Onishi Yasushi, Higuchi Jun, Ogawa Tatuji, Namekawa Akio, Hayashi Hidemori, Odakura Hironori, Goto Kanako, Hayashi Yukiko K
Department of Neurology, Sendai City Hospital.
Rinsho Shinkeigaku. 2002 Feb;42(2):140-4.
Emery-Dreifuss muscular dystrophy (EDMD) is a muscular disorder characterized by 1) early contracture of the elbows. Achilles tendons and post-cervical muscles, 2) slowly progressive muscle wasting and weakness with a humeroperoneal distribution, and 3) life-threatening cardiomyopathy with conduction block. Most of families with EDMD show X-linked recessive inheritance with mutations in the STA gene on chromosome Xq28, which encodes a protein named emerin. A rare autosomal dominant form of EDMD (AD-EDMD) is caused by mutations in lamin A/C gene (LMNA) on chromosome 1q21. Both emerin and lamin A/C are located in the inner surface membrane of the nucleus. A 49-year-old woman was skinny and slow runner from childhood and suspected as having a certain muscular disorder. At 35 years, she was found to have the second degree atrioventricular block. At 45 years, she was admitted to a hospital for right-side hemiplegia after cerebral infarction. Cardiac involvement was also observed including high degree atrioventricular block with chronic atrial fibrillation and frequent paroxysmal ventricular contraction on the electrocardiogram. At 49 years, she was referred to our hospital for further evaluation. She had possible dilated cardiomyopathy with conduction block. She also had muscular atrophy and weakness in all extremities, predominantly in the right-side, and contracture of bilateral Achilles tendon, knee and elbow joints, and postcervical muscles. Biopsied skeletal muscle and electromyogram showed myopathic changes. Since a novel point mutation of Ser303Pro was found in exon 5 of LMNA gene, she was diagnosed as having AD-EDMD and had a permanent pacemaker implantation. Her daughter also had some abnormalities on electrocardiogram. This is the first Japanese case of AD-EDMD. Amiodaron was effective for non-sustained ventricular tachycardia. Early diagnosis and following cardiological examinations and treatments are important and necessary to improve the prognosis of the patients with EDMD.
埃默里-德赖富斯肌营养不良症(EDMD)是一种肌肉疾病,其特征为:1)肘部、跟腱和颈后肌肉早期挛缩;2)肱骨-腓骨分布区出现缓慢进展的肌肉萎缩和无力;3)伴有传导阻滞的危及生命的心肌病。大多数EDMD家族表现为X连锁隐性遗传,X染色体q28上的STA基因发生突变,该基因编码一种名为emerin的蛋白质。一种罕见的常染色体显性形式的EDMD(AD-EDMD)由1号染色体q21上的核纤层蛋白A/C基因(LMNA)突变引起。Emerin和核纤层蛋白A/C都位于细胞核的内膜。一名49岁女性自幼消瘦且跑步缓慢,怀疑患有某种肌肉疾病。35岁时,她被发现患有二度房室传导阻滞。45岁时,她因脑梗死导致右侧偏瘫入院。心电图检查还发现心脏受累,包括高度房室传导阻滞伴慢性心房颤动以及频发阵发性室性收缩。49岁时,她被转诊至我院进一步评估。她可能患有扩张型心肌病伴传导阻滞。她还存在四肢肌肉萎缩和无力,以右侧为主,双侧跟腱、膝关节、肘关节和颈后肌肉挛缩。骨骼肌活检和肌电图显示有肌病改变。由于在LMNA基因外显子5中发现了新的Ser303Pro点突变,她被诊断为AD-EDMD,并植入了永久性心脏起搏器。她的女儿心电图也有一些异常。这是日本首例AD-EDMD病例。胺碘酮对非持续性室性心动过速有效。早期诊断以及后续的心脏检查和治疗对于改善EDMD患者的预后非常重要且必要。