Cocaine induced midline destructive lesions I77.6
Definition
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Cocaine induced midline destructive lesion is a localized erosive or ulcerative lesion of the mucosa induced by cocaine/levamisole use, caused by rapid inhalation of cocaine crystals, drug adulteration, nasal picking and superficial necrosis. However, in some habitual users, the damage extends to the underlying bony and cartilaginous structures of the nose, resulting in extensive destructive nasal lesions that often spread centrifugally.
Occurrence/Epidemiology
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In 2020, 22 million people worldwide used cocaine, a figure that is increasing year on year (UNODC 2022). In the European Union, cocaine is the second most commonly used drug after cannabis. Sniffing cocaine crystals through the nose is the most common form of consumption.
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Etiopathogenesis
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Vascular ischemia is the primary mechanism responsible for causing local destructive nasal lesions, which can be attributed to direct damage to the endothelium, an induced prothrombotic state, and, above all, the vasoconstrictive effects of cocaine, which are associated with stimulation of the sympathetic nervous system and endothelial cells (Trimarchi M et al. 2001; Goodger NM et al. 2005). Furthermore, cocaine induces significant dose- and time-dependent apoptosis of nasal mucosal cells, airway epithelial cells, and inflammatory cells in the nasal cavity.
These symptoms are also linked to cocaine’s ability to induce the expression of genes involved in the oxidative stress response and DNA damage, as well as genes associated with apoptosis, autophagy/lysosomal activity, tissue regeneration, cell proliferation, and collagen integrity (Trimarchi M et al. 2021). Furthermore, necrosis and apoptosis, as well as the massive vasodilation that occurs as part of the healing process as the effects of cocaine wear off, lead to frequent bleeding, crust formation, and extensive crusting that impedes breathing and requires removal, leading to further damage.
Other factors contributing to the development of lesions in the mid-nose include local decongestant treatments, smoking, a history of diabetes mellitus, and an individual predisposition to bacterial superinfections of the damaged nasal mucosa, which is influenced by personal nasal hygiene and the use of antibiotics. Different patterns of cocaine use in terms of frequency and duration do not appear to correlate with the extent of the lesions.
Pathophysiology
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Cocaine, a highly potent and addictive drug, is the most commonly used psychostimulant in Europe and is derived from the leaves of the coca plant (Erythroxylum coca). Cocaine increases dopamine levels in the synaptic cleft of the central nervous system by inhibiting its presynaptic reuptake and the presynaptic reabsorption of norepinephrine and serotonin. This leads to changes in behavior and mental health.
Levamisole: Levamisole is a synthetic compound derived from imidazothiazole that was originally used as an anthelmintic in veterinary medicine. Due to its immunomodulatory properties, it was also previously used in humans as an anticancer agent and to treat various autoimmune diseases. In 1999, reports of severe neutropenia led to the drug’s withdrawal from the market. Approximately 70–80% of cocaine is “cut” with levamisole, which is added to increase its volume and stimulant properties. Levamisole is used for this purpose because it has a similar white, powdery consistency to cocaine and cannot be detected in common adulteration tests such as the “bleach test,” a popular street test for checking cocaine purity. Furthermore, levamisole enhances cocaine’s addictive effects by acting as a nicotinic antagonist and prolonging and intensifying the release of glutamate.
Diagnostics
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Cocaine can be detected in urine by screening for its metabolite benzoylecgonine, which is detectable for 48 to 72 hours after use and can persist for up to two weeks in frequent users. Cocaine is detectable in blood and saliva for less than 48 hours, in sweat for several weeks and in hair for several months.
The quantification of levamisole can only be carried out in specialized laboratories using liquid chromatography in conjunction with mass spectrometry on serum and urine samples. In addition, levamisole is difficult to detect due to its limited renal excretion and relatively short half-life of 5.6 hours (Marquez J et al. 2017).
Laboratory
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ANCA-positive!
- p-ANCA is often positive at high titers
- HNE-ANCA is particularly characteristic of CIMDL
- PR3-ANCA possible, but less common
- MPO-ANCA possible, but less common
Literature
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- Aseem F et al. (2024) ANCA-associated vasculitis presenting with isolated neurological manifestations in a patient with cocaine abuse: A case report and literature review. Clin. Rheumatol 43:1401-1407.
- Chevalier X et al.(1995) Schoenlein-Henoch purpura with necrotizing vasculitis after cocaine snorting. Clin. Nephrol. 43:348-349.
- Collister D et al. (2017) ANCA Associated Vasculitis Secondary to Levamisole-Adultered Cocaine with Associated Membranous Nephropathy: A Case Series. Am J Nephrol 45:209-216.
- Dy IA et al. (2012) Cocaine-levamisole thrombotic vasculopathy. Semin Thromb Hemost 38:780-782.
- Gómez-Puerta JA et al. (2017) Anti C1q antibodies. A promising biomarker for cocaine-levamisole induced vasculitis. Reum Clin 15:e66-e67.
- Goodger NM et al. (2005) Palatal and nasal necrosis resulting from cocaine misuse. Br. Dent. J. 198:333-334.
- Iorio L et al. (2024) Cocaine- and Levamisole-Induced Vasculitis: Defining the Spectrum of Autoimmune Manifestations. J Clin Med 13:5116.
- Iorio L et al. (2024) Cocaine- and Levamisole-Induced Vasculitis: Defining the Spectrum of Autoimmune Manifestations. J Clin Med 13:5116.
- Jacob RS et al. (2012) Levamisole-induced vasculopathy: A report of 2 cases and a novel histopathologic finding. Am J Dermatopathol 34:208-213.cocaine-induced vasculopathies.
- Jenkins J et al. (2011) ANCA-positive necrotizing vasculitis and thrombotic vasculopathy induced by levamisole-adulterated cocaine: a distinctive clinicopathologic presentation. J Am Acad Dermatol 65:e14-6.
- Lötscher F et al (2019) Cocaine-induced ANCA-associated renal disease: A case-based review. Rheumatol Int 39:2005-2014.
- Marquez J et al. (2017) Cocaine-Levamisole-Induced Vasculitis/Vasculopathy Syndrome. Curr. Rheumatol. Rep19:36.
- McGrath MM et al. (2011) Contaminated cocaine and antineutrophil cytoplasmic antibody-associated disease. Clin. J. Am. Soc. Nephrol. 6:2799-2805.
- Major T et al. (2024) Granulomatosis with polyangiitis or its mimic? A case report. J Int Med Res 52:3000605241237876.
- Neynaber S et al. (2008) PR3-ANCA-positive necrotizing multi-organ vasculitis following cocaine abuse. Acta Derm. Venereol 88:594-596.
- Pearson T et al. (2012) Vasculopathy related to cocaine adulterated with levamisole: A review of the literature. Dermatol Online J18:1
- Seedahmed K et al. (2025) Midline Destructive Lesions: Differentiating Granulomatosis With Polyangiitis From Cocaine-Induced Perforations. Cureus 17:e83425.
- Specks U (2011) The growing complexity of the pathology associated with cocaine use. J. Clin. Rheumatol17:167-168.
- Trimarchi M et al. (2001) Cocaine-induced midline destructive lesions: Clinical, radiographic, histopathologic, and serologic features and their differentiation from Wegener granulomatosis. Medicine 80:391-404.
- Trimarchi M et al. (2021) Gene Expression Analysis in Patients with Cocaine-Induced Midline Destructive Lesions. Medicine57:861.
- UNODC (2022). World Drug Report 2022. United Nations Publication; Vienna, Austria: 2022: p. 72.
- Wu VC et al. (2006) Levamisole-induced multifocal inflammatory leukoencephalopathy: Clinical characteristics, outcome, and impact of treatment in 31 patients. Medicine 85:203-213.
Incoming links (5)
Cocaine; Cocaine- and Levamisole-Induced Vasculitis; Cocain induced Vasculitis ; Granulomatosis with polyangiitis; Levamisole;Disclaimer
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