Palate perforation differentiates cocaine-induced midline destructive lesions from granulomatosis with polyangiitis.

Cocaine abuse occasionally causes extensive destruction of the osteocartilaginous structures of the nose, sinuses and palate, which mimics the clinical picture of other diseases associated with necrotising midfacial lesions. The differentiation of cocaine-induced midline destructive lesions (CIMDL) and limited granulomatosis with polyangiitis (GPA) may be difficult, particularly if patients do not readily admit substance abuse. We studied 10 patients with CIMDL and palate perforation referred to our Unit between 2002 and 2015.

An accordion not to be played.

We present the case of a 52-year-old man with normal coronary arteries admitted to our department after being resuscitated from ventricular fibrillation. Transthoracic echocardiography raised suspicion of left-ventricular non-compaction. Cardiac magnetic resonance excluded this, but showed several systolic bulgings of the right ventricle and a characteristic focal 'crinkling' of the right-ventricular outflow tract known as the 'accordion' sign, a specific marker of desmosomal gene mutations, thus suggesting the presence of an arrhythmogenic cardiomyopathy.

Massive apoptosis erodes nasal mucosa of cocaine abusers.

Background: A threatening occurrence in some cocaine abusers is the progressive destruction of nasal structures (cocaine-induced midline destructive lesions [CIMDL]) that may end in a highly severe disease.

Methods: Thirty patients with CIMDL, 10 healthy patients, 10 patients affected by nasal polyposis, and 10 patients affected by Wegener granulomatosis were observed. Biopsy specimens of nasal mucosa were analyzed by immunohistochemistry for caspases-3, -9 and -8 and by the terminal deoxynucleotidyl transferase-mediated dUTP-digoxygenin nick end labeling (TUNEL) method.