Su Yi-Chia, Wu Chih-Chien
Department of Pharmacy, Kaohsiung Veterans General Hospital, No. 386, Dazhong 1st Rd., Zuoying Dist., Kaohsiung, Taiwan, ROC.
Department of Surgery, Kaohsiung Veterans General Hospital, No. 386, Dazhong 1st Rd., Zuoying Dist., Kaohsiung, Taiwan, ROC.
Drug Saf Case Rep. 2015 Dec;2(1):16. doi: 10.1007/s40800-015-0020-6.
A 54-year-old woman presented at the emergency department after experiencing lower limb weakness and bilateral ankle pain for 2 days. She had a history of type 2 diabetes mellitus, diabetes mellitus nephropathy with chronic kidney disease, and chronic gouty arthritis. She had received 0.6 mg colchicine orally once or twice daily for 8 months. Four days prior to her emergency department visit, she was discharged from our nephrology ward, where she had been admitted because of a urinary tract infection. During hospitalization, she was treated with intravenous cefazolin for 7 days. Because of persistent symptoms, we performed repeated urinalysis, which revealed the presence of yeast. She was diagnosed with fungal cystitis, and was administered a 7-day course of once-daily oral fluconazole (100 mg). On day 5 of the course, she was discharged and asked to continue taking oral colchicine (0.6 mg, twice daily), as well as fluconazole for the full 7-day course. Neurological examination revealed marked symmetrical weakness (Medical Research Council grade 4/5). Her sensation and coordination were intact. Initial laboratory investigation revealed hyperkalemia (6.2 mmol/L), and blood urea nitrogen, serum creatinine, and creatine kinase levels of 181, 11.16 mg/dL, and 803 U/L respectively. Her liver function tests showed elevated alanine aminotransferase levels (112 U/L). Electromyographic results were consistent with colchicine neuromyopathy. Ten days after treatment cessation, muscle enzyme levels normalized and weakness gradually disappeared. We used the Drug Interaction Probability Scale to evaluate our patient's case. A score of 5 was calculated, indicating that the drug-drug interaction was the probable cause of neuromuscular toxicity.
一名54岁女性在出现下肢无力和双侧踝关节疼痛2天后到急诊科就诊。她有2型糖尿病、糖尿病肾病合并慢性肾脏病以及慢性痛风性关节炎病史。她曾口服秋水仙碱0.6毫克,每日1次或2次,共8个月。在她到急诊科就诊前4天,她从我们的肾脏病病房出院,她因尿路感染入住该病房。住院期间,她接受了7天的静脉注射头孢唑林治疗。由于症状持续存在,我们进行了多次尿液分析,结果显示有酵母菌存在。她被诊断为真菌性膀胱炎,并接受了为期7天的每日1次口服氟康唑(100毫克)治疗。在疗程的第5天,她出院了,并被要求继续服用口服秋水仙碱(0.6毫克,每日2次)以及完成整个7天疗程的氟康唑治疗。神经系统检查发现明显的对称性无力(医学研究委员会肌力分级为4/5级)。她的感觉和协调能力正常。初始实验室检查显示高钾血症(6.2毫摩尔/升),血尿素氮、血清肌酐和肌酸激酶水平分别为181、11.16毫克/分升和803单位/升。她的肝功能检查显示丙氨酸转氨酶水平升高(112单位/升)。肌电图结果与秋水仙碱中毒性神经病一致。停药10天后,肌肉酶水平恢复正常,无力症状逐渐消失。我们使用药物相互作用概率量表对我们患者的病例进行评估。计算得出的评分为5分,表明药物相互作用可能是神经肌肉毒性的原因。