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1. Longitudinal Outcomes in Young Patients with Alpha-1-Antitrypsin Deficiency with Native Liver Reveal that Neonatal Cholestasis is a Poor Predictor of Future Portal Hypertension

Author

Teckman, Jeffrey, primary, Rosenthal, Philip, additional, Hawthorne, Kieran, additional, Spino, Cathie, additional, Bass, Lee M., additional, Murray, Karen F., additional, Kerkar, Nanda, additional, Magee, John C., additional, Karpen, Saul, additional, Heubi, James E., additional, Molleston, Jean P., additional, Squires, Robert H., additional, Kamath, Binita M., additional, Guthery, Stephen L., additional, Loomes, Kathleen M., additional, Sherker, Averell H., additional, Sokol, Ronald J., additional, Alonso, Estella, additional, Bass, Lee, additional, Kelly, Susan, additional, Riordan, Mary, additional, Melin-Aldana, Hector, additional, Bezerra, Jorge, additional, Bove, Kevin, additional, Heubi, James, additional, Miethke, Alexander, additional, Tiao, Greg, additional, Denlinger, Julie, additional, Chapman, Erin, additional, Sokol, Ronald, additional, Feldman, Amy, additional, Mack, Cara, additional, Narkewicz, Michael, additional, Suchy, Frederick, additional, Sundaram, Shikha, additional, Van Hove, Johan, additional, Garcia, Benigno, additional, Kauma, Mikaela, additional, Kocher, Kendra, additional, Steinbeiss, Matthew, additional, Lovell, Mark, additional, Loomes, Kathleen, additional, Piccoli, David, additional, Rand, Elizabeth, additional, Russo, Pierre, additional, Spinner, Nancy, additional, Erlichman, Jessi, additional, Stalford, Samantha, additional, Pakstis, Dina, additional, King, Sakya, additional, Squires, Robert, additional, Sindhi, Rakesh, additional, Venkat, Veena, additional, Bukauskas, Kathy, additional, McKiernan, Patrick, additional, Haberstroh, Lori, additional, Squires, James, additional, Bull, Laura, additional, Curry, Joanna, additional, Langlois, Camille, additional, Kim, Grace, additional, Teckman, Jeffery, additional, Kociela, Vikki, additional, Nagy, Rosemary, additional, Patel, Shraddha, additional, Cerkoski, Jacqueline, additional, Bozic, Molly, additional, Subbarao, Girish, additional, Klipsch, Ann, additional, Sawyers, Cindy, additional, Cummings, Oscar, additional, Horslen, Simon, additional, Murray, Karen, additional, Hsu, Evelyn, additional, Cooper, Kara, additional, Young, Melissa, additional, Finn, Laura, additional, Kamath, Binita, additional, Ng, Vicky, additional, Quammie, Claudia, additional, Putra, Juan, additional, Sharma, Deepika, additional, Parmar, Aishwarya, additional, Guthery, Stephen, additional, Jensen, Kyle, additional, Rutherford, Ann, additional, Lowichik, Amy, additional, Book, Linda, additional, Meyers, Rebecka, additional, Hall, Tyler, additional, Wang, Kasper, additional, Michail, Sonia, additional, Thomas, Danny, additional, Goodhue, Catherine, additional, Kohli, Rohit, additional, Wang, Larry, additional, Soufi, Nisreen, additional, Thomas, Daniel, additional, Gupta, Nitika, additional, Romero, Rene, additional, Vos, Miriam B., additional, Tory, Rita, additional, Berauer, John-Paul, additional, Abramowsky, Carlos, additional, McFall, Jeanette, additional, Shneider, Benjamin, additional, Harpavat, Sanjiv, additional, Hertel, Paula, additional, Leung, Daniel, additional, Tessier, Mary, additional, Schady, Deborah, additional, Cavallo, Laurel, additional, Olvera, Diego, additional, Banks, Christina, additional, Tsai, Cynthia, additional, Thompson, Richard, additional, Doo, Edward, additional, Hoofnagle, Jay, additional, Sherker, Averell, additional, Torrance, Rebecca, additional, Hall, Sherry, additional, Magee, John, additional, Merion, Robert, additional, and Ye, Wen, additional

Published
2020
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3. Longitudinal Outcomes in Young Patients with Alpha-1-Antitrypsin Deficiency with Native Liver Reveal that Neonatal Cholestasis is a Poor Predictor of Future Portal Hypertension

Author

Jeffrey Teckman, Philip Rosenthal, Kieran Hawthorne, Cathie Spino, Lee M. Bass, Karen F. Murray, Nanda Kerkar, John C. Magee, Saul Karpen, James E. Heubi, Jean P. Molleston, Robert H. Squires, Binita M. Kamath, Stephen L. Guthery, Kathleen M. Loomes, Averell H. Sherker, Ronald J. Sokol, Estella Alonso, Lee Bass, Susan Kelly, Mary Riordan, Hector Melin-Aldana, Jorge Bezerra, Kevin Bove, James Heubi, Alexander Miethke, Greg Tiao, Julie Denlinger, Erin Chapman, Ronald Sokol, Amy Feldman, Cara Mack, Michael Narkewicz, Frederick Suchy, Shikha Sundaram, Johan Van Hove, Benigno Garcia, Mikaela Kauma, Kendra Kocher, Matthew Steinbeiss, Mark Lovell, Kathleen Loomes, David Piccoli, Elizabeth Rand, Pierre Russo, Nancy Spinner, Jessi Erlichman, Samantha Stalford, Dina Pakstis, Sakya King, Robert Squires, Rakesh Sindhi, Veena Venkat, Kathy Bukauskas, Patrick McKiernan, Lori Haberstroh, James Squires, Laura Bull, Joanna Curry, Camille Langlois, Grace Kim, Jeffery Teckman, Vikki Kociela, Rosemary Nagy, Shraddha Patel, Jacqueline Cerkoski, Molly Bozic, Girish Subbarao, Ann Klipsch, Cindy Sawyers, Oscar Cummings, Simon Horslen, Karen Murray, Evelyn Hsu, Kara Cooper, Melissa Young, Laura Finn, Binita Kamath, Vicky Ng, Claudia Quammie, Juan Putra, Deepika Sharma, Aishwarya Parmar, Stephen Guthery, Kyle Jensen, Ann Rutherford, Amy Lowichik, Linda Book, Rebecka Meyers, Tyler Hall, Kasper Wang, Sonia Michail, Danny Thomas, Catherine Goodhue, Rohit Kohli, Larry Wang, Nisreen Soufi, Daniel Thomas, Nitika Gupta, Rene Romero, Miriam B. Vos, Rita Tory, John-Paul Berauer, Carlos Abramowsky, Jeanette McFall, Benjamin Shneider, Sanjiv Harpavat, Paula Hertel, Daniel Leung, Mary Tessier, Deborah Schady, Laurel Cavallo, Diego Olvera, Christina Banks, Cynthia Tsai, Richard Thompson, Edward Doo, Jay Hoofnagle, Averell Sherker, Rebecca Torrance, Sherry Hall, John Magee, Robert Merion, and Wen Ye

Subjects
Adult, Male, medicine.medical_specialty, Cirrhosis, Adolescent, medicine.medical_treatment, Cholestasis, Intrahepatic, Liver transplantation, Article, Young Adult, 03 medical and health sciences, Liver disease, 0302 clinical medicine, Cholestasis, alpha 1-Antitrypsin Deficiency, 030225 pediatrics, Internal medicine, Hypertension, Portal, medicine, Humans, Longitudinal Studies, 030212 general & internal medicine, Neonatal cholestasis, Child, Alpha 1-antitrypsin deficiency, business.industry, Infant, Newborn, Infant, medicine.disease, Liver Transplantation, Transplantation, Child, Preschool, Pediatrics, Perinatology and Child Health, Disease Progression, Portal hypertension, Female, business
Abstract

Objectives To identify predictors of portal hypertension, liver transplantation, and death in North American youth with alpha-1-antitrypsin (AAT) deficiency, and compare with patients with AAT deficiency elsewhere. Study design The Childhood Liver Disease Research Network Longitudinal Observational Study of Genetic Causes of Intrahepatic Cholestasis is a prospective, cohort study of pediatric cholestatic liver diseases, including AAT deficiency, enrolling PIZZ and PISZ subjects 0-25 years of age seen since November 2007 at 17 tertiary care centers in the US and Canada. Data from standard-of-care baseline and annual follow-up visits were recorded from medical records, history, physical examination, and laboratory studies. Participants with portal hypertension were identified based on data collected. Results We enrolled 350 participants (60% male) with a native liver; 278 (79%) entered the cohort without portal hypertension and 18 developed portal hypertension during follow-up. Thirty participants required liver transplantation; 2 patients died during 1077 person-years of follow-up. There was no difference in participants with or without preceding neonatal cholestasis progressing to transplantation or death during the study (12% vs 7%; P = .09), or in experiencing portal hypertension (28% vs 21%; P = .16); the hazard ratio for neonatal cholestasis leading to portal hypertension was P = .04. Development of portal hypertension was associated with a reduced height Z-score. Conclusions Portal hypertension in youth with AAT deficiency impacts growth measures. Progression to liver transplantation is slow and death is rare, but the risk of complications and severe liver disease progression persists throughout childhood. A history of neonatal cholestasis is a weak predictor of severe disease.

Published
2020
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4. Incidence and Prevalence of Pediatric Eosinophilic Esophagitis in Utah Based on a 5-Year Population-Based Study

Author

Robson, Jacob, primary, O’Gorman, Molly, additional, McClain, Amber, additional, Mutyala, Krishna, additional, Davis, Cassandra, additional, Barbagelata, Carlos, additional, Wheeler, Justin, additional, Firszt, Rafael, additional, Smith, Ken, additional, Patel, Raza, additional, Peterson, Kathryn, additional, Lowichik, Amy, additional, and Guthery, Stephen, additional

Published
2019
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5. Eosinophilic Esophagitis in Adults Is Associated With IgG4 and Not Mediated by IgE

Author

Kristen Cox, John C. Fang, Gerald J. Gleich, Frederic Clayton, Molly O'Gorman, Laura A. Vinson, Lyska Emerson, Alfredo J. Lucendo, Xinjian Chen, Kathryn A. Peterson, José María Olalla, and Amy Lowichik

Subjects
medicine.medical_specialty, Lamina propria, Allergy, Pathology, Hepatology, biology, medicine.diagnostic_test, business.industry, Gastroenterology, Omalizumab, Eosinophil, medicine.disease, Immunoglobulin E, medicine.anatomical_structure, Internal medicine, parasitic diseases, Biopsy, medicine, biology.protein, Eosinophilic esophagitis, business, Esophagitis, medicine.drug
Abstract

Background & Aims Eosinophilic esophagitis is usually triggered by foods, by unclear mechanisms. We evaluated the roles of IgE and IgG4 in the development of eosinophilic esophagitis. Methods We performed a prospective, randomized, double-blind, placebo-controlled trial of adults with eosinophilic esophagitis given an antibody against IgE (omalizumab, n = 16) or placebo (n = 14) every 2–4 weeks for 16 weeks, based on weight and serum level of IgE. Endoscopy was performed, esophageal biopsy specimens were collected, and symptoms were assessed at baseline and at 16 weeks. Maximum numbers of eosinophils/high-power field were determined. Homogenates of esophageal biopsy specimens from 11 subjects with eosinophilic esophagitis and 8 without (controls) were assessed for IgM, IgA, and IgG subclasses. In a retrospective analysis, we performed immunofluorescence analysis of IgG4 in fixed esophageal tissues from 2 patients with eosinophilic esophagitis who underwent esophagectomy and 47 consecutive autopsies (controls). We also performed immunofluorescence analysis of IgG4 in esophageal mucosal biopsy specimens from 24 subjects with eosinophilic esophagitis and 9 without (controls). Finally, sera were collected from 15 subjects with eosinophilic esophagitis and from 41 without (controls), and assayed for total and food-reactive IgG4. Results Omalizumab did not alter symptoms of eosinophilic esophagitis or eosinophil counts in biopsy samples compared with placebo. Homogenates of esophageal tissues from patients with eosinophilic esophagitis had a 45-fold increase in IgG4 compared with controls ( P -5 ), but no significant increases in other IgG subclasses, IgM, or IgA. Sparse stromal deposits resembling immune complexes were found in 2 of 5 eosinophilic esophagitis biopsy specimens based on ultrastructural analysis. Esophagectomy samples from 2 patients with eosinophilic esophagitis contained 180 and 300 IgG4 plasma cells/maximal high-power field, mainly in the deep lamina propria; these levels were greater than in tissues from controls. Fibrosis essentially was exclusive to the lamina propria. Granular extracellular IgG4 was detected in biopsy specimens from 21 of 24 patients with eosinophilic esophagitis, but in none of the specimens from 9 controls ( P = 6 × 10 -6 ). The total serum level of IgG4 increased only slightly in patients with eosinophilic esophagitis, compared with controls. Subjects with eosinophilic esophagitis had increased serum levels of IgG4 that reacted with milk, wheat, egg, and nuts—the 4 foods that most commonly trigger this condition ( P ≤ 3 × 10 -4 for each food). Conclusions In a prospective trial, omalizumab did not reduce symptoms of eosinophilic esophagitis or tissue eosinophil counts compared with placebo. This finding, along with observed granular deposits of IgG4, abundant IgG4-containing plasma cells, and serum levels of IgG4 reactive to specific foods, indicate that, in adults, eosinophilic esophagitis is IgG4-associated, and not an IgE-induced allergy. ClinicalTrials.gov number: NCT 00123630.

Published
2014
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6. Incidence and Prevalence of Pediatric Eosinophilic Esophagitis in Utah Based on a 5-Year Population-Based Study

Author

Amy Lowichik, Rafael Firszt, Molly O'Gorman, Justin Wheeler, Kathryn A. Peterson, Raza Patel, Jacob Robson, Stephen L. Guthery, Amber McClain, Krishna Mutyala, Carlos Barbagelata, Ken R. Smith, and Cassandra Davis

Subjects
Male, medicine.medical_specialty, Pediatrics, Adolescent, Biopsy, Population, 03 medical and health sciences, Esophagus, 0302 clinical medicine, Risk Factors, Utah, Epidemiology, Prevalence, Humans, Medicine, Eosinophilia, Child, education, Eosinophilic esophagitis, education.field_of_study, Hepatology, Histocytochemistry, business.industry, Incidence, Medical record, Incidence (epidemiology), Infant, Newborn, Gastroenterology, Infant, Eosinophilic Esophagitis, medicine.disease, medicine.anatomical_structure, Child, Preschool, 030220 oncology & carcinogenesis, Female, 030211 gastroenterology & hepatology, medicine.symptom, business, Rare disease
Abstract

Background & Aims Eosinophilic esophagitis (EoE) is often detected in children and is considered to be a rare disease, with prevalence values reported to be below 60 cases per 100,000 persons. To determine whether the incidence of EoE in children in Utah exceeds estimates from regional reports, we calculated incidence and prevalence values over a 5-year period. Methods Using consensus guidelines for the diagnosis of EoE, we reviewed pathology records from the Intermountain Healthcare pathology database, from July 1, 2011 through June 31, 2016. We collected data on 10,619 pediatric patients with available esophageal biopsy results, and identified cases of esophageal eosinophilia (>14 eosinophils in a high-power microscopy field in an endoscopic biopsy). An EoE case required the presence of esophageal eosinophilia, symptoms of esophageal dysfunction, and the absence of co-morbid conditions that may cause esophageal eosinophilia. Annual pediatric EoE incidence and prevalence values were calculated per 100,000 children, based on averaged pediatric population estimates from census figures of Utah in 2010 and 2016. Results We identified 1281 unique pediatric patients who met criteria for esophageal eosinophilia. Of those, 1060 patients met criteria for newly diagnosed EoE. Over the 5-year period studied, the average annual pediatric EoE incidence in Utah was 24 cases per 100,000 children. The prevalence in year 5 of the study was 118 cases per 100,000 children. Conclusion In a population-based study of children in Utah, we found the incidence and prevalence of pediatric EoE to be higher than previously reported. This could be due to the prominence of EoE risk factors in this region, as well as Utah’s searchable medical record system that allows for reliable case ascertainment. Further studies of this type could increase disease awareness, prompting early referral to pediatric gastroenterologists and trials to strengthen evidence-based, algorithmic approaches to EoE diagnosis and treatment in children.

Published
2019
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7. Neurodevelopmental Outcome of Young Children with Biliary Atresia and Native Liver: Results from the ChiLDReN Study

Author

Ng, Vicky L., primary, Sorensen, Lisa G., additional, Alonso, Estella M., additional, Fredericks, Emily M., additional, Ye, Wen, additional, Moore, Jeff, additional, Karpen, Saul J., additional, Shneider, Benjamin L., additional, Molleston, Jean P., additional, Bezerra, Jorge A., additional, Murray, Karen F., additional, Loomes, Kathleen M., additional, Rosenthal, Philip, additional, Squires, Robert H., additional, Wang, Kasper, additional, Arnon, Ronen, additional, Schwarz, Kathleen B., additional, Turmelle, Yumirle P., additional, Haber, Barbara H., additional, Sherker, Averell H., additional, Magee, John C., additional, Sokol, Ronald J., additional, Hertel, Paula M., additional, Harpavat, Sanjiv, additional, Brandt, Mary L., additional, Leung, Daniel H., additional, Karnsakul, Wikrom, additional, Torrance, Rebecca, additional, Hall, Sherry, additional, Doo, Edward, additional, Hoofnagle, Jay H., additional, Whitington, Peter, additional, Bass, Lee, additional, Miethke, Alexander G., additional, Heubi, James E., additional, Setchell, Kenneth, additional, Bove, Kevin E., additional, Tiao, Greg, additional, Mack, Cara L., additional, Narkewicz, Michael R., additional, Feldman, Amy G., additional, Sundaram, Shikha S., additional, Suchy, Frederick J., additional, Karrer, Frederick M., additional, Lovell, Mark, additional, Van Hove, Johan L., additional, Rand, Elizabeth B., additional, Squires, James E., additional, Venkat, Veena L., additional, Sindhi, Rakesh, additional, Ranganathan, Sarangarajan, additional, Bull, Laura, additional, Teckman, Jeffrey, additional, Bozic, Molly, additional, Subbarao, Girish, additional, Horslen, Simon, additional, Hsu, Evelyn, additional, Finn, Laura, additional, Healey, Patrick, additional, Kohli, Rohit, additional, Thomas, Danny, additional, Soufi, Nisreen, additional, Michail, Sonia, additional, Clifton, Matt, additional, Gupta, Nitika, additional, Romero, Rene, additional, Vos, Miriam, additional, Caltharp, Shelley, additional, Kamath, Binita M., additional, Ling, Simon C., additional, Gold, Anna, additional, Fecteau, Annie, additional, Guthery, Stephen L., additional, Jensen, Kyle, additional, Meyers, Rebecka, additional, Lowichik, Amy, additional, Book, Linda, additional, Merion, Robert M., additional, Spino, Cathie, additional, and Jones, Karen, additional

Published
2018
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8. Evidence by Spectral Karyotyping that 8q11.2 Is Nonrandomly Involved in Lipoblastoma

Author

Rebecca Shepard, Amy Lowichik, Bonnie Issa, Zhong Chen, Arthur R. Brothman, Steven Scott, Cheryl M. Coffin, David R. Forsyth, Avery A. Sandberg, and Aurelia Meloni-Ehrig

Subjects
Male, Chromosomal translocation, Chromosomal rearrangement, Biology, Translocation, Genetic, Pathology and Forensic Medicine, Polyploidy, medicine, Humans, In Situ Hybridization, Fluorescence, Neoplasms, Adipose Tissue, Chromosome Aberrations, Genetics, Chromosomes, Human, Pair 13, medicine.diagnostic_test, Infant, Chromosome, Karyotype, Lipoma, medicine.disease, Molecular biology, Karyotyping, Molecular Medicine, Lipoblastoma, Chromosomes, Human, Pair 16, Chromosomes, Human, Pair 7, Chromosomes, Human, Pair 8, Regular Articles, Fluorescence in situ hybridization
Abstract

We report two cases of lipoblastoma with chromosome 8-related aberrations, ie, a 92,XXYY,t(7;8Xp22;q11.2)x2 [8]/46,XY[16] in Case 1 and a 46,XY,-8,-13,add(16) (q22),+mar, +r [cp13]/46,XY[7] in Case 2. Using spectral karyotyping and fluorescence in situ hybridization techniques, the karyotype of Case 2 was redesignated as 46,XY, r(8), del(13)(q12), der(16)ins(16;8)(q22; q24q11.2)[cp13]/46,XY[7]. This report delineates a new chromosome rearrangement, ie, der(16)ins(16;8)(q22; q24q11.2) in lipoblastoma, and also confirms the t(7; 8)(p22;q11.2), reported only once previously, as a recurrent translocation involved in such a tumor. These findings provide valuable information for clinical molecular cytogenetic diagnosis of lipoblastoma. Furthermore, this report highlights the value of cytogenetic and molecular cytogenetic analysis in differential diagnosis of childhood adipose tissue tumors and adds to the number of lipoblastomas reported with chromosomal abnormalities at 8q11.2.

Published
2000
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