---
title: "Vedolizumab for Immunodeficiency-Associated Enteropathy: Full Article Not Included in Source"
id: "frontiers-in-immunology-16-vedolizumab-treatment-in-adults-with-immunodeficiency-associated-enteropathy-a"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-16-vedolizumab-treatment-in-adults-with-immunodeficiency-associated-enteropathy-a"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953966"
published_at: "2026-10-05T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Vedolizumab for Immunodeficiency-Associated Enteropathy: Full Article Not Included in Source
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-16-vedolizumab-treatment-in-adults-with-immunodeficiency-associated-enteropathy-a
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1953966)
- **Published At:** 2026-10-05T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The provided source content contained only website navigation, journal section listings, and page scaffolding from Frontiers in Immunology; the actual article text for "Vedolizumab treatment in adults with immunodeficiency-associated enteropathy: a case series" was not present in the supplied source body. - The article title and journal (Frontiers in Immunology) were visible, but no abstract, methods, results, case descriptions, patient numbers, outcomes, safety data, or author conclusions were available to extract. - Because the source body lacked substantive content, no clinical or trial data about **Vedolizumab** or **immunodeficiency-associated enteropathy** could be summarized or interpreted from this input. - Key elements typically expected in a case-series report—diagnostic criteria, patient demographics, baseline immunodeficiency diagnoses, vedolizumab dosing schedule, clinical response metrics, adverse events, follow-up duration, and authors' recommendations—were not reported in the supplied text. - This limitation prevents evidence-based synthesis, clinical interpretation, or guidance based on the article; users seeking detailed clinical information should retrieve the full article directly from the journal or contact the corresponding author. - The rewrite emphasizes the absence of source data, lists specifically which article components are missing, and provides practical next steps for locating the full report for clinical use or review.
## Clinical Analysis & Structured Key Points
Frontiers | Vedolizumab treatment in adults with immunodeficiency-associated enteropathy: a case series BRIEF RESEARCH REPORT article Front. Immunol. , 05 October 2026 Sec. B Cell Biology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1953966 Published in Frontiers in Immunology B Cell Biology 7 impact factor 11.3 citescore Part of a Research Topic Emerging Insights into Gastrointestinal Complications in patients with Inborn Errors of Immunity Submission open 4391 views 4 articles Editor & Reviewers Edited by A G Alexandros Grammatikos Reviewed by F F Farida Fortune E D Enrico Drago I J Ivan Jonathan Fuss Outline Figures and Tables Figure 1 View in article Table 1 Clinical, laboratory and endoscopic/histopathological findings before and after treatment with vedolizumab. View in article Table 2 Clinical and immunological features in patients treated with vedolizumab. View in article BRIEF RESEARCH REPORT article Front. Immunol. , 05 October 2026 Sec. B Cell Biology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1953966 Vedolizumab treatment in adults with immunodeficiency-associated enteropathy: a case series E A Ernestina Angarola 1,2 * M J María Josefina Etchevers 3 J A Juan Andres De Paula 3 M F Maria Florencia Sanchez 4 J P Juan Pablo Santino 4 D L Diana Liberatore 1 1. Immunology Section, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina 2. Internal Medicine Department, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina 3. Gastroenterology Section, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina 4. Pathology Department, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina See more Article metrics View details Abstract Background: Inflammatory gastrointestinal disease is a common manifestation of inborn errors of immunity (IEI) and may affect any segment of the gastrointestinal tract. Vedolizumab, a gut-selective anti-integrin approved for inflammatory bowel disease, has been scarcely studied in IEI. We describe our experience with vedolizumab in adults with immunodeficiency-associated enteropathy. Methods: We conducted a retrospective case series of adults with humoral or combined immunodeficiency and inflammatory gastrointestinal disease treated with vedolizumab at a single tertiary referral center. Clinical, endoscopic, laboratory and histopathological responses were assessed. Results: Four adult patients with immunodeficiency-associated enteropathy received vedolizumab. Two patients achieved sustained clinical and endoscopic/histological remission, both of whom had predominant villous atrophy (one with TRAF3 haploinsufficiency, and the other had multiple autoimmune manifestations, refractory immune thrombocytopenia and agammaglobulinemia following rituximab). Another patient with combined immunodeficiency and protein-losing enteropathy had marked clinical improvement with mild histologic response, but relapsed at two years in the setting of norovirus and Clostridium difficile infection. In contrast, a woman with common variable immunodeficiency, autoimmune hepatitis, and severe refractory pancolitis failed to respond to vedolizumab and subsequently developed CMV superinfection, requiring treatment escalation. Conclusions: In this case series, vedolizumab was associated with clinical improvement predominantly in patients with villous atrophy rather than refractory colitis. These findings are hypothesis-generating and support further evaluation of vedolizumab as a therapeutic option for selected patients with immunodeficiency-associated enteropathy. Introduction Inborn errors of immunity (IEIs), also known as primary immunodeficiencies, comprise more than 550 genetically defined entities affecting humoral, cellular, combined, and innate immune function ( 1 ). Immune dysregulation leading to symptomatic gastrointestinal disorders affects 5% to 50% of patients with IEI, including celiac disease-like, lymphocytic gastritis, granulomatous disease, microscopic colitis, inflammatory bowel disease (IBD)-like and lymphoma ( 2 ). Among patients with IEI and gastrointestinal involvement requiring endoscopic evaluation, immune dysregulation disorders - particularly CTLA4 deficiency, X-linked lymphoproliferative syndrome, and IPEX syndrome- and phagocyte defects, predominantly chronic granulomatous disease, are the most frequently represented categories, followed by predominantly antibody deficiencies ( 3 ). More than 80 monogenic causes of IBD have now been identified, the majority overlapping with IEI; among these, interleukin-10 (IL-10) and IL-10 receptor signaling defects represent the most striking example of life-threatening, infantile-onset IBD ( 4 ). Gastrointestinal manifestations in IEI are often debilitating, notoriously difficult to treat and contribute to increased morbidity and mortality ( 5 ). The infectious risk associated with conventional systemic immunosuppressants for inflammatory gastrointestinal disorders is of significant concern in patients with IEI. Vedolizumab, a humanized monoclonal antibody against the α4β7 integrin that inhibits lymphocyte migration into intestinal tissue, was approved for the treatment of adults with moderate to severe IBD in 2014 ( 6 ). Unlike systemic immunosuppressants, its mechanism of action is restricted to gut-homing lymphocytes, sparing systemic immune surveillance. The gut-selective mechanism of action has not been linked to an increased risk of opportunistic infections, positioning this medication as a potentially beneficial option for patients with immunodeficiencies ( 7 ). However, there is insufficient evidence about the utility of vedolizumab in patients with IEI. Some authors reported benefits treating gut inflammation in common variable immunodeficiency (CVID) patients, whereas others did not find it helpful ( 5 , 7 , 8 ). Also, there are limited data regarding the utility of vedolizumab in other IEI. Methods We conducted a retrospective, descriptive case series at a single tertiary care center, Hospital Italiano de Buenos Aires, Argentina. We reviewed the Institutional Registry of Rare Diseases. Patients were included in the IEI section if immunological and/or genetic evaluation fulfilled the IUIS criteria for an IEI ( 1 ). Patients with a secondary immunodeficiency followed in our section were excluded. Nevertheless, we opted to include one remarkable patient (Case 4) who received rituximab but has a high clinical suspicion of an underlying IEI that could not yet be genetically confirmed. We included patients aged 18 years or older with humoral or combined immunodeficiency and inflammatory gastrointestinal disorders who received treatment with vedolizumab between January 2020 and June 2026. Vedolizumab was administered intravenously at a standard dose of 300 mg at weeks 0, 2 and 6, followed by maintenance infusions every 8 weeks. Clinical response was defined as improvement in stool frequency/consistency, weight gain, and/or discontinuation or reduction of corticosteroid dose. Endoscopic response was defined as resolution or improvement of mucosal lesions compared with baseline. Histopathological response was defined as reduction in inflammatory infiltrate or improvement of villous architecture on consecutive biopsies. Laboratory response was additionally assessed when available, and was defined as an increase in serum IgG (without changes in doses) and/or albumin levels, and/or a decrease in fecal calprotectin and/or alpha-1 antitrypsin clearance, compared with pretreatment values. As this is a retrospective case series, these parameters were not obtained at pre-specified time points but were recorded whenever available in the clinical records, and are summarized for every patient in Table 1 . Table 1 Case Findings before treatment with vedolizumab Follow-up 1 Follow-up 2 Follow-up 3 Overall response Case 1 Weight: 67 kg Stool frequency: 3–4 watery/day Use of steroids: prednisone 6 mg Hospitalization: No PN: No Albumin + : 3.5 g/dL IgG levels: 539 mg/dL Calprotectin*: 2065 µg/g Duodenum: Marsh IIIc, active duodenitis Ileum: follicular hyperplasia, chronic ileitis Colon: chronic active colitis ~1 year Weight: 69 kg Stool frequency: 1/day normal Use of steroids:add prednisone 10 mg Hospitalization: No PN: No Albumin:3.6 g/dL IgG levels: 692 mg/dL Calprotectin:838 µg/g Duodenum: villous architecture restored; active duodenitis persists Ileum: follicular hyperplasia Colon: focal active colitis in rectum ~2 years Weight: 75 kg Stool frequency: 1/day normal Use of steroids: No Hospitalization: No PN: No Albumin: 4.08 g/dL IgG levels: 989 mg/dL Calprotectin: 225 µg/g Duodenum: villous architecture restored; peptic ulcer Clinical remission Histological/endoscopic response Case 2 Weight: 41 kg Stool frequency:3-4/day Use of steroids: 9 mg budesonide Hospitalization: Yes PN: Yes Albumin: 3.9 g/dL IgG levels: 134 mg/dL Alpha-1-antitrypsin clearance: 422 mL/24 h Calprotectin: 187 µg/g Duodenum: Marsh IIIc, intraepithelial lymphocytosis >25%, absent plasma cells ~1 year: Weight: 44.5 kg Stool frequency: 1/day Use of steroids: 3 mg budesonide Hospitalization: No PN: No Albumin: 4.2 g/dL IgG levels: 412 mg/dL Alpha-1-antitrypsin clearance: 18.7 mL/24 h (normalized) - Duodenum: chronic atrophic duodenitis Marsh IIIb, intraepithelial lymphocytes, single non-necrotizing granuloma ~2 years: Weight: 41.8 kg Stool frequency: 4-5/day Steroids: 6 mg budesonide Hospitalization: Yes PN: No Albumin: 3.4 g/dL IgG levels: 227 mg/dL Alpha-1-antitrypsin clearance: 132 mL/24 h - Duodenum: persistent villous atrophy Marsh IIIb, intraepithelial lymphocytes >25% Initial clinical response, mild histologic response. Subsequent clinical relapse after two years of treatment, norovirus and C.difficile Case 3 Weight: 64 kg Stool frequency: 9–10 watery/day Use of steroids: 9 mg budesonide Hospitalization: Yes PN: Yes Albumin + : 3.6 g/dL IgG levels: 743 mg/dL Calprotectin: 371 µg/g Duodenum: normal Ileum: follicular hyperplasia, active ileitis Colon: severe active chronic colitis, absent plasma cells After 4 doses: Weight: 64 kg Stool frequency: 6-10/day Use of steroids: 9 mg budesonide Hospitalization: Yes PN: No Albumin: 3.2 g/dL IgG levels: 553 mg/dL Colon: severe active colitis with CMV viral inclusions — No response; CMV superinfection Case 4 Weight: 52 kg Stool frequency: 3–4 watery/day Use of steroids: 9 mg budesonide Hospitalization: No PN: No Albumin + : 3.1 g/dL IgG levels: 610 mg/dL Calprotectin: 332 µg/g Duodenum: Marsh IIIc, intraepithelial lymphocytosis >30%, absent plasma cells Ileum: follicular hyperplasia Colon: no inflammatory activity ~1 year: Weight: 59 kg Stool frequency: 1/day Use of steroids: No Hospitalization: No PN: No Albumin: 3.1 g/dL IgG levels: 717 mg/dL Calprotectin: 794 µg/g Duodenum: restored villous architecture, normal intraepithelial lymphocyte count, absent plasma cells ~2 years: Weight: 62 kg Stool frequency: 1/day Use of steroids: add 6 mg budesonide 2 months Hospitalization: No PN: No Albumin: 4.3 g/dL IgG levels: 806 mg/dL Calprotectin: 203 µg/g Duodenum: partial villous atrophy ~4 years: Weight: 65 kg Stool frequency: 1/day Use of steroids: No Hospitalization: No PN: No Albumin: 4.5 g/dL IgG levels: 1049 mg/dL Calprotectin: 48 µg/g Duodenum: restored villous architecture Ileum and colon: no inflammatory activity Sustained clinical and histologic remission with one mild histologic relapse resolved with short-course of oral budesonide, in remission for two years since then Clinical, laboratory and endoscopic/histopathological findings before and after treatment with vedolizumab. + Albumin normal range: 3.2–5 g/dL *Calprotectin normal range: 5–45 ug/g # Alpha-1-antitrypsin clearance normal range: <20 mL/24 h. PN, parenteral nutrition. Prior to initiation of biologic therapy, all patients underwent evaluation by an infectious disease specialist to rule out active gastrointestinal infection, including stool cultures and PCR testing, as well as histopathological assessment of tissue samples for cytopathic effect complemented by PCR-based testing for viral pathogens such as cytomegalovirus (CMV). This Institutional Registry of Rare Disease was approved by the Ethics Committee (Project number 7014) at Hospital Italiano de Buenos Aires. Written informed consent for research purposes is obtained before starting follow-up at this institution and also to be included in the registry. Results A total of 105 adult patients across all IUIS categories were identified (86 with predominantly antibody deficiencies, 8 with combined immunodeficiency, and 11 with other IUIS categories), of whom 12 (11%) had inflammatory gastrointestinal disease, all within the subgroup with predominantly antibody or combined immunodeficiency (12/94, 12.8%). Four received vedolizumab at some point during follow-up. We describe the clinical features of gastrointestinal involvement and treatment response in this subgroup. Case 1 A 38-year-old man with combined immunodeficiency with immune dysregulation had a longstanding history of enteropathy with chronic diarrhea with 3–4 watery stools per day. beginning at the age of 14 years, with duodenal, ileal, and colonic involvement requiring recurrent topical and systemic corticosteroid therapy. By the age of 29 years, biopsies demonstrated complete villous atrophy with an inflammatory infiltrate in the lamina propria and increased eosinophils and chronic proctocolitis with foci of neutrophilic exocytosis. He also experienced recurrent respiratory tract infections, prompting his first immunological evaluation in 2020 at the age of 33 years. The finding of hypogammaglobulinemia, impaired response to both protein and polysaccharide vaccines, and CD4+ lymphopenia established the diagnosis of combined immunodeficiency. Immunoglobulin replacement therapy and antibiotic prophylaxis were initiated, resulting in no further infections. He continued to experience persistent diarrhea, and repeat endoscopic evaluation showed persistent complete villous atrophy, with active ileitis and colitis. Although corticosteroids achieved clinical improvement, he became steroid-dependent. Vedolizumab was therefore initiated in 2021, achieving good symptomatic control with successful steroid withdrawal and normalization of stool frequency. After one year of treatment, mild endoscopic activity was noted only in the rectum, which resolved after the addition of low-dose prednisone for 2 months. He was later able to discontinue corticosteroids and remained asymptomatic on vedolizumab for three years, with a weight gain of 8 kg over this period. IgG levels also increased, likely reflecting improved control of enteropathy. In 2023, a genetic diagnosis was established with the identification of a de novo pathogenic TRAF3 variant resulting in haploinsufficiency. In 2024, he developed polyarthritis, requiring the addition of tofacitinib, and vedolizumab was discontinued. Tofacitinib provided good control of both the articular and gastrointestinal manifestations. He subsequently self-discontinued tofacitinib for one year, during which villous atrophy, ileitis, and colitis relapsed. Reintroduction of tofacitinib resulted in a favorable clinical response. Case 2 A 24-year-old man with combined immunodeficiency had a history of recurrent pneumonia since the age of one year, as well as short stature with delayed bone age. At the age of four years he was diagnosed with combined immunodeficiency and started immunoglobulin replacement therapy and antibiotic prophylaxis. At the age of 16 years, he was diagnosed with high-risk stage IVB Hodgkin lymphoma with pulmonary involvement and bulky mediastinal disease, for which he received ESHAP chemotherapy followed by radiotherapy. A heterozygous variant of uncertain significance in TNFRSF13B ( TACI ) was identified. As this finding did not fully explain the patient’s phenotype, whole-exome sequencing remains under periodic reanalysis. At the age of 20 years, he developed autoimmune enteropathy characterized by chronic diarrhea and severe nutritional compromise, requiring hospitalization with temporary parenteral nutrition and enteral nutritional support. Endoscopic biopsies demonstrated complete villous atrophy, and a markedly elevated fecal alpha-1 antitrypsin clearance (422 mL/24 h; normal <20 mL/24 h). Despite corticosteroid therapy, clinical response was poor. Vedolizumab was subsequently initiated, resulting in normalization of stool frequency, weight gain, discontinuation of parenteral nutrition, and normalization of alpha-1 antitrypsin clearance to 18.7 mL/24 h. One year later, follow-up upper endoscopy showed mild endoscopic and histologic response, with residual chronic atrophic duodenitis, and although he had better symptomatic control, he was not able to discontinue budesonide. Two years after initiating vedolizumab, he experienced worsening diarrhea. Repeat endoscopy revealed chronic duodenitis with inflammatory activity, complete villous atrophy, and recurrent elevation of alpha-1 antitrypsin clearance. He required rehospitalization, during which norovirus and Clostridium difficile infection were identified. His gastrointestinal symptoms improved following treatment with oral vancomycin. At present, escalation to an alternative therapeutic regimen is being considered. Case 3 A 51-year-old woman with common variable immunodeficiency (CVID) and autoimmune hepatitis, diagnosed at the age of 38 years. She developed chronic diarrhea at the age of 42 years and an initial endoscopic evaluation demonstrated active proctocolitis, with partial clinical improvement following treatment with topical and systemic corticosteroids and mesalamine. Subsequent endoscopic examinations revealed ileitis in addition to persistent proctocolitis. Histopathological analysis showed chronic proctocolitis with foci of acute inflammatory activity, including cryptitis, crypt abscesses, and a mixed inflammatory infiltrate in the lamina propria. Azathioprine was initiated, resulting in a favorable clinical response, but was discontinued due to severe leukopenia. She subsequently developed progressively worsening bloody diarrhea, with up to 10 stools per day, requiring hospitalization. During hospitalization, following an infectious disease evaluation that ruled out active infection, infliximab was initiated; however, no significant clinical benefit was observed. By that time, endoscopic and histologic findings had progressed to severe active chronic pancolitis. At 48 years of age, she received four doses of vedolizumab without clinical improvement and subsequently developed extensive CMV-associated colitis. Treatment was then switched to ustekinumab. Although endoscopic and laboratory findings continue to demonstrate ongoing inflammatory activity, she has shown gradual clinical improvement, with weight gain, reduced diarrhea (although not complete resolution) and healing of the previously observed deep colonic ulcers. She continues to require a low dose of prednisone. Case 4 A 53-year-old woman was diagnosed with alopecia areata at the age of 16, which progressed to alopecia universalis at 45, and with vitiligo and Hashimoto thyroiditis at the age of 26. At the same age, she developed refractory immune thrombocytopenia requiring rituximab and splenectomy, with subsequent agammaglobulinemia. Also at the age of 26, she was diagnosed with celiac disease based on characteristic histological findings in endoscopic duodenal biopsies, despite negative celiac-specific antibodies. At the age of 45, her diarrhea worsened; upper gastrointestinal endoscopy and capsule endoscopy revealed complete villous atrophy extending from the duodenal bulb to the proximal ileum, refractory to corticosteroid therapy. Azathioprine was initiated but discontinued due to severe leukopenia. During this period, she developed pulmonary CMV infection and severe COVID-19. At 47 years of age, considering persistent diarrhea and severe infec
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