Treatment of Rituximab-induced Crohn’s Disease With Ustekinumab Induction and Long-term Maintenance of Remission

Shankar, Uday; Vijayasekar, Kavitha; Bansal, Raghav; Walfish, Aaron

doi:10.1093/ibd/izz270

Cited by 6 publications

(14 citation statements)

References 4 publications

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“…Immune dysregulation in the gastrointestinal tract may contribute to Crohn's disease as a secondary complication in rituximab-susceptible cases. 1 Ustekinumab was highly effective in this case. Though ustekinumab is not approved for children with IBD in Japan, its use was deemed appropriate based on its widespread use in other countries and its effectiveness in similar cases in the past.…”

mentioning

confidence: 66%

“…Eliminating B cells to resolve autoimmunity can also result in regulatory B‐cell depletion, which hinders the suppression of inflammation 5 . Inhibiting the interaction between B and T cells due to B‐cell depletion can result in T‐regulatory cell dysfunction and, consequently, activation of Th1 and Th17 cells 1 and dysregulated mucosal immune response, which may then cause Crohn's disease. Immune dysregulation in the gastrointestinal tract may contribute to Crohn's disease as a secondary complication in rituximab‐susceptible cases 1 .…”

Section: Figmentioning

confidence: 99%

“…Though ustekinumab is not approved for children with IBD in Japan, its use was deemed appropriate based on its widespread use in other countries and its effectiveness in similar cases in the past. 1 In conclusion, IBD should be considered in patients with gastrointestinal symptoms following rituximab use, regardless of the period of time after administration.…”

mentioning

confidence: 99%

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Rituximab‐induced Crohn's disease in a child with refractory nephrotic syndrome

Machida

Kobayashi

Yodoshi

2022

Pediatrics International

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mentioning

confidence: 66%

Section: Figmentioning

confidence: 99%

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Rituximab‐induced Crohn's disease in a child with refractory nephrotic syndrome

Machida

Kobayashi

Yodoshi

2022

Pediatrics International

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“…Indeed, Shahmohammadi et al reported that the concomitant use of 5-ASA and CSs was effective in 43% (3/7) of patients (6). Biologics can be added because the efficacy of ustekinumab for RTXinduced Chron's disease has been reported (18).…”

Section: Discussionmentioning

confidence: 99%

Rituximab-induced Ileocolitis in a Patient with Gastric MALToma: A Case Report and Literature Review

et al. 2021

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Rituximab (RTX) is effective for treating cancer, but reports of RTX-associated enterocolitis are limited. We herein report the case of a 65-year-old man who developed RTX-induced ileocolitis. He was diagnosed with gastric mucosa-associated lymphoid tissue lymphoma (MALToma) and treated with RTX. He complained of bloody diarrhea after RTX. Mucosal inflammation on colonoscopy indicated RTX-induced ileocolitis. He was treated with corticosteroids, and his symptoms improved. We reviewed the RTX-associated gastrointestinal adverse events and classified the features into ulcerative colitis, Crohn's disease, microscopic colitis, and ileocolitis. To our knowledge, this is the first case of a Japanese patient who developed RTXinduced ileocolitis.

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“…Similarly, next-generation biologics that target CD20, such as ocrelizumab, obinutuzumab, and veltuzumab, may be similarly effective [143]. However, rituximab has been implicated in GI complications and reports of rituximab-induced colitis [144][145][146]. Further, rituximab may target follicular B cells expressing CD20 and prevent their differentiation into plasmablasts, but would not target chronically active plasmablasts already formed prior to initiation of treatment [147].…”

Section: Implications For Immunotherapymentioning

confidence: 99%

The Possible Pathogenic Role of IgG4-Producing Plasmablasts in Stricturing Crohn’s Disease

Bushara¹,

Escobar²,

Weinberg³

et al. 2022

Pathobiology

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Background: Crohn’s disease (CD) is a condition on the spectrum of inflammatory bowel disease that affects up to 20 people per 100,000 in the US annually, and with incidence increasing. One of the most significant sources of morbidity in CD is the formation of strictures, with resultant intestinal blockage a common indication for hospitalization and surgical intervention in these patients. The pathophysiology of stricture formation is not fully understood. However, the fibroplasia that leads to fibrostenotic stricture formation may have shared pathophysiology with IgG4-related fibrosis. Summary: Initial intestinal inflammation recruits innate immune cells, such as neutrophils, that secrete IL-1β and IL-23, which induces a type 17 CD4+ T-helper T-cell (Th17)-mediated adaptive immune response. These CD4+ Th17 T cells also contribute to inflammation by secreting proinflammatory cytokines such as IL-17 and IL-21. IL-21 recruits and stimulates CD4+ T follicular helper (Tfh) cells, which secrete more IL-21. This causes ectopic germinal center formation, recruiting and stimulating naïve B cells. The IL-17 and IL-21 produced by Th17 cells and Tfh cells also induce IgG4 plasmablast differentiation. Finally, these IgG4-producing plasmablasts secrete platelet-derived growth factor (PDGF), which activates local PDGF-receptor expressing fibroblasts and myofibroblasts, resulting in uncontrolled fibroplasia.

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Treatment of Rituximab-induced Crohn’s Disease With Ustekinumab Induction and Long-term Maintenance of Remission

Cited by 6 publications

References 4 publications

Rituximab‐induced Crohn's disease in a child with refractory nephrotic syndrome

Rituximab‐induced Crohn's disease in a child with refractory nephrotic syndrome

Rituximab-induced Ileocolitis in a Patient with Gastric MALToma: A Case Report and Literature Review

The Possible Pathogenic Role of IgG4-Producing Plasmablasts in Stricturing Crohn’s Disease

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