Cocaine induced midline destructive lesions I77.6

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.

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.

Vascular ischemia is the primary mechanism causing local destructive nasal lesions due to direct damage to the endothelium, an induced prothrombotic state and, most importantly, the vasoconstrictive effects of cocaine associated with stimulation of the sympathetic nervous system and endothelial cells (Trimarchi M et al. 2001; Goodger NM et al. 2005). In addition, 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 related to the ability of cocaine 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 during the wearing off of the effects of cocaine, lead to frequent bleeding, crust formation and extensive encrustations that impede breathing and require removal, resulting in further damage.

Other factors contributing to the development of lesions in the center of the nose may include local decongestant treatments, smoking, history of diabetes mellitus, and an individual predisposition to bacterial superinfection of the damaged nasal mucosa, which is influenced by personal nasal hygiene and antibiotic use. Different patterns of cocaine use in terms of frequency and duration do not appear to correlate with the extent of the lesions.

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).

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