Adalimumab, a tumor necrosis factor-alpha inhibitor, is widely used for chronic plaque psoriasis and psoriatic arthritis. While cutaneous adverse effects are known, perforating dermatosis is rare and poorly understood. A 34-year-old woman with psoriasis and psoriatic arthritis developed acquired perforating dermatosis after switching from adalimumab biosimilar GP2017-CTP17. She presented painful, ulcerated plaques on the thighs, gluteal area, and elbows. Histopathology confirmed the diagnosis. The biosimilar drug was discontinued and a 4-week course of systemic corticosteroids led to complete resolution. Both conditions were later managed with methotrexate and ixekizumab. Perforating dermatosis following anti-tumor necrosis factor is rare and underreported with adalimumab. No other known triggers (e.g., diabetes and renal failure) were present. Hypothesized mechanisms include fibronectin dysregulation and advanced glycation end accumulation, disrupting keratinocyte function. Perforating dermatosis should be recognized as a rare adverse effect of tumor necrosis factor-alpha inhibitors. Early recognition and discontinuation may prevent progression. Further studies are needed to clarify pathogenesis.
