Klein Christopher J, Boes Christopher J, Chapin John E, Lynch Christopher D, Campeau Norbert G, Dyck P James B, Dyck Peter J
Department of Neurology, Mayo Clinic and Mayo Foundation, 200 First Street SW, Rochester, Minnesota 55905, USA.
Muscle Nerve. 2004 Feb;29(2):323-8. doi: 10.1002/mus.10520.
A non-Jewish patient is described who had adult polyglucosan body disease (APBD) and glycogen branching enzyme (GBE) deficiency without GBE mutation. A heterozygous polymorphism (Val160Ile) was found, and also discovered in 1 of 50 normal individuals. Magnetic resonance imaging demonstrated increased T2 signal in the midbrain, medullary olives, dentate nuclei, cerebellar peduncles, and internal and external capsules, with vermian atrophy. Both muscle and nerve biopsy revealed perivascular inflammatory infiltrates. These findings expand the clinical and genetic spectrum of APBD. Factors other than mutation of the expressed GBE gene may cause enzyme deficiency and varied expression and development of APBD.
描述了一名非犹太患者,其患有成人多聚葡萄糖体病(APBD)且存在糖原分支酶(GBE)缺乏但无GBE突变。发现了一种杂合多态性(Val160Ile),在50名正常个体中的1名也发现了该多态性。磁共振成像显示中脑、延髓橄榄核、齿状核、小脑脚以及内囊和外囊的T2信号增强,伴有蚓部萎缩。肌肉和神经活检均显示血管周围炎性浸润。这些发现扩展了APBD的临床和遗传谱。除了所表达的GBE基因突变之外的因素可能导致酶缺乏以及APBD的不同表现和发展。