Suppr超能文献

延髓和脊髓性肌萎缩症(肯尼迪病):综述

Bulbar and spinal muscular atrophy (Kennedy's disease): a review.

作者信息

Finsterer J

机构信息

Krankenanstalt Rudolfstiftung, Vienna, Austria.

出版信息

Eur J Neurol. 2009 May;16(5):556-61. doi: 10.1111/j.1468-1331.2009.02591.x.

Abstract

Bulbar and spinal muscular atrophy (BSMA) is an adult-onset, X-linked recessive trinucleotide, polyglutamine disorder, caused by expansion of a polymorphic CAG tandem-repeat in exon 1 of the androgen-receptor (AR) gene on chromosome Xq11-12. Pathogenetically, mutated AR accumulates in nuclei and cytoplasm of motor neurons, resulting in their degeneration and loss. Phenotypically, patients present with amyotrophic, proximal or distal weakness and wasting of the facial, bulbar and limb muscles, occasionally sensory disturbances, and endocrinologic disturbances, such as androgen resistance, gynecomastia, elevated testosterone or progesterone, and reduced fertility. There may be mild hyper-CK-emia, abnormal motor and sensory nerve conduction studies, and neuropathic and myopathic alterations on muscle biopsy. The golden standard for diagnosing BSMA is genetic analysis, demonstrating a CAG-repeat number >40. No causal therapy is available, but symptomatic therapy should be provided for tremor, endocrinologic abnormalities, sensory disturbances, or muscle cramps. The course is slowly progressive, the ability to walk lost only late in life, only few patients require ventilatory support, and life expectancy only slightly reduced.

摘要

延髓和脊髓性肌萎缩症(BSMA)是一种成年发病的X连锁隐性三核苷酸多聚谷氨酰胺疾病,由位于Xq11 - 12染色体上雄激素受体(AR)基因外显子1中多态性CAG串联重复序列的扩增引起。在发病机制上,突变的AR在运动神经元的细胞核和细胞质中积累,导致其变性和丧失。在表型上,患者表现为肌萎缩、近端或远端无力,面部、延髓和肢体肌肉萎缩,偶尔有感觉障碍以及内分泌紊乱,如雄激素抵抗、男性乳房发育、睾酮或孕酮升高以及生育能力下降。可能存在轻度高肌酸激酶血症、运动和感觉神经传导研究异常以及肌肉活检显示的神经病变和肌病改变。诊断BSMA的金标准是基因分析,显示CAG重复数>40。目前尚无因果治疗方法,但对于震颤、内分泌异常、感觉障碍或肌肉痉挛应给予对症治疗。病程进展缓慢,仅在生命后期才会丧失行走能力,只有少数患者需要通气支持,预期寿命仅略有缩短。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验