Modi Jitu R, Cratty Michael S
Department of Pediatrics, Walter Reed Army Medical Center, Washington, DC, USA.
Ann Pharmacother. 2002 Dec;36(12):1870-4. doi: 10.1345/aph.1C029.
To demonstrate a case of rhabdomyolysis with acute renal failure in a patient receiving fluvastatin and to present evidence that this was an adverse drug reaction to fluvastatin.
A 51-year-old white man with a past medical history significant for hyperlipidemia treated with fluvastatin presented with malaise, myalgias, nausea, and lumbar back pain. The patient had azotemia with elevated creatine kinase (CK), lactate dehydrogenase, and transaminases. He developed hematuria and proteinuria. Laboratory results demonstrated a normal antinuclear antibody, rheumatoid factor, angiotensin-converting enzyme, antineutrophil cytoplasmic antibody, and thyroid-stimulating hormone. Cytomegalovirus and Epstein-Barr virus titers were negative for recent infection. There were no signs of systemic infection; the white blood cell count was normal and blood and urine cultures were negative. Renal ultrasound showed hyperechoic renal cortices with no obstruction. The discontinuation of fluvastatin and hemodialysis led to a rapid decrease in CK and improvement in symptoms.
Hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitors have the potential to cause rhabdomyolysis. However, fluvastatin is rarely associated with rhabdomyolysis when compared to other statins. Differences in biochemical and pharmacokinetic properties between fluvastatin and other HMG-CoA reductase inhibitors may be important in the development of rhabdomyolysis.
Fluvastatin was the precipitating factor causing rhabdomyolysis in this case report. This patient had no other findings to suggest infection or other disorder inducing rhabdomyolysis. An objective causality assessment revealed that the adverse drug reaction was probable as determined by the Naranjo probability scale. Fluvastatin has the potential to cause serious adverse effects. Therefore, a heightened awareness by the patient and physician for potential signs of myopathy is recommended.
证实一例接受氟伐他汀治疗的患者发生横纹肌溶解症并伴有急性肾衰竭的病例,并提供证据表明这是氟伐他汀的药物不良反应。
一名51岁白人男性,既往有高脂血症病史,接受氟伐他汀治疗,出现全身不适、肌痛、恶心和腰痛。患者出现氮质血症,肌酸激酶(CK)、乳酸脱氢酶和转氨酶升高。他出现了血尿和蛋白尿。实验室检查结果显示抗核抗体、类风湿因子、血管紧张素转换酶、抗中性粒细胞胞浆抗体和促甲状腺激素均正常。巨细胞病毒和EB病毒滴度近期感染呈阴性。没有全身感染的迹象;白细胞计数正常,血培养和尿培养均为阴性。肾脏超声显示肾皮质回声增强,无梗阻。停用氟伐他汀并进行血液透析后,CK迅速下降,症状改善。
羟甲基戊二酰辅酶A(HMG-CoA)还原酶抑制剂有导致横纹肌溶解症的潜在风险。然而,与其他他汀类药物相比,氟伐他汀很少与横纹肌溶解症相关。氟伐他汀与其他HMG-CoA还原酶抑制剂在生化和药代动力学特性上的差异可能在横纹肌溶解症的发生中起重要作用。
在本病例报告中,氟伐他汀是导致横纹肌溶解症的诱发因素。该患者没有其他发现提示感染或其他导致横纹肌溶解症的疾病。客观的因果关系评估显示,根据Naranjo概率量表确定,该药物不良反应很可能发生。氟伐他汀有导致严重不良反应的潜在风险。因此,建议患者和医生提高对肌病潜在体征的认识。