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Paradoxical Psoriasis — SCE Rheumatology MCQ

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HardRheumatoid ArthritisParadoxical PsoriasisSCE Rheumatology

A 55-year-old woman with seropositive rheumatoid arthritis has achieved good disease control with adalimumab 40 mg every 2 weeks for 10 months. She develops sharply demarcated erythematous, scaly plaques with sterile pustules, predominantly affecting her palms and soles. She has no personal or family history of psoriasis, no new topical or occupational exposures, and no preceding diarrhoea or urethritis. Treponemal serology is negative. The lesions improve during a 6-week perioperative interruption of adalimumab and recur after treatment is restarted. Which mechanism best explains this eruption?

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Correct answer: A — TNF blockade causing dysregulated type I interferon-predominant psoriasiform inflammation

Adalimumab can paradoxically induce new-onset psoriasis, particularly a palmoplantar pustular phenotype. The strongest clues are TNF-inhibitor exposure, absence of previous psoriasis, and improvement on withdrawal followed by recurrence after restarting treatment. The leading mechanistic model is that TNF blockade permits sustained plasmacytoid dendritic-cell production of type I interferons, especially interferon-alpha, producing psoriasiform inflammation despite TNF inhibitors being treatments for conventional psoriasis. Contact dermatitis is unsupported by an allergen exposure and the drug-linked course. Negative treponemal serology argues against secondary syphilis, while the absence of a preceding infection or associated features makes reactive arthritis unlikely. Coincidental idiopathic psoriasis is possible in principle, but the positive dechallenge–rechallenge relationship strongly favours a paradoxical drug reaction.

Reference: Electronic Medicines Compendium (eMC), Humira 40 mg solution for injection in pre-filled pen, Summary of Product Characteristics, section 4.8 Undesirable effects, updated 16 February 2026. https://www.medicines.org.uk/emc/product/7986/smpc