Staphylococcal infections may mimic paradoxical psoriasis in patients receiving TNF-alpha inhibitors for systemic conditions

Patients treated with TNF-α antagonists may develop psoriasis-like skin lesions. Clinical manifestations include palmoplantar, inverse, localized or generalized guttate, plaque-type, eczematous, and pustular lesions; deep inflammatory nodes; and nonscarring alopecia, often with overlapping reaction patterns. They are classified as paradoxical psoriasis and interpreted as an inflammatory reaction resulting from the disturbed maturation of plasmacytoid dendritic cells, with overproduction of type I interferons due to tumor necrosis factor α (TNF-α) inhibition. Management frequently necessitates discontinuation of therapy. Here, we review the clinical presentation of six patients who were initially diagnosed with paradoxical psoriasis during TNF-α blockade due to the development of corresponding skin lesions. Dermatologic examination revealed that the lesions were impetigo contagiosa, ecthyma, folliculitis decalvans, ostiofolliculitis, nummular microbial eczema, or abscessing furunculosis—all caused by Staphylococcus aureus, likely spreading from the colonized nasal mucosa to the skin. The cutaneous symptoms resolved with topical antimicrobial therapy and systemic antibiotic treatment. We conclude that many cases diagnosed as paradoxical psoriasis may, in fact, represent generalized abscessing staphyloderma resulting from impaired antimicrobial immunity under TNF-α blockade. The diagnosis of paradoxical psoriasis should therefore be critically re-evaluated on a case-by-case basis. Identification and eradication of S. aureus may substantially improve the prognosis for patients experiencing paradoxical psoriasis-like manifestations during treatment with TNF-α antagonists.