Judith R. Kelsen
VerifiedUniversity of Pennsylvania · Rehabilitation Medicine
Active 2008–2026
About
Judith R. Kelsen, M.D., is an Associate Professor of Pediatrics specializing in Gastroenterology, Hepatology, and Nutrition at the Children's Hospital of Philadelphia. She serves as the Director of the Fecal Microbiome Center and the Very Early Onset IBD Center at the Children's Hospital of Philadelphia. Her work focuses on pediatric inflammatory bowel disease (IBD), including ulcerative colitis in children, and translational research related to gastrointestinal health. Dr. Kelsen completed her B.A. at Stern College, Yeshiva University in 1996, earned her M.D. from Cornell University, Weill Medical School in 2001, and completed her translational research training at the University of Pennsylvania in 2013.
Research topics
- Biology
- Genetics
- Computational biology
Selected publications
Gastrointestinal Endoscopy · 2026-05-01
articleGastrointestinal Endoscopy · 2026-05-01
articleSenior authorGastroenterology · 2026-05-01
articleSenior authorGastroenterology · 2026-05-01
articleAlimentary Pharmacology & Therapeutics · 2025-02-08 · 18 citations
articleOpen accessBACKGROUND: There are scarce data available on upadacitinib in children with Crohn's disease (CD). AIM: To evaluate the effectiveness and safety of upadacitinib as an induction therapy in paediatric CD. METHODS: This was a multicentre retrospective study between 2022 and 2024 of children treated with upadacitinib for induction of remission of active CD conducted in 30 centres worldwide affiliated with the IBD Interest and Porto group of the ESPGHAN. We recorded demographic, clinical and laboratory data and adverse events (AEs) at week 8 post-induction. The analysis of the primary outcome was based upon the intention-to-treat (ITT) principle. RESULTS: We included 100 children (median age 15.8 [interquartile range 14.3-17.2]). All were previously treated with biologic therapies including 89 with ≥ 2 biologics. At the end of the 8-week induction period, we observed clinical response, clinical remission and corticosteroid- and exclusive enteral nutrition-free clinical remission (CFR) in 75%, 56% and 52%, respectively. By the end of induction, 68% had achieved normalisation of C-reactive protein, and 58% had faecal calprotectin (FC) < 150 mcg/g. There was combined CFR and FC remission in 13/31 children with available data at 8 weeks (13% of the ITT population). AEs were recorded in 24 children; the most frequent was acne in 12. Two AEs (severe acne and hypertriglyceridemia) led to discontinuation of therapy. CONCLUSION: Upadacitinib is an effective induction therapy for refractory paediatric CD. Efficacy should be weighed against the potential risks of AEs.
The Journal of Pediatrics · 2025-06-05 · 2 citations
articleOpen accessAn Epigenetic Basis for Sustained Inflammatory Epithelial Progenitor Cell States in Crohn’s Disease
Cellular and Molecular Gastroenterology and Hepatology · 2025-10-21 · 1 citations
articleOpen accessBACKGROUND & AIMS: Defining consequential differences in intestinal epithelial stem cells in healthy humans vs those with inflammatory bowel disease (Crohn's disease and ulcerative colitis) is essential for the development of much needed therapies to restore the epithelial barrier and maintain its fidelity. METHODS: We used single-cell transcriptomic and epigenomic approaches in matched patient tissues and organoids to investigate epithelial gene expression and function in children with no pathological diagnosis in the lower gastrointestinal tract and healthy adults compared with those with Crohn's disease. RESULTS: We identify an inflammatory secretory progenitor (ISP) cell state present almost exclusively in patients with Crohn's disease compared with healthy subjects. ISPs exhibit gene expression profiles consistent with normal secretory progenitor cells but concomitantly express a suite of distinguishing pro-inflammatory genes. Mechanistically, ISPs exhibit open chromatin at ISP gene loci. Although ISP-specific genes are not expressed in intestinal stem cells, their chromatin is accessible in Crohn's disease stem cells, suggesting that ISP genes are epigenetically poised in stem cells and subsequently transcriptionally activated in ISPs in the presence of inflammatory stimuli. Consistently, Crohn's disease colonoids exhibit sustained ISP gene expression that can be elicited further with pro-inflammatory cytokines or via co-culture with pro-inflammatory macrophages. CONCLUSIONS: We have defined differences in the epithelial stem and progenitor compartment of patients with Crohn's disease that suggest aberrant stem cell differentiation and inflammatory gene expression arise and persist during disease.
Acute Liver Failure Unmasking XIAP Deficiency in Very Early-Onset Inflammatory Bowel Disease
Journal of Human Immunity · 2025-04-25
articleOpen accessSenior authorIntroduction X-linked inhibitor of apoptosis (XIAP) deficiency is a rare inborn error of immunity with particularly pleiomorphic spectrum of manifestations. These include hemophagocytic lymphohistiocytosis (HLH) with and without primary EBV infection, inflammatory bowel disease (IBD), uveitis, and episodic fevers. Liver manifestations have been rarely reported. Herein we describe severe acute liver failure (ALF) in a patient with very early-onset IBD found to have XIAP deficiency. Case Presentation The patient presented at 5 years of age with intermittent bloody stools, a perianal skin tag, and a history of intermittent fevers since infancy. Endoscopic evaluation at 6 years of age showed ulcerations and histologic colitis and granulomas. He was initiated on infliximab with good clinical response. Concurrent with his IBD evaluation, he was noted to have elevated liver enzymes. Twenty-one months after diagnosis, he developed fever, right upper quadrant pain, nausea, scleral icterus, liver enzymes to the 2000s, and cholestasis without synthetic dysfunction. EBV serologies were IgM positive. Transaminases improved spontaneously, but five days later, he re-presented with marked transaminitis, worsened cholestasis, and new synthetic dysfunction. He was transferred to a tertiary academic referral center ICU with high fevers and encephalopathy for management of ALF. HLH biomarkers were only modestly elevated: ferritin 290, Hgb 9.2, Plts 177, ANC 1620, fibrinogen 103, sIL-2Ra 1500, IFNg 128, and CXCL9 2959. EBV serologies and serial PCRs were negative. IL-18 was 12079. He was treated with IV glucocorticoids and emapalumab with stabilization. Flow cytometry showed XIAP deficiency, and anakinra was added with gradual resolution of liver dysfunction. Whole-genome sequencing revealed an XIAP frameshift variant (c.1021_1022del, p.(N341Yfs*8)). Emapalumab was replaced with ruxolitinib as the patient was preparing for hematopoietic stem cell transplant. Discussion XIAP-deficiency is remarkable for its range and severity of inflammatory phenotypes, including HLH and refractory IBD. Here we present a rare case of ALF in XIAP-deficiency. Antecedent, transient EBV infection was a likely trigger. His ALF improved with steroids, emapalumab, and IL-1 blockade. A high index of suspicion for immune dysregulation should be employed in all cases of VEO-IBD and/or liver failure. Figure 1. Laboratory trends and therapeutics. Day 0 represents initial hospitalization for acute liver failure.
Gastroenterology · 2025-05-01
articleSenior authorThe Journal of Pediatrics · 2025-10-01
letter
Recent grants
Very Early-onset inflammatory bowel disease
NIH · $720k · 2014–2019
Very Early-onset inflammatory bowel disease
NIH · $173k · 2014–2019
NIH · $772k · 2018–2021
Frequent coauthors
- 104 shared
Máire Conrad
Children's Hospital of Philadelphia
- 73 shared
Robert N. Baldassano
- 73 shared
Marcella Devoto
National Research Council
- 73 shared
Kathleen E. Sullivan
Children's Hospital of Philadelphia
- 61 shared
Noor Dawany
- 33 shared
Petar Mamula
- 32 shared
Trusha Patel
Children's Hospital of Philadelphia
- 31 shared
Kathryn E. Hamilton
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