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Psoriasis and Pustular Dermatitis Triggered by TNF- Inhibitors in Patients With Rheumatologic Conditions
Gillian C. de Gannes, MD;
Mehran Ghoreishi, MD, PhD;
Janet Pope, MD, FRCPC;
Anthony Russell, MA, MB BChir, FRCPC;
David Bell, MD, FRCPC;
Stewart Adams, MD, FRCPC;
Kamran Shojania, MD, FRCPC;
Magdalena Martinka, MD, FRCPC;
Jan P. Dutz, MD, FRCPC
Arch Dermatol. 2007;143(2):223-231.
Background New onset or worsening of psoriasis has been reported in patients treated with tumor necrosis factor  (TNF-) inhibitors for a variety of rheumatologic conditions. There is mounting evidence that a key innate immune pathway for triggering common human autoimmune disease, including psoriasis, involves plasmacytoid dendritic cell precursors (PDCs) and type 1 interferon (IFN) production. We present herein a case series with clinical and histopathologic evidence of psoriasis in patients with rheumatologic disease treated with TNF- inhibitors. We propose that the cross regulation between TNF- and IFN may have a role in the pathogenesis of this reaction.
Observations We observed new-onset psoriasis (n = 13) or severe exacerbation of psoriasis (n = 2) in 15 patients with a variety of rheumatologic conditions—rheumatoid arthritis (n = 13), psoriatic arthritis (n = 1), and seronegative arthritis (n = 1)—during treatment with etanercept (n = 6), infliximab (n = 5), and adalimumab (n = 4). Immunohistochemical staining of skin biopsy specimens for myxovirus-resistance protein A (MxA, a surrogate marker for lesional type 1 IFN activity) showed increased staining in TNF- inhibitor–induced psoriasis compared with psoriasis vulgaris.
Conclusions New onset or severe exacerbation of psoriasis is a rare complication of TNF- inhibitor therapy. The finding of increased production of IFN- in TNF- inhibitor–induced psoriasis is a possible pathophysiologic explanation for this reaction.
Author Affiliations: Department of Dermatology and Skin Science (Drs de Gannes, Ghoreishi, and Dutz) and Division of Rheumatology (Drs Shojania and Dutz), Department of Medicine, University of British Columbia, Vancouver; Division of Rheumatology, Department of Medicine, University of Western Ontario, London (Drs Pope and Bell); Division of Rheumatology, Department of Medicine, University of Alberta, Edmonton (Dr Russell); Division of Dermatology, Department of Medicine, University of Calgary, Calgary, Alberta (Dr Adams); and Department of Pathology, Vancouver General Hospital, Vancouver (Dr Martinka).
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