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Background: Cocaine is the second most widely abused illicit substance worldwide and exerts potent sympathomimetic effects by inhibiting the reuptake of norepinephrine, dopamine, and serotonin. While cardiovascular and neurological complications are well recognized, gastrointestinal (GI) manifestations are increasingly reported. These arise from multifactorial mechanisms including vasospasm, endothelial dysfunction, thrombosis, ischemia, and direct mucosal toxicity, often with severe clinical consequences. Objective: This narrative review summarizes the mechanisms, pharmacokinetics, pharmacodynamics, routes of use, and spectrum of GI complications associated with cocaine exposure, with emphasis on ischemic, ulcerative, hemorrhagic, inflammatory, fibrotic, hepatobiliary, and pancreatic sequelae. Methods: We reviewed published case reports, cohort studies, and systematic reviews indexed in PubMed and major databases up to 2023. Articles focusing on pathophysiology, clinical presentation, diagnostic features, and outcomes of cocaine-induced GI disorders were included. References with available abstracts were prioritized. Results: Cocaine induces GI injury through vasoconstriction, pro-thrombotic effects, microvascular dysfunction, and direct cytotoxicity. Pharmacokinetically, cocaine demonstrates rapid absorption via intranasal, inhalational, or intravenous routes, with hepatic metabolism and elimination through benzoylecgonine and ecgonine methyl ester. Clinical gastrointestinal complications include: • Ischemic/Vascular: Mesenteric ischemia/infarction, colonic ischemia, ischemic/ hemorrhagic colitis, Vascular thrombosis • Ulcerative/Perforative: Peptic ulcer disease, Gastric, duodenal, small and large bowel perforations • Inflammatory/Fibrotic: Enteritis, enterocolitis, strictures, retroperitoneal fibrosis • Hepatobiliary & Pancreatic • Splenic • Other: GAVE, IBD mimic Rare complications such as intussusception and small bowel hematomas have also been described. Cocaine adulteration with levamisole increases risk of agranulocytosis and ischemic necrosis. Mortality is particularly high in cases of acute mesenteric ischemia, infarction, and fulminant ischemic colitis. Conclusion: Cocaine use is a significant and under-recognized contributor to severe GI morbidity and mortality. Its complications span from ischemia and perforation to hepatopancreatic injury, often requiring emergent intervention. Clinicians should maintain high suspicion for cocaine-related GI disease in young patients presenting with abdominal pain or ischemic features, as early recognition and management may improve outcomes.