Etanercept-Induced Cutaneous Necrotizing Vasculitis in a Patient With Rheumatoid Arthritis: A Case Report and Literature Review.
- 1Department of Rheumatology B, Ayachi Hospital, Faculty of Medicine and Pharmacy of Rabat, Mohammed V University, Rabat, MAR.
- 2Laboratory of Physiology, Mohammed V University, Faculty of Medicine and Pharmacy of Rabat, Rabat, MAR.
Abstract
Tumor necrosis factor-alpha (TNF-α) inhibitors are effective therapies for rheumatoid arthritis (RA) but may rarely induce paradoxical autoimmune complications, including vasculitis. We report the case of a 53-year-old woman with seropositive RA and secondary Sjögren's syndrome who developed bilateral dependent petechial and purpuric lesions of the lower extremities after approximately 33 months of etanercept therapy at a dose of 25 mg twice weekly. At symptom onset, her RA was well controlled, with no clinical or ultrasonographic synovitis and a Disease Activity Score in 28 joints of 2.1. Skin biopsy demonstrated fibrinoid necrosis of dermal vessels, consistent with necrotizing angiitis. No gastrointestinal, renal, neurological, pulmonary, or ear, nose, and throat involvement was identified. The etiologic workup showed a normal complete blood count, preserved renal function, normal urinalysis and complement levels, negative anti-myeloperoxidase, anti-proteinase 3, anti-double-stranded DNA antibodies and cryoglobulins, and negative hepatitis B, hepatitis C, and human immunodeficiency virus serologies. Serum protein electrophoresis showed no monoclonal gammopathy. Antinuclear antibodies were weakly positive at a titer of 1:80 without clear pathological significance. Etanercept was permanently discontinued, and the active lesions resolved completely within approximately 20 days, leaving only residual hyperpigmented and cicatricial changes. No recurrence was documented during follow-up. Rechallenge was not performed, and tocilizumab was subsequently selected for RA control. The compatible latency, histological confirmation, positive dechallenge, sustained absence of recurrence, and lack of a more plausible alternative cause strongly supported the diagnosis of cutaneous necrotizing vasculitis probably induced by etanercept. This case highlights that anti-TNF-α-associated vasculitis may occur after prolonged treatment and requires systematic assessment for systemic involvement and competing autoimmune, infectious, and hematologic causes.
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BibTeX
@article{nouri2026etanerceptinduced,
title = {{Etanercept-Induced Cutaneous Necrotizing Vasculitis in a Patient With Rheumatoid Arthritis: A Case Report and Literature Review.}},
author = {Chaimae Nouri and Latifa Tahiri and Hanan Rkain and Fatine Kronbi and Fadoua Allali},
journal = {Cureus},
year = {2026},
month = sep,
doi = {10.7759/cureus.116548},
url = {https://europepmc.org/article/MED/42899311},
note = {CC BY},
}
RIS
TY - JOUR
TI - Etanercept-Induced Cutaneous Necrotizing Vasculitis in a Patient With Rheumatoid Arthritis: A Case Report and Literature Review.
AU - Chaimae Nouri
AU - Latifa Tahiri
AU - Hanan Rkain
AU - Fatine Kronbi
AU - Fadoua Allali
PY - 2026
DA - 2026/09/19
JO - Cureus
DO - 10.7759/cureus.116548
UR - https://europepmc.org/article/MED/42899311
AB - Tumor necrosis factor-alpha (TNF-α) inhibitors are effective therapies for rheumatoid arthritis (RA) but may rarely induce paradoxical autoimmune complications, including vasculitis. We report the case of a 53-year-old woman with seropositive RA and secondary Sjögren's syndrome who developed bilateral dependent petechial and purpuric lesions of the lower extremities after approximately 33 months of etanercept therapy at a dose of 25 mg twice weekly. At symptom onset, her RA was well controlled, with no clinical or ultrasonographic synovitis and a Disease Activity Score in 28 joints of 2.1. Skin biopsy demonstrated fibrinoid necrosis of dermal vessels, consistent with necrotizing angiitis. No gastrointestinal, renal, neurological, pulmonary, or ear, nose, and throat involvement was identified. The etiologic workup showed a normal complete blood count, preserved renal function, normal urinalysis and complement levels, negative anti-myeloperoxidase, anti-proteinase 3, anti-double-stranded DNA antibodies and cryoglobulins, and negative hepatitis B, hepatitis C, and human immunodeficiency virus serologies. Serum protein electrophoresis showed no monoclonal gammopathy. Antinuclear antibodies were weakly positive at a titer of 1:80 without clear pathological significance. Etanercept was permanently discontinued, and the active lesions resolved completely within approximately 20 days, leaving only residual hyperpigmented and cicatricial changes. No recurrence was documented during follow-up. Rechallenge was not performed, and tocilizumab was subsequently selected for RA control. The compatible latency, histological confirmation, positive dechallenge, sustained absence of recurrence, and lack of a more plausible alternative cause strongly supported the diagnosis of cutaneous necrotizing vasculitis probably induced by etanercept. This case highlights that anti-TNF-α-associated vasculitis may occur after prolonged treatment and requires systematic assessment for systemic involvement and competing autoimmune, infectious, and hematologic causes.
SN - 2168-8184
ER -