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III型糖原贮积病的神经肌肉受累情况

Neuromuscular involvement in glycogen storage disease type III.

作者信息

Moses S W, Gadoth N, Bashan N, Ben-David E, Slonim A, Wanderman K L

出版信息

Acta Paediatr Scand. 1986 Mar;75(2):289-96. doi: 10.1111/j.1651-2227.1986.tb10201.x.

Abstract

Sixteen patients with glycogen storage disease type III (GSD III) aged 3 to 22 years underwent a detailed neuromuscular evaluation. A minimal impairment of skeletal muscle function was presented in eight patients, slight impairment in four and severe impairment in one patient. Serum creatinine phosphokinase (CPK) was elevated in all patients studied. In the nine patients, in whom electromyography (EMG) was performed; six exhibited a myopathic pattern while a "mixed" (neurogenic-myopathic) pattern was present in three. Muscle biopsies performed in 12 patients, revealed in all cases amylo-1,6,-glucosidase deficiency and biochemical as well as morphological evidence of glycogen accumulation. Two brothers suffered from late onset myopathy, which in the older sibling was associated with clinical, EMG and EM findings of a peripheral neuropathy. Fifteen patients had either electrocardiographic and or echographic evidence of cardiomyopathy. Observations based on this patient material suggest a widespread myopathy in GSD III patients with heterogeneous expression, while peripheral nerve involvement is rarely encountered.

摘要

16例3至22岁的III型糖原贮积病(GSD III)患者接受了详细的神经肌肉评估。8例患者存在骨骼肌功能轻度损害,4例轻度损害,1例重度损害。所有研究患者的血清肌酸磷酸激酶(CPK)均升高。在接受肌电图(EMG)检查的9例患者中,6例表现为肌病模式,3例表现为“混合”(神经源性-肌病性)模式。12例患者进行了肌肉活检,所有病例均显示淀粉-1,6-葡萄糖苷酶缺乏以及糖原积累的生化和形态学证据。两兄弟患有迟发性肌病,在年长的兄弟中,伴有周围神经病变的临床、肌电图和神经传导检查结果。15例患者有心电图和/或超声心动图显示的心肌病证据。基于该患者资料的观察结果表明,GSD III患者存在广泛的肌病,表现具有异质性,而周围神经受累很少见。

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