Immunoglobulin A vasculitis associated with inflammatory bowel disease: a retrospective cohort study

Villatoro-Villar, Michel; Crowson, Cynthia S.; Warrington, Kenneth J.; Makol, Ashima; Koster, Matthew J.

doi:10.1080/03009742.2020.1732460

Cited by 3 publications

(2 citation statements)

References 22 publications

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“…Serum TNF-a is elevated in patients with IgAV, and the level is associated with disease severity, suggesting the participation of other inflammatory cells (135). Paradoxically, TNF-a inhibitors may induce IgAV in patients with inflammatory bowel disease or psoriasis, but the causality is not confirmed (136)(137)(138). A possible explanation is that TNF-a inhibitors form immune complexes with endogenic TNF-a and deposits at vessel walls.…”

Section: Othersmentioning

confidence: 99%

Pathogenesis of IgA Vasculitis: An Up-To-Date Review

Song

Huang

et al. 2021

Front. Immunol.

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Immunoglobin A (IgA) vasculitis (IgAV), formerly called the Henoch-Schönlein purpura (HSP), is a small vessel vasculitis, characterized by IgA1-dominant immune deposition at diseased vessel walls. IgAV is the most common form of vasculitis in children; typical symptoms include palpable purpura, arthritis or arthralgia, abdominal pain, and hematuria or proteinuria. Galactose-deficient IgA1 is detected in the tissues of the kidney and skin in patients with IgAV; it forms immune complexes leading to subsequent immune reactions and injuries. This report provides the recent advances in the understanding of environmental factors, genetics, abnormal innate and acquired immunity, and the role of galactose-deficient IgA1 immunocomplexes in the pathogenesis of IgAV.

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Section: Othersmentioning

confidence: 99%

Pathogenesis of IgA Vasculitis: An Up-To-Date Review

Song

Huang

et al. 2021

Front. Immunol.

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“…One study reported that two cases showed the deposition of IgA in the renal biopsy among 39 cases of vasculitis during treatment with TNF inhibitors [ 79 ]. Another study showed that six out of nine patients experienced IgA vasculitis onset during TNF inhibitors; however, three of five patients continued to use TNF inhibitors and fully recovered while maintaining TNF inhibitor treatment [ 80 ]. IL-17A inhibitors have also been reported as triggers of IgA vasculitis [ 81 ].…”

Section: Triggers and Pathogenesis Of Iga Vasculitismentioning

confidence: 99%

IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes

Sugino

Sawada

Nakamura

2021

IJMS

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IgA, previously called Henoch-Schönlein vasculitis, is an essential immune component that drives the host immune response to the external environment. As IgA has the unique characteristic of a flexible response to broad types of microorganisms, it sometimes causes an autoreactive response in the host human body. IgA vasculitis and related organ dysfunction are representative IgA-mediated autoimmune diseases; bacterial and viral infections often trigger IgA vasculitis. Recent drug developments and the presence of COVID-19 have revealed that these agents can also trigger IgA vasculitis. These findings provide a novel understanding of the pathogenesis of IgA vasculitis. In this review, we focus on the characteristics of IgA and symptoms of IgA vasculitis and other organ dysfunction. We also mention the therapeutic approach, biomarkers, novel triggers for IgA vasculitis, and epigenetic modifications in patients with IgA vasculitis.

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IgA vasculitis in patients with inflammatory bowel disease: new insights into the role of TNF-α blockers

et al. 2021

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Objective Association of IgA vasculitis (IgAV) and inflammatory bowel diseases (IBD) is rarely described, mainly during anti-TNF-α therapy. We aimed to describe the association of IgAV and IBD. Methods We retrospectively analyzed the association of IgAV and IBD through the implication of the GETAID and FVSG networks. Characteristics of IBD and IgAV were collected using a standardized case report form. Results Forty-three cases were included. IBD (mainly Crohn’s disease (CD) in 58%) preceded IgAV in 38 (88%), with median interval of 9.2 (IQR 5.4–15.4) years. In these 38 patients, at IgAV diagnosis, 5 (13%) had active IBD and 28 (74%) were treated with anti-TNF-α for a median duration of 31.5 (IQR 19–56) months. Main IgAV manifestations were purpura all patients (100%), joints in 20/35 (57%), renal in 15/35 (43%) and gastrointestinal in 11/35 (31%) involvement. IgAV was treated with glucocorticoids in 25 (66%), colchicine in 6 (16%), cyclophosphamide in 6 (16%), and anti-TNF-α were discontinued in 15/28 (54%). No IgAV relapse occurred when TNF-α blockers were stopped, vs 23% in patients pursuing it. Conversely, 5 (33%) had IBD flare or complication after anti-TNF-α cessation vs 1 (8%) in those continuing biologics. Anti-TNF-α were resumed in 6 (40%), with subsequent IgAV relapse in 4 (67%). Conclusions This large cohort suggests that TNF-α blockers may promote the onset of IgAV in IBD. Discontinuation of anti-TNF-α was associated with vasculitis remission but increased risk of IBD relapses, whereas continuation of anti-TNF-α was associated with IBD remission but vasculitis relapse.

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Immunoglobulin A vasculitis associated with inflammatory bowel disease: a retrospective cohort study

Cited by 3 publications

References 22 publications

Pathogenesis of IgA Vasculitis: An Up-To-Date Review

Pathogenesis of IgA Vasculitis: An Up-To-Date Review

IgA Vasculitis: Etiology, Treatment, Biomarkers and Epigenetic Changes

IgA vasculitis in patients with inflammatory bowel disease: new insights into the role of TNF-α blockers

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