他汀类药物肌毒性与炎症性肌炎的鉴别诊断

Q4 Medicine
A. D. Tudorancea, Romania Pharmacy Craiova, P. Ciurea, C. D. Pârvănescu, S. Firulescu, C. Bogdan, E. Vintilă, R. Dumitrașcu, C. Ene, C. Criveanu, Florentin Vreju Ananu, Ș. Dinescu
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引用次数: 0

摘要

炎性肌病,包括多发性肌炎、皮肌炎、包体肌炎和坏死性肌病,但他们的诊断需要一个全面的鉴别,以优化治疗和有最好的结果。在这种情况下,最具争议的诊断之一是药物相关的肌毒性,因为症状可能变化很大,但通常包括肌肉无力和肌痛,并伴有肌酸激酶血清水平升高。我们报告一例70岁的患者,接受他汀类药物治疗,自一年前开始出现可耐受的肌痛症状,随后不久伴有轻度肌肉无力,并在最近几个月逐渐恶化。根据目前的症状和肌肉酶升高建议中断他汀类药物:肌酸激酶(CK) x3倍和天冬氨酸转氨酶(AST) x2倍正常范围。调查。自身免疫检查包括抗核抗体和3-羟基-3-甲基戊二酰辅酶A还原酶(HMGCR)抗体均为阴性。针刺肌电图异常,几乎所有研究部位都有弥漫性颤动电位,包括近端和远端肌肉。在大多数测试肌肉中也观察到复杂的重复性放电。针刺肌电图上明显的肌原性征象揭示了临床表现为肌原性的可能原因。讨论。他汀类药物诱导的肌病(SIM)通常是自限性的,在他汀类药物停用后的几周或几个月内表现出缓解。尽管肌电图研究支持SIM中存在典型的肌病特征,但它不能指出归因于他汀类药物相关功能障碍的特定变化。患者出院时预后良好。在为期两周的检查中,她报告了肌肉力量、活动范围和肌痛的改善。反复血检显示CK和AST均呈下降趋势,在正常范围内。结论。临床病例,整个算法的临床评估和临床旁的测试,导致最终诊断和文献回顾,强调了一个详尽的方法的重要性。电生理检查对潜在中毒性肌病患者的初步诊断、随访和必要时的活检结果提供了重要的帮助。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differential diagnosis between statin myotoxicity and inflammatory myositis – case presentation
Inflammatory myopathies, include polymyositis, dermatomyositis, inclusion body myositis and necrotising myopathy, but their diagnosis requires a comprehensive differential, in order to optimise treatment and to have the best outcome. One of the most controversial diagnosis in this situation is drug related myotoxicity, since the symptoms may vary significantly, but usually include muscle weakness and myalgia accompanied by elevated creatine kinase serum levels Patient background. We report a case of a 70 year-old patient, treated with statins, with onset of symptoms since one year with tolerable myalgia, accompanied by mild muscle weakness shortly after and progressive worsening in the last couple of months. Interruption of statins was recommended based on current symptoms and elevated muscle enzymes: creatine kinase (CK) x3 fold and aspartate aminotransferase (AST) x2 fold normal range. Investigations. Autoimmunity panel including anti-nuclear and 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) antibodies was negative. The needle EMG was abnormal, with diffuse fibrillation potentials in almost all investigated sites, both in the proximal and distal muscles. Complex repetitive discharges were also observed in most muscles tested. Existence of clear myogenic signs on needle EMG revealed the probable cause for the clinical presentation as being myogenic in nature. Discussion. Statin-induced myopathy (SIM) is typically self-limited showing remission in the following weeks or months after statin cessation. Although EMG studies support the presence of typical myopathy features in SIM, it cannot point-out specific changes attributed to a statin-related dysfunction. Patient outcome was favorable on hospital discharge. On a two week check-up, she reported improvement in muscle strength, range of motion and remitted myalgia. Repeated blood work showed a descending trend in both CK and AST, with values in normal range. Conclusions. The clinical case, the whole algorithm of clinical evaluation and paraclinical tests that lead to final diagnosis and the literature review, highlight the importance of an exhaustive approach. Electrophysiology tests offer important aid to the physician in the approach of patients with an underlying toxic myopathy in initial diagnosis, follow-up and biopsy yield if necessary.
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CiteScore
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