Udd B, Krahe R, Wallgren-Pettersson C, Falck B, Kalimo H
Neurological Department, Vasa Central Hospital, Finland.
Neuromuscul Disord. 1997 Jun;7(4):217-28. doi: 10.1016/s0960-8966(97)00041-2.
We describe a family with an autosomal dominant, multisystem disorder, consisting of late-onset proximal muscular dystrophy, electrophysiological myotonia, cataracts, late-onset deafness and male hypogonadism. Four patients were available for clinical examinations. Examination of asymptomatic family members revealed another patient with bilateral cataracts but without definite muscle disorder. Five deceased members of the family had proximal muscle weakness, reportedly or confirmed in medical records. Molecular examination of genomic DNA showed no expansion of the unstable (CTG)n trinucleotide repeat on chromosome 19q13.3 associated with myotonic dystrophy (DM). Linkage to two loci implicated in other myotonic disorders, the muscle chloride channel (CLCN1) gene, and the muscle sodium channel (SCN4A) gene, was assessed and excluded. The clinical findings differ from those described in proximal myotonic myopathy (PROMM), in terms of the more severe muscle involvement with atrophy of affected muscles and the hearing loss. These findings suggest phenotypic and probably genetic heterogeneity among the proximal myotonic syndromes.
我们描述了一个患有常染色体显性多系统疾病的家族,该疾病包括迟发性近端肌营养不良、电生理肌强直、白内障、迟发性耳聋和男性性腺功能减退。有4名患者可供临床检查。对无症状家庭成员的检查发现另一名患者有双侧白内障,但无明确的肌肉疾病。该家族的5名已故成员有近端肌无力,据报告或在医疗记录中得到证实。对基因组DNA的分子检查显示,19号染色体q13.3上与强直性肌营养不良(DM)相关的不稳定(CTG)n三核苷酸重复序列没有扩增。评估并排除了与其他强直性疾病相关的两个基因座的连锁关系,即肌肉氯通道(CLCN1)基因和肌肉钠通道(SCN4A)基因。临床发现与近端强直性肌病(PROMM)中所描述的不同,表现为受累肌肉萎缩导致的更严重的肌肉受累和听力丧失。这些发现提示近端强直性综合征之间存在表型和可能的遗传异质性。