Fernández Solá J, Pedrol Clotet E, Campistol Plana J M, Masanés Torán F, Grau Junyent J M, Urbano Márquez A
Servicio de Medicina Interna General Hospital Clínico y Provincial, Barcelona.
Rev Clin Esp. 1993 Sep;193(4):182-4.
A forty-six year old man with chronic renal failure and a toxic chronic liver disease developed progressive muscle weakness after a long trial with colchicine. Physical exam revealed muscle weakness and proximal muscle atrophy with hyporeflexia. Serum levels of creatine kinase were high and signs of myopathy and axonal and demyelinating polyneuropathy was evidenced in electrophysiological studies. Muscle biopsy disclosed a vacuolar myopathy, disruption of myofibers and dilatation of sarcoplasmic reticulum. The clinical pictures was attributed to a toxic myopathy and polyneuropathy due to colchicine, thus this treatment was discontinued. Four week later, the patient was symptom free, the levels of seric creatine kinase were normal and a new muscle biopsy was normal, with disappearance of previous histological findings.
一名患有慢性肾衰竭和中毒性慢性肝病的46岁男性,在长期服用秋水仙碱后出现进行性肌肉无力。体格检查发现肌肉无力、近端肌肉萎缩伴反射减退。血清肌酸激酶水平升高,电生理研究证实存在肌病以及轴索性和脱髓鞘性多发性神经病的体征。肌肉活检显示为空泡性肌病、肌纤维破坏和肌浆网扩张。临床症状归因于秋水仙碱所致的中毒性肌病和多发性神经病,因此停用了该治疗。四周后,患者症状消失,血清肌酸激酶水平正常,再次进行肌肉活检结果正常,之前的组织学表现消失。