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.

An educational intervention may improve FPs' knowledge and diagnosis of skin cancer. Our results may guide future studies with larger sample sizes in developing a skin cancer continuing medical education (CME) course for FPs.

An educational intervention may improve FPs' knowledge and diagnosis of skin cancer. Our results may guide future studies with larger sample sizes in developing a skin cancer continuing medical education (CME) course for FPs.

We conclude from our study that patients with a personal or family history of atopy have an increased risk of allergic contact dermatitis (ACD). These results provide further evidence for the link between atopy and ACD and suggest that children of atopic parents should avoid potential contact allergens and would likely benefit from prophylactic emollient use.