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Cocaine is an alkaloid substance extracted from Erytroxylon coca, originating in Latin American countries, which acts by inhibiting the reuptake of serotonin at synaptic terminals. In recent decades, recreational cocaine use has substantially increased, becoming a significant public health issue. Approximately 5.3% of the population between the ages of 12 and 65 have used cocaine at some point in their lives, marking a 100% increase compared to the 2010 study. In comparison with 2010, lifetime cocaine use has tripled among adolescents. Approximately 1.5% of the population reported cocaine use in the last year, with 2.4% of males and 0.7% of females being consumers. Levamisole, a veterinary antiparasitic, is currently used to increase the volume and potency of cocaine. The combination of these two substances can lead to a condition characterized by cocaine-related effects, such as nasal septal cartilage involvement resulting in septal perforation, cutaneous small vessel vasculitis affecting the auricular pavilions and nasal cartilage, a condition known as cocaine-levamisole-induced vasculitis (CLIV) that can progress to necrosis and even cutaneous ulcers, associated with agranulocytosis, arthralgia, and glomerulonephritis with pulmonary-renal syndrome.
Cocaine-levamisole-induced vasculitis generates a set of systemic symptoms characterized by dermatological and pulmonary lesions, small vessel vasculitis, agranulocytosis, fever, arthralgia, earlobe necrosis, and also includes rheumatological manifestations. The diagnosis is clinical but must be supported by laboratory tests to rule out differential diagnoses. The aim of this case report is to consider early suspicion of dermatological vasculitis and pulmonary-renal syndrome of cocaine-levamisole vasculitis for diagnosis and initiation of treatment to prevent complications and progression to chronic kidney disease. The diagnosis of cocaine-levamisole-induced vasculitis poses a diagnostic challenge because levamisole can only be detected by laboratory methods within 24 hours of consumption. Therefore, medical history, a history of cocaine use, and clinical presentation are essential tools for diagnosis
Clinical Case: A 25-year-old patient with a history of intravenous drug use, hepatitis C, admitted to another institution 3 months ago with febrile syndrome, rapidly progressing renal injury requiring hemodialysis, hemoptysis due to necrotizing pneumonia, presented with fever, dyspnea, and increased lower limb circumference.
Physical examination: Cutaneous mucosal pallor, multiple upper limb puncture lesions due to intravenous substance abuse, erythematous lesions with crusts and scales of different sizes on the lower limbs. Tachypnea with bilateral rales. Lower limb edema. Urine sediment and complete urine with hematic cylinders, dysmorphic erythrocytes, serology for Hepatitis B negative, Hepatitis C positive, HIV negative, Fan Anti DNA negative , ANCA C negative , ANCA P negative, cryoglobulins negative. Laboratory: hto
Pleural Efus: glu 102mg/dl. LDH 1057/L, Protein 4g/l, PH 7 Hemat 1000/mm3
Chest computed tomography: Disseminated cavitated lesions, Doppler echocardiogram: 13mm vegetation on tricuspid valve. Renal ultrasound: kidneys of preserved size and shape. Skin biopsy: lymphocytic vasculitis with erythrocyte extravasation.
Levamisole is a veterinary antiparasitic drug used as an enhancer of cocaine's effects. In recent years, there has been an increase in reported cases associated with vasculitis due to cocaine adulteration with levamisole. Cascio and Jen have proposed naming this constellation of alterations as cocaine-levamisole autoimmune syndrome (CLAAS). The literature describes vasculitis in patients with a history of substance abuse, primarily cocaine. They typically present purpuric skin lesions on the lower limbs and areas with distal finger necrosis due to small vessel occlusion. Skin lesion biopsies often reveal leukocytoclastic vasculitis or vasculitis with thrombosis leading to necrosis. Hematological manifestations include sometimes severe, challenging-to-manage anemia due to probable inflammatory reaction, leukopenia, and hypocomplementemia.
Levamisole-induced vasculitis manifests with pulmonary-renal syndrome, featuring rapidly progressive renal damage, urinary sediment with hematic cylinders, dysmorphic erythrocytes, and the detection of ANCA C, ANCA P, anti MBG, antinuclear antibodies, and anticardiolipins to rule out other causes. The literature primarily describes pulmonary involvement, with fewer cases showing renal damage.
There is no specific treatment for this condition, although reports indicate a good response and remission of symptoms with corticosteroid pulse therapy combined with cyclophosphamide, along with discontinuation of drug use. We must sistematize study in this population of patiens to acelerate diagnostic.