Pustular psoriasis is a rare and severe form of psoriasis, characterized by the presence of desquamative plaques with pustules on an erythematous base. Psoriasis is thought to result from plasmacytoid dendritic cell (PDC)-mediated T-cell activation, which stimulates keratinocyte proliferation via type 1 interferon signaling. Studies suggest that TNF-alpha inhibition can paradoxically enhance interferon-alpha activity, leading to the development of pustular psoriasis in some cases. A 58-year-old patient with hidradenitis suppurativa began adalimumab therapy. One month later, she presented with a diffuse pustular rash. A punch biopsy revealed pustular psoriasis with negative direct immunofluorescence (DIF) and periodic acid-Schiff (PAS) stain. Despite treatment with topical steroids, the rash worsened. Her therapy was switched to guselkumab, alongside continued topical steroids. This resulted in significant improvement within a week, with continued resolution at the one-month follow-up. Psoriasis and hidradenitis suppurativa are driven by chronic inflammation involving TNF-alpha and the IL-23/IL-17 axis. While TNF-alpha inhibitors like adalimumab reduce inflammation, paradoxical reactions like pustular psoriasis can occur due to enhanced interferon-alpha activity. In patients on this therapy who develop a new-onset diffuse pustular rash, an index of suspicion for this condition should be maintained. TNF-alpha inhibitors should be discontinued if pustular psoriasis develops, with IL-23 inhibitors providing a viable alternative.
Keywords: adalimumab (humira); biologic treatment; generalized pustular psoriasis; guselkumab; hidradenitis suppurativa; paradoxical psoriasis.
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