他汀类药物诱导的免疫介导的坏死性肌病导致近端肌肉无力。

Mohammed S Abdalla, Qishuo Zhang, Monzer O Abdalla, Suhair S Abdel-Jalil
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引用次数: 0

摘要

他汀类药物诱导的免疫介导坏死性肌病(IMNM)是一种与他汀类药物暴露相关的IMNM亚型,其特征是抗羟甲基戊二酰(HMG)辅酶a还原酶(HMGCR)抗体阳性。虽然很少见,但随着他汀类药物的广泛应用,这种疾病越来越被认为是近端肌无力的原因。与典型的他汀类药物相关肌肉症状不同,IMNM肌病通常会导致严重的肌肉损伤,肌肉无力在他汀类药物停药后持续存在或有时恶化。在服用他汀类药物的患者出现肌肉无力时,医生需要对他汀类药物引起的IMNM保持高度的临床怀疑指数。这种疾病可能使人衰弱,尽管在诊断方面取得了进展,但治疗策略还没有很好地确立。本文报告2例他汀类药物致IMNM的临床特点及病程。两例患者在长期接受他汀类药物治疗时均出现进行性近端肌无力和肌痛,停药后症状无明显改善。怀疑IMNM,两名患者均发现抗hmg辅酶A还原酶抗体滴度高,显微镜特征与肌肉活检的IMNM诊断一致。由于肌肉无力,患者经历了严重的残疾,需要长期的免疫抑制治疗。虽然很少见,但在服用他汀类药物的患者中,如果出现肌肉无力,在停止他汀类药物后没有改善或恶化,则应怀疑IMNM。早期诊断和免疫抑制治疗是预防疾病发展的重要手段。
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 Immune-Mediated Necrotizing Myopathy Resulting in Proximal Muscle Weakness.

Statin-Induced Immune-Mediated Necrotizing Myopathy Resulting in Proximal Muscle Weakness.

Statin-Induced Immune-Mediated Necrotizing Myopathy Resulting in Proximal Muscle Weakness.

Statin-induced immune-mediated necrotizing myopathy (IMNM) is a subtype of IMNM linked to exposure to statins and is characterized by positive anti-hydroxymethylglutaryl (HMG) coenzyme A reductase (HMGCR) antibodies. Although rare, this entity has become increasingly recognized as a cause of proximal muscle weakness, especially with the widespread use of statin therapy. Unlike typical statin-associated muscle symptoms, IMNM myopathy often causes severe muscle injury, and muscle weakness persists or sometimes worsens following the withdrawal of statin therapy. Medical practitioners need to keep a high index of clinical suspicion for statin-induced IMNM in patients taking statins who present with muscle weakness. The disease can be debilitating, and treatment strategies are not well established despite the advances that have been made in the diagnosis. Here we present the clinical characteristics and disease course of two cases of statin-induced IMNM. Both patients presented with progressive proximal muscle weakness and myalgias while on long-term statin therapy without significant improvement in their symptoms following the withdrawal of statin therapy. IMNM was suspected, and both patients were found to have high titers of anti-HMG coenzyme A reductase antibodies and demonstrated microscopic features consistent with a diagnosis of IMNM on muscle biopsy. The patients experienced significant disability due to muscle weakness and required a protracted course of escalated immunosuppressive therapy. Although rare, IMNM should be suspected in patients taking statins who present with muscle weakness that fails to improve or worsens when statins were stopped. Early diagnosis and institution of immunosuppressive therapy are important to prevent the progression of the disease.

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