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Colchicine poisoning occurs due to the ingestion of colchicine, a drug derived from the plant colchicum autumnale, and can be life-threatening.
Pathophysiology
Colchicine's toxicity arises primarily from its mechanism of action, which involves binding to tubulin and disrupting microtubule formation, leading to impaired cellular processes. This disruption affects rapidly dividing cells, particularly in the gastrointestinal tract and bone marrow, resulting in significant gastrointestinal symptoms such as nausea, vomiting, and diarrhea due to rapid turnover of intestinal mucosal cells. The drug is metabolized in the liver, primarily by cytochrome P450 enzymes, leading to the formation of several metabolites, including 3-demethylcolchicine (3DMC) and 2-demethylcolchicine (2DMC). These metabolites can exhibit increased toxicity compared to the parent compound, contributing to hepatic injury and other systemic effects. As colchicine inhibits mitosis by preventing spindle formation, it leads to multi-organ dysfunction. The early phase (10-24 hours post-ingestion) is characterized by gastrointestinal distress and initial leukocytosis. In the subsequent phase (24 hours to 7 days), patients may experience severe complications including renal failure, disseminated intravascular coagulation (DIC), and cardiac issues due to direct toxicity on cardiac myocytes. The high affinity of colchicine for tissues like the liver and kidneys contributes to its rapid accumulation in these organs, leading to further complications.