of histologic, endoscopic, or patient-reported outcomes are used to determine whether pharmacologic agents produce a response or remission in patients with EoE. A core outcome set is needed to reduce heterogeneity in outcome reporting and facilitate trial interpretation and comparison of results from trials.

Published
2018

40. Updated International Consensus Diagnostic Criteria for Eosinophilic Esophagitis: Proceedings of the AGREE Conference

Author

Dellon, Evan S, Liacouras, Chris A, Molina-Infante, Javier, Furuta, Glenn T, Spergel, Jonathan M, Zevit, Noam, Spechler, Stuart J, Attwood, Stephen E, Straumann, Alex, Aceves, Seema S, Alexander, Jeffrey A, Atkins, Dan, Arva, Nicoleta C, Blanchard, Carine, Bonis, Peter A, Book, Wendy M, Capocelli, Kelley E, Chehade, Mirna, Cheng, Edaire, Collins, Margaret H, Davis, Carla M, Dias, Jorge A, Di Lorenzo, Carlo, Dohil, Ranjan, Dupont, Christophe, Falk, Gary W, Ferreira, Cristina T, Fox, Adam, Gonsalves, Nirmala P, Gupta, Sandeep K, Katzka, David A, Kinoshita, Yoshikazu, Menard-Katcher, Calies, Kodroff, Ellyn, Metz, David C, Miehlke, Stephan, Muir, Amanda B, Mukkada, Vincent A, Murch, Simon, Nurko, Samuel, Ohtsuka, Yoshikazu, Orel, Rok, Papadopoulou, Alexandra, Peterson, Kathryn A, Philpott, Hamish, Putnam, Philip E, Richter, Joel E, Rosen, Rachel, Rothenberg, Marc E, Schoepfer, Alain, Scott, Melissa M, Shah, Neil, Sheikh, Javed, Souza, Rhonda F, Strobel, Mary J, Talley, Nicholas J, Vaezi, Michael F, Vandenplas, Yvan, Vieira, Mario C, Walker, Marjorie M, Wechsler, Joshua B, Wershil, Barry K, Wen, Ting, Yang, Guang-Yu, Hirano, Ikuo, and Bredenoord, Albert J

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Food Allergies, Digestive Diseases, Clinical Research, Algorithms, Consensus, Diagnostic Techniques, Digestive System, Eosinophilic Esophagitis, Gastroenterology, Humans, Predictive Value of Tests, Prognosis, Proton Pump Inhibitors, Diagnosis, Esophageal Eosinophilia, Proton Pump Inhibitor, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology, Clinical sciences, Nutrition and dietetics
Abstract

Background & aimsOver the last decade, clinical experiences and research studies raised concerns regarding use of proton pump inhibitors (PPIs) as part of the diagnostic strategy for eosinophilic esophagitis (EoE). We aimed to clarify the use of PPIs in the evaluation and treatment of children and adults with suspected EoE to develop updated international consensus criteria for EoE diagnosis.MethodsA consensus conference was convened to address the issue of PPI use for esophageal eosinophilia using a process consistent with standards described in the Appraisal of Guidelines for Research and Evaluation II. Pediatric and adult physicians and researchers from gastroenterology, allergy, and pathology subspecialties representing 14 countries used online communications, teleconferences, and a face-to-face meeting to review the literature and clinical experiences.ResultsSubstantial evidence documented that PPIs reduce esophageal eosinophilia in children, adolescents, and adults, with several mechanisms potentially explaining the treatment effect. Based on these findings, an updated diagnostic algorithm for EoE was developed, with removal of the PPI trial requirement.ConclusionsEoE should be diagnosed when there are symptoms of esophageal dysfunction and at least 15 eosinophils per high-power field (or approximately 60 eosinophils per mm2) on esophageal biopsy and after a comprehensive assessment of non-EoE disorders that could cause or potentially contribute to esophageal eosinophilia. The evidence suggests that PPIs are better classified as a treatment for esophageal eosinophilia that may be due to EoE than as a diagnostic criterion, and we have developed updated consensus criteria for EoE that reflect this change.

Published
2018

41. 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

42. 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

43. Pathophysiology of Eosinophilic Esophagitis

Author

O’Shea, Kelly M, Aceves, Seema S, Dellon, Evan S, Gupta, Sandeep K, Spergel, Jonathan M, Furuta, Glenn T, and Rothenberg, Marc E

Subjects
Digestive Diseases, Food Allergies, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Adult, Age Factors, Allergens, Biopsy, Child, Cytokines, Ehlers-Danlos Syndrome, Eosinophilic Esophagitis, Eosinophils, Epigenesis, Genetic, Esophageal Stenosis, Esophagus, Female, Fibrosis, Food Hypersensitivity, Gastroesophageal Reflux, Gastrointestinal Microbiome, Genetic Predisposition to Disease, Glucocorticoids, Humans, Loeys-Dietz Syndrome, Male, Mast Cells, Prevalence, Proton Pump Inhibitors, Sex Factors, Transcriptome, Allergy, Desmosome, Genetics, Inflammation, Clinical Sciences, Neurosciences, Paediatrics and Reproductive Medicine, Gastroenterology & Hepatology
Abstract

Eosinophilic esophagitis is an emerging disease that is distinguished from gastroesophageal reflux disease by the expression of a unique esophageal transcriptome and the interplay of early life environmental factors with distinct genetic susceptibility elements at 5q22 (TSLP) and 2p23 (CAPN14). Rare genetic syndromes have uncovered the contribution of barrier disruption, mediated in part by defective desmosomes and dysregulated transforming growth factor beta production and signaling, to eosinophilic esophagitis pathophysiology. Experimental modeling has defined a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods. Understanding these processes is opening the way to better treatment based on disrupting allergic inflammatory and type 2 cytokine-mediated responses, including anti-cytokine therapeutics and dietary therapy.

Published
2018

44. Pathophysiology of Eosinophilic Esophagitis.

Author

O'Shea, Kelly M, Aceves, Seema S, Dellon, Evan S, Gupta, Sandeep K, Spergel, Jonathan M, Furuta, Glenn T, and Rothenberg, Marc E

Subjects
Esophagus, Eosinophils, Mast Cells, Humans, Gastroesophageal Reflux, Esophageal Stenosis, Ehlers-Danlos Syndrome, Food Hypersensitivity, Genetic Predisposition to Disease, Fibrosis, Allergens, Cytokines, Glucocorticoids, Biopsy, Prevalence, Age Factors, Sex Factors, Epigenesis, Genetic, Adult, Child, Female, Male, Proton Pump Inhibitors, Loeys-Dietz Syndrome, Eosinophilic Esophagitis, Transcriptome, Gastrointestinal Microbiome, Allergy, Desmosome, Genetics, Inflammation, Clinical Research, Digestive Diseases, Food Allergies, 2.1 Biological and endogenous factors, Inflammatory and Immune System, Epigenesis, Genetic, Gastroenterology & Hepatology, Clinical Sciences, Paediatrics and Reproductive Medicine, Neurosciences
Abstract

Eosinophilic esophagitis is an emerging disease that is distinguished from gastroesophageal reflux disease by the expression of a unique esophageal transcriptome and the interplay of early life environmental factors with distinct genetic susceptibility elements at 5q22 (TSLP) and 2p23 (CAPN14). Rare genetic syndromes have uncovered the contribution of barrier disruption, mediated in part by defective desmosomes and dysregulated transforming growth factor beta production and signaling, to eosinophilic esophagitis pathophysiology. Experimental modeling has defined a cooperative role of activated eosinophils, mast cells, and the cytokines IL-5 and IL-13, mediated by allergic sensitization to multiple foods. Understanding these processes is opening the way to better treatment based on disrupting allergic inflammatory and type 2 cytokine-mediated responses, including anti-cytokine therapeutics and dietary therapy.

Published
2018

45. 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

47. Addendum guidelines for the prevention of peanut allergy in the United States: Report of the National Institute of Allergy and Infectious Diseases–sponsored expert panel

Author

Togias, Alkis, Cooper, Susan F, Acebal, Maria L, Assa'ad, Amal, Baker, James R, Beck, Lisa A, Block, Julie, Byrd-Bredbenner, Carol, Chan, Edmond S, Eichenfield, Lawrence F, Fleischer, David M, Fuchs, George J, Furuta, Glenn T, Greenhawt, Matthew J, Gupta, Ruchi S, Habich, Michele, Jones, Stacie M, Keaton, Kari, Muraro, Antonella, Plaut, Marshall, Rosenwasser, Lanny J, Rotrosen, Daniel, Sampson, Hugh A, Schneider, Lynda C, Sicherer, Scott H, Sidbury, Robert, Spergel, Jonathan, Stukus, David R, Venter, Carina, and Boyce, Joshua A

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Health Services, Clinical Research, Nutrition, Food Allergies, Pediatric, Foodborne Illness, Digestive Diseases, Prevention, Inflammatory and immune system, Good Health and Well Being, Allergens, Arachis, Eczema, Egg Hypersensitivity, Humans, Immunoglobulin E, Infant, National Institute of Allergy and Infectious Diseases (U.S.), Peanut Hypersensitivity, Skin Tests, United States, Food, peanut, allergy, prevention, guidelines, Immunology, Allergy
Abstract

BackgroundFood allergy is an important public health problem because it affects children and adults, can be severe and even life-threatening, and may be increasing in prevalence. Beginning in 2008, the National Institute of Allergy and Infectious Diseases, working with other organizations and advocacy groups, led the development of the first clinical guidelines for the diagnosis and management of food allergy. A recent landmark clinical trial and other emerging data suggest that peanut allergy can be prevented through introduction of peanut-containing foods beginning in infancy.ObjectivesPrompted by these findings, along with 25 professional organizations, federal agencies, and patient advocacy groups, the National Institute of Allergy and Infectious Diseases facilitated development of addendum guidelines to specifically address the prevention of peanut allergy.ResultsThe addendum provides 3 separate guidelines for infants at various risk levels for the development of peanut allergy and is intended for use by a wide variety of health care providers. Topics addressed include the definition of risk categories, appropriate use of testing (specific IgE measurement, skin prick tests, and oral food challenges), and the timing and approaches for introduction of peanut-containing foods in the health care provider's office or at home. The addendum guidelines provide the background, rationale, and strength of evidence for each recommendation.ConclusionsGuidelines have been developed for early introduction of peanut-containing foods into the diets of infants at various risk levels for peanut allergy.

Published
2017

Catalog

Books, media, physical & digital resources
See catalog results