Borrás-Blasco J, Enriquez R, Sirvent A E, Amoros F, Navarro-Ruiz A, Reyes A
Pharmacy Service, Hospital General Universitario de Elche, Spain.
Int J Clin Pharmacol Ther. 2005 Oct;43(10):480-4.
A 47-year-old man with a history of polyarticular gout was admitted to the nephrology service because of severe renal insufficiency (creatinine 6.25 mg/dl). Three days before admission he had a pain crisis in his knees and ankles and self-administered 20 x 1 mg granules of colchicine p.o. over a period of 4 - 5 hours together with six suppositories each containing 100 mg of indomethacin. The patient began vomiting within 24 hours, experienced diarrhea which persisted for three days and then came to the hospital. The patient reported oliguria during the preceding 24 hours. In hospital, attempts to correct water and electrolyte balance were initiated. The patient became stabilized hemo-dynamically, the diarrhea disappeared within 24 hours, diuresis resumed and the renal function progressively improved. Leukopenia and thrombopenia were diagnosed, the transaminases increased: AST = 79 U/l, ALT = 132 U/l on the eighth day after taking the colchicine. The serology for hepatitis A, B, C and HIV viruses was negative; the serology for CMV and VEB revealed a previous infection. After being discharged from hospital 11 days after admission, the patient presented with the following parameters: hematocrit 39%, leukocytes 5,920/microl (3 470 neutrophils), prothrombin time 13 seconds, urea 44 mg/dl, creatinine 1.29 mg/dl, AST 16 U/l and ALT 35 U/l.
The patient mistakenly ingested 20 mg ofcolchicine p.o. (0.22 mg/kg). The intoxication was associated with gastroenterocolitis, dehydration and renal failure during the first three days after ingestion. The patient also developed leukopenia, thrombopenia and mild hepatocellular injury. Renal failure due to colchicine intoxication is due to various factors such as depletion of volume/hypotension, rhabdomyolysis and multiorgan failure. In this case, the hypovolemia was probably the fundamental cause of the acute renal insufficiency as demonstrated by the quick recovery after administering fluids. It is possible that indomethacin may have enhanced the toxic effect of colchicine on the kidneys and bone marrow. Some colchicine intoxications, as in this case, are caused by an error in interpreting the dose for treating an acute attack of gout. A way to prevent these errors would be to use a low-dose treatment protocol.
一名47岁多关节痛风病史男性因严重肾功能不全（肌酐6.25mg/dl）入住肾内科。入院前三天，他出现双膝和踝关节疼痛发作，在4至5小时内自行口服了20粒1mg秋水仙碱颗粒，并同时使用了6枚每枚含100mg吲哚美辛的栓剂。患者在24小时内开始呕吐，腹泻持续三天后前来医院就诊。患者自述前24小时尿量减少。在医院，开始尝试纠正水和电解质平衡。患者血流动力学稳定，腹泻在24小时内消失，尿量恢复，肾功能逐渐改善。诊断为白细胞减少和血小板减少，服用秋水仙碱后第八天转氨酶升高：AST = 79U/l，ALT = 132U/l。甲型、乙型、丙型肝炎病毒及HIV病毒血清学检查均为阴性；巨细胞病毒和EB病毒血清学检查显示既往感染。入院11天后出院时，患者的各项指标如下：血细胞比容39%，白细胞5920/微升（中性粒细胞3470），凝血酶原时间13秒，尿素44mg/dl，肌酐1.29mg/dl，AST 16U/l，ALT 35U/l。
患者误服了20mg口服秋水仙碱（0.22mg/kg）。中毒在摄入后前三天伴有胃肠结肠炎、脱水和肾衰竭。患者还出现了白细胞减少、血小板减少和轻度肝细胞损伤。秋水仙碱中毒导致的肾衰竭是由多种因素引起的，如血容量减少/低血压、横纹肌溶解和多器官功能衰竭。在本病例中，低血容量可能是急性肾功能不全的根本原因，补液后迅速恢复即证明了这一点。吲哚美辛可能增强了秋水仙碱对肾脏和骨髓的毒性作用。正如本病例所示，一些秋水仙碱中毒是由于对痛风急性发作治疗剂量的错误解读所致。预防这些错误的一种方法是采用低剂量治疗方案。
