IgA vasculitis during secukinumab therapy

Perković, Dijana; Šimac, Petra; Katić, Josip

doi:10.1007/s10067-020-05364-1

Cited by 12 publications

(18 citation statements)

References 11 publications

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“…The onset time of those AESI ranged from 3 days 52 to 96 weeks 60 . A total of 24 AESI was identified (Table 1), including adiposity, 14 alopecia areata, 15 acute autoimmune hemolytic anemia, 16 bullous eruption, 17,18,32 crystalline corneal deposition, 19 drug‐associated vasculitis (including leucocytoclastic vasculitis, IgA vasculitis [henoch‐schönlein purpura], and Behcet's disease), 5,20–24,61 eczematous drug eruption, 11,25–31,62 erectile dysfunction, 35 granuloma annulare, 36–38 hidradenitis suppurativa, 39,40 hypertrichosis, 41 IBD (including Crohn disease [CD], ulcerative colitis [UC], and IBD undefined [IBDU]), 9,12,13 interstitial pneumonia, 42,43 drug‐induced lupus erythematosus, 6,45–47 multiple lentigines, 48 perianal dermatophytosis, 51 pompholyx (dyshidrotic eczema), 33,34 pseudolymphoma, 52 pyoderma gangrenosum, 53,54 raynaud's phenomenon, 55 scleroderma, 57 stomatitis (such as lichenoid mucositis, oral lichen planus, and angular cheilitis), 44,49,50,56 uveitis, 58 and vitiligo 59,60 …”

Section: Resultsmentioning

confidence: 99%

Review of secukinumab‐induced adverse events of special interest and its potential pathogenesis

Liang

Zhang

et al. 2022

Dermatologic Therapy

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Although secukinumab has demonstrated high efficacy and favorable safety in moderate‐to‐severe psoriasis and psoriatic arthritis, patients developing adverse events of special interest (AESI) were reported increasingly in real‐world practice. A systematic literature search of the PubMed database was conducted to identify clinical studies or case reports on secukinumab‐induced AESI. More than 1077 patients (aged 18–74 years) from 55 studies were reported to have 24 AESI 3 days to 96 weeks after secukinumab treatment. The four most common AESI was inflammatory bowel disease (n > 1000), eczematous drug eruption (n > 30), drug‐associated vasculitis (n = 8), and drug‐induced lupus erythematosus (n = 4). Most of these AESI were only mild to moderately severe and resolved after secukinumab discontinuation without or with symptomatic treatment. Secukinumab has the potential to develop a number of AESI by probably dysregulating the different expression of polar T‐cell axes (Th1, Th2, Th17, Th22, and/or Treg) and driving various cytokines in some patients. Physicians should be aware of these AESI for timely diagnosis and proper treatment.

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Section: Resultsmentioning

confidence: 99%

Review of secukinumab‐induced adverse events of special interest and its potential pathogenesis

Liang

Zhang

et al. 2022

Dermatologic Therapy

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“…In patients with active IgAV, serum levels of IL-17 were elevated, and the number of Th17 in peripheral blood increased ( 128 , 129 ). Interestingly, a monoclonal antibody against IL-17A (secukinumab) can trigger IgAV ( 130 ). It is speculated that the secukinumab breaks the balance of regulators of Th17 cells, leading to increased proinflammatory cytokines that induce IgAV.…”

Section: Immunopathogenesis Of Igavmentioning

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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“…Of 6 previously reported cases of secukinumab-associated vasculitis, at least 4 were IgA vasculitis (Table ). [1][2][3][4][5][6] Another case described one patient with rheumatoid arthritis undergoing secukinumab treatment who experienced necrotizing glomerulonephritis; however, the authors concluded secukinumab likely was not causative in that case, as serologies and urinalyses suggested gradual onset of the process prior to initiating the medication. 7 The exact pathogenesis of IgA vasculitis is unclear, but a prevailing theory involves the dysregulation of IgA synthesis and metabolism.…”

Section: Commentmentioning

confidence: 99%

IgA Vasculitis in the Setting of Biologic Therapy for Psoriasis and Recurrent Cutaneous Methicillin-Resistant Staphylococcus aureus Colonization

Young¹

2022

Cutis

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IgA vasculitis is a form of cutaneous small-vessel leukocytoclastic vasculitis (LCV) that has various triggers, including anti-tumor necrosis factor (TNF) α therapy. As the use of more targeted biologic therapies such as the IL-17 inhibitor secukinumab increases, so do reports of associated adverse events. Herein, we describe an uncommon case of IgA vasculitis in a man undergoing biologic therapy with adalimumab and secukinumab for psoriasis with recurrent cutaneous methicillin-resistant Staphylococcus aureus (MRSA) colonization. A review of the current literature also is provided.Cutis. 2022;110:E4-E10.

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IgA vasculitis during secukinumab therapy

Cited by 12 publications

References 11 publications

Review of secukinumab‐induced adverse events of special interest and its potential pathogenesis

Review of secukinumab‐induced adverse events of special interest and its potential pathogenesis

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

IgA Vasculitis in the Setting of Biologic Therapy for Psoriasis and Recurrent Cutaneous Methicillin-Resistant Staphylococcus aureus Colonization

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