他汀类药物诱导的坏死性自身免疫性肌病合并复杂糖尿病患者的治疗

Emma M Laspe, Nathaniel Daugherty
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引用次数: 0

摘要

背景:在极少数情况下,他汀类药物治疗降低脂质水平可能引起肌肉相关的不良反应,导致自身免疫性肌病。他汀类药物诱导的坏死性自身免疫性肌病(SINAM)通常伴有对称性近端肌无力和肌酸磷酸激酶(CPK)升高。糖皮质激素是一线治疗,但治疗可能升级到包括甲氨蝶呤和/或静脉免疫球蛋白治疗(IVIG)。病例介绍:男性,59岁,证实阿托伐他汀依从1年,出现4个月的疲劳、神经病变和进行性近端肌无力史。实验室检测显示CPK升高高达12990微克/升。抗3-羟基-3-甲基戊二酰辅酶A还原酶(抗hmgcr)抗体检测阳性,患者开始免疫抑制治疗,IVIG单药治疗(2 g/kg),疗程3天。由于2型糖尿病难以控制,未使用糖皮质激素治疗。出院后,患者继续每月进行IVIG治疗。在总共7轮(入院后6轮)IVIG治疗后,患者报告活动改善,日常活动强度增加,CPK水平继续下降至680 mcg/L。结论:出现近端肌无力和CPK升高的患者,即使在他汀类药物停药后,也应考虑对潜在的SINAM进行全面检查。检测抗hmgcr抗体或存在坏死的肌肉活检是必要的正式诊断。该病例显示IVIG单药治疗成功,尽管先前的研究表明肌肉症状改善的最佳机会是糖皮质激素、甲氨蝶呤和IVIG的联合治疗。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Statin-Induced Necrotizing Autoimmune Myopathy in a Patient With Complex Diabetes Management.

Background: In rare cases, statin therapy for the reduction of lipid levels may cause muscle-related adverse effects leading to autoimmune myopathy. Statin-induced necrotizing autoimmune myopathy (SINAM) is typically accompanied by symmetrical proximal muscle weakness and elevated creatine phosphokinase (CPK). Glucocorticoids are the first-line treatment, but therapy may escalate to include methotrexate and/or intravenous immune globulin therapy (IVIG).

Case presentation: A male aged 59 years with confirmed atorvastatin adherence for 1 year presented with a 4-month history of fatigue, neuropathy, and progressive proximal muscle weakness. Laboratory tests revealed elevated CPK as high as 12,990 mcg/L. The anti-3-hydroxy-3-methlyglutaryl coenzyme A reductase (anti-HMGCR) antibody test was positive, and the patient started immunosuppressive therapy with IVIG therapy monotherapy (2 g/kg) over 3 days. Gluocorticoid therapy was not used due to difficult to control type 2 diabetes. After hospital discharge, the patient continued monthly IVIG treatment. Following 7 total rounds (6 rounds postadmission) of IVIG, the patient reported an improvement in activity, increased strength in his daily activities, and his CPK level continued decreasing to 680 mcg/L.

Conclusions: Patients presenting with proximal muscle weakness and elevated CPK, even after statin discontinuation, should be considered for a full workup for potential SINAM. The detection of anti-HMGCR antibodies or presence of necrosis on muscle biopsy are necessary for a formal diagnosis. This case displayed success with IVIG monotherapy, although previous research suggests the best chance of muscle symptom improvement is with a combination of a glucocorticoid, methotrexate, and IVIG.

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