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Clinical outcomes after colchicine overdose: A case report

机译:Colchicine Overdose后的临床结果:案例报告

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Rationale: Colchicine can inhibit cell division and intracellular transport in affected organs by fixing intracellular tubulin and preventing its polymerization into microtubules. A lethal dose of colchicine is considered to be 0.8 mg/kg. The wide distribution of colchicine through 70% of the body following an overdose makes it difficult to eliminate. Patient concerns: A 56-year-old man with a clear history of colchicine overdose was admitted to our hospital nearly 40 hours after taking 12 mg (0.17 mg/kg) of colchicine . He had a history of gout and chronic kidney disease. As the disease progressed, he showed most of the clinical manifestations and pathological features of colchicine overdose. Diagnoses and interventions: Colchicine overdose was clear, with symptoms of multiple organ failure including primary gastrointestinal failure, bone marrow hematopoietic inhibition, rhabdomyolysis, cardiac damage, hepatocyte damage. The patient developed secondary septic shock , renal failure, circulatory failure, and respiratory failure. We performed continuous renal replacement therapy and gastric lavage, and administered norepinephrine, frozen plasma, proton-pump inhibitors, adenosylmethionine, antibiotics, granulocyte colony stimulating factor, and total parenteral nutrition. Outcomes: The patient rapidly developed complete hematopoietic function inhibition, gastrointestinal failure, and cardiac damage 32 hours after admission. Sustained severe infection and circulatory instability caused a progressive deterioration of respiratory function. Tracheal intubation was performed but the patient continued to deteriorate, and death occurred approximately 132 hours after admission. Lessons: Excessive colchicine levels cause continuous organ damage due to extensive tissue distribution, eventually leading to multiple organ failure . Colchicine metabolism is delayed in patients with liver or kidney dysfunction, and even a low dose of colchicine may result in poisoning in these individuals. Early diagnosis and reduction of colchicine levels is critical to improve prognosis, and colchicine poisoning should be considered in patients with poor liver or kidney function even when the ingested dose is low.
机译:理由:通过固定细胞内小管蛋白并防止其聚合到微管中,Colchicine可以抑制受影响器官中的细胞分裂和细胞内转运。致命剂量的血基含量被认为是0.8mg / kg。通过在过量的70%通过70%的狼曲细胞的广泛分布使得难以消除。患者担忧:一名56岁的男子历史明显历史悠闲地在服用12毫克(0.17毫克/千克)的秋水仙碱后近40小时内接纳了我们的医院。他有痛风和慢性肾病的历史。随着疾病的进展,他表现出大部分临床表现和秋水化妆病的病理特征。诊断和干预措施:血氯氨酸过量透明,具有多种器官衰竭的症状,包括原发性胃肠失败,骨髓造血抑制,横纹肌溶解,心脏损伤,肝细胞损伤。患者开发了继发性化脓性休克,肾衰竭,循环衰竭和呼吸衰竭。我们进行连续肾置换疗法和胃灌洗,并施用脱甲肾上腺素,冷冻等离子体,质子泵抑制剂,腺苷甲基硫醚,抗生素,粒细胞菌落刺激因子,以及全肠胃外营养。结果:患者在入院后32小时迅速发展完全造血功能抑制,胃肠衰竭和心脏损伤。持续严重的感染和循环不稳定导致呼吸功能的逐渐恶化。进行气管插管,但患者持续恶化,入院后大约132小时发生死亡。课程:过量的秋水仙碱水平导致由于广泛的组织分布导致连续的器官损坏,最终导致多器官失败。肝脏或肾功能不全的患者延迟了血氯化汀代谢,甚至低剂量的血清序可能导致这些个体中毒。早期诊断和降低血小藻水平对于改善预后至关重要,即使摄入剂量低,肝脏或肾功能较差的患者,应考虑血小藻霉素中毒。

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