Drug-induced vasculitis

Drug-induced vasculitis is a form of vasculitis (inflammation of blood vessels) that occurs as an adverse reaction to certain medications. Unlike primary vasculitides, which arise from autoimmune or idiopathic causes, drug-induced vasculitis is triggered by exposure to specific pharmaceutical agents. Commonly implicated drugs include hydralazine, propylthiouracil, minocycline, allopurinol, certain antibiotics (such as penicillins and cephalosporins), nonsteroidal anti-inflammatory drugs (NSAIDs), and tumor necrosis factor (TNF) inhibitors. The condition may also be referred to as drug-associated vasculitis or medication-induced vasculitis. Many cases are associated with the development of antineutrophil cytoplasmic antibodies (ANCA), particularly when triggered by drugs such as hydralazine or propylthiouracil. The disease can affect multiple organ systems depending on the size and location of the blood vessels involved. The skin is most commonly affected, presenting with palpable purpura, petechiae, skin ulcers, or nodules, typically on the lower extremities. In more severe cases, the kidneys (glomerulonephritis), lungs (pulmonary hemorrhage or infiltrates), joints (arthralgia or arthritis), peripheral nerves, and gastrointestinal tract may be involved. Patients may also experience systemic symptoms such as fever, malaise, weight loss, and myalgia. ANCA-associated drug-induced vasculitis can mimic primary ANCA-associated vasculitides such as granulomatosis with polyangiitis or microscopic polyangiitis. The cornerstone of treatment is prompt identification and discontinuation of the offending drug, which often leads to significant improvement or complete resolution of symptoms. In mild cases limited to the skin, withdrawal of the causative medication may be sufficient. For more severe or systemic disease, immunosuppressive therapy may be required, including corticosteroids and, in refractory cases, additional agents such as cyclophosphamide or rituximab. The prognosis is generally favorable when the causative drug is identified and removed early, though some patients may experience persistent symptoms or organ damage requiring ongoing management. Regular monitoring of organ function and ANCA titers may be warranted during recovery.

Common questions about Drug-induced vasculitis