Peer Reviewed
Levamisole Toxicity From Adulterated Cocaine
Diagnostic tests. Laboratory test results were as follows: white blood cell count, 7020/µL; hemoglobin, 10.7 g/dL; platelet count, 535 × 103/µL; C-reactive protein, 2.85 mg/L; and lactate, 1.70 mg/dL. Results of a basic metabolic panel were within normal limits.
HIV test results were nonreactive, antinuclear antibody (ANA) test results were negative, and perinuclear antineutrophil cytoplasmic antibody (p-ANCA) and cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA) titers were all less than 1:20.
Chest radiography and chest computed tomography angiography showed opacities in the left lower lobe and right upper lobe, along with splenomegaly and bilateral axillary lymphadenopathy.
Diagnosis. The differential diagnosis for retiform purpura included Wegener granulomatosis, cryoglobulinemia, cocaine levamisole toxicity, septic vasculitis, polyarteritis nodosa, calciphylaxis, and warfarin necrosis. Based on the patient’s history and clinical presentation, a diagnosis of levamisole toxicity from adulterated cocaine was made.
Discussion. Levamisole was withdrawn from in the US market in 1999 due to serious adverse effects related to agranulocytosis, along with development of safer alternative anthelminthic agents.1 It is still in use as an anthelminthic agent for livestock and in aquariums and thus remains available as a cutting agent in cocaine.2 Approximately 70% of cocaine in the United States is contaminated with levamisole.3,4 It adds bulk and a purity factor due to its color, weight, and white powdery consistency. There may also be an added stimulant effect of levamisole, making it ideal for passing street tests by users and dealers.4
Cutaneous manifestations of levamisole toxicity can range from exanthems, urticaria, angioedema, and lichenoid eruptions to vasculitis and Stevens-Johnson syndrome.5 A distinguishing feature are the characteristic necrotic and purpuric skin lesions that preferentially involve the earlobes and cheeks.3,6
Biopsy of a representative skin lesion reveals a leukocytoclastic vasculitis, with varying involvement of superficial and deep dermal vessels, and often vasculopathy with fibrin thrombi in vessel walls.7