Abstract:

Introduction: Skin blistering is an uncommon cutaneous reaction to imatinib. Vesicles or bullae are typically photo-distributed and classified as drug-induced pseudoporphyria or rarely porphyria. We present a unique case of a bullous drug eruption occurring on photo-protected skin. Our distinct histologic findings support an alternative pathomechanism for imatinib-induced skin blistering. Case presentation: A 70-year-old male with a history of chronic myeloid leukemia treated with imatinib 400mg daily for 18 months developed recurrent blistering of his ventral fingers and wrist. He denied alcohol and NSAID use. Histopathology: Sections showed a cell poor subepidermal vesicle with mild superficial perivascular lymphocytic infiltrate without eosinophils. PAS/GMS stains were negative. There were no eosinophilic deposits within the roof of the blister cavity nor within the dermis. DIF was negative for immunoglobulin deposition. Hyalinization of the dermis and loss of elastin below the blister cavity was noted on VVG stain. Porphyrin screen was negative. Discussion/conclusion: Imatinib is a tyrosine kinase inhibitor with additional targets that may explain the diverse presentation of blistering. On photo-exposed skin, C-kit inhibition may lead to altered melanogenesis and accumulation of endogenous porphyrins. Whereas, on photo-protected skin, platelet-derived growth factor receptor inhibition may lead to basement membrane instability and loss of elastic microfibrils in the dermis. Treatment includes sun protection for porphyria/pseudoporphyria related cases, dose reduction, or switching to a newer tyrosine kinase inhibitor.

Financial Disclosure:
No current or relevant financial relationships exist.

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Sama Alazawi, DO