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Abstract

A 59-year-old woman with hypertension and chronic kidney disease was transferred for hemorrhagic shock following a renal biopsy. During hospitalization, she underwent iodine-loaded renal artery embolization and was noted to have a 5-year history of hydralazine use. Seven days after admission, she developed rapidly progressive bullous hemorrhagic plaques on the face, upper trunk, and upper extremities. Laboratory evaluation revealed p-ANCA, anti-histone, and dsDNA positivity. Kidney biopsy demonstrated tubular injury with features suggestive of post-infectious-associated nephritis. Skin biopsy showed a dense dermal neutrophilic infiltrate containing mononucleated vacuolated structures with a cryptococcoid appearance. PAS and other infectious stains were negative. Rheumatology did not favor systemic lupus erythematosus or drug-induced lupus; however, a hydralazine-induced cutaneous reaction remained a consideration. High-dose corticosteroids and dialysis led to rapid arrest of new lesions and resolution of purpuric plaques. This presentation mirrors an increasingly recognized clinicopathologic pattern of acute hemorrhagic bullous eruptions with dense neutrophilic infiltrates containing cryptococcoid cells. Most published cases have described this entity as a variant of Sweet syndrome, hydralazine-induced Sweet syndrome, or iododerma neutrophilic dermatosis. Our patient’s abrupt onset following iodine exposure, in the setting of CKD and hydralazine use, supports an exogenous-induced process—potentially iododerma or medication-related—rather than idiopathic Sweet syndrome. Our literature review highlights recurrent associations with recent iodine contrast, renal dysfunction, specific medications, and autoantibody positivity, suggesting this phenotype may represent a distinct clinicopathologic entity. Recognition of this pattern should prompt targeted evaluation of recent exposures and autoimmune markers to guide therapy and prevent recurrence.