Vasculitis associated with tumor necrosis factor-α inhibitors.
OBJECTIVE
To describe the clinical characteristics, histopathologic features, and outcomes of patients in whom vasculitis developed in association with use of tumor necrosis factor-α (TNF-α) inhibitors.


METHODS
This is a retrospective review of patients evaluated at Mayo Clinic, Rochester, Minnesota, from January 1, 1998, through March 31, 2011, with a diagnosis of vasculitis induced by anti-TNF-α therapy.


RESULTS
Of 8 patients with vasculitis associated with anti-TNF-α therapy (mean age, 48.5 years), 6 (75%) were female. Four (50%) had rheumatoid arthritis, 1 (13%) had Crohn disease, and 3 (38%) had ulcerative colitis. Five (63%) were treated with infliximab, 2 (25%) with etanercept, and 1 (13%) with adalimumab. The mean duration of treatment before development of vasculitis was 34.5 months. The skin was the predominant organ affected (5 patients [63%]), with the most common cutaneous lesion being palpable purpura (4 of 5 [80%]). Two organs involved in systemic vasculitis were the peripheral nervous system (4 patients [50%]) and kidney (1 patient [13%]). All cases of vasculitis were histopathologically confirmed. Seven of 8 patients improved with discontinuation of therapy (mean time to resolution, 6.9 months) and adjuvant treatment (all 8 received prednisone; another agent was also used in 7); rechallenge with anti-TNF-α therapy was not attempted in any patient. At last follow-up, no patients had experienced a recurrence of vasculitis after therapy discontinuation.


CONCLUSIONS
Cutaneous small-vessel vasculitis was the most common finding, but systemic vasculitis, including peripheral nerve and renal vasculitis, was also frequently observed.
Department of Dermatology, Mayo Clinic, Rochester, MN 55905, USA.
Olayemi
O
Sokumbi
David A
DA
Wetter
Ashima
A
Makol
Kenneth J
KJ
Warrington
D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000893:Anti-Inflammatory Agents / Q000009:adverse effects*; D000911:Antibodies, Monoclonal / Q000009:adverse effects*; D061067:Antibodies, Monoclonal, Humanized / Q000009:adverse effects; D058846:Antibodies, Monoclonal, Murine-Derived / Q000627:therapeutic use; D001172:Arthritis, Rheumatoid / Q000188:drug therapy; D001379:Azathioprine / Q000627:therapeutic use; D003093:Colitis, Ulcerative / Q000188:drug therapy; D003424:Crohn Disease / Q000188:drug therapy; D003520:Cyclophosphamide / Q000627:therapeutic use; D000068800:Etanercept; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D006417:Hematuria / Q000209:etiology; D006801:Humans; D007074:Immunoglobulin G / Q000009:adverse effects; D007155:Immunologic Factors / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D009173:Mycophenolic Acid / Q000031:analogs & derivatives / Q000627:therapeutic use; D011115:Polyneuropathies / Q000209:etiology; D011241:Prednisone / Q000627:therapeutic use; D011507:Proteinuria / Q000209:etiology; D018124:Receptors, Tumor Necrosis Factor; D012189:Retrospective Studies; D000069283:Rituximab; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014657:Vasculitis / Q000139:chemically induced* / Q000188:drug therapy; D055815:Young Adult
D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D005938:Glucocorticoids; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069283:Rituximab; D003520:Cyclophosphamide; D000069285:Infliximab; D000068879:Adalimumab; D009173:Mycophenolic Acid; D001379:Azathioprine; D000068800:Etanercept; D011241:Prednisone; D008727:Methotrexate