Wokke J H, Ausems M G, van den Boogaard M J, Ippel E F, van Diggelene O, Kroos M A, Boer M, Jennekens F G, Reuser A J, Ploos van Amstel H K
Rudolf Magnus Institute of the Neurosciences, Laboratory of Neuromuscular Disorders, University Utrecht, Netherlands.
Ann Neurol. 1995 Sep;38(3):450-4. doi: 10.1002/ana.410380316.
We performed a clinical, biochemical, and genetic study in 16 patients from 11 families with adult-onset acid maltase deficiency. All patients were compound heterozygotes and carried the IVS1(-13T --> G) transversion on one allele; the second allele harbored either a deletion of a T at position 525 in exon 2 (7 probands, 64%) or a deletion of exon 18 (1 proband, 9%). Deterioration of handicap was related to age, and decrease in vital capacity to duration of the symptomatic stage. Respiratory insufficiency was never the first manifestation. The levels of activity of serum creatine kinase and of alpha-glucosidase in peripheral blood cells or muscle were helpful for the diagnosis, but did not have prognostic value. The adult form of acid maltase deficiency appears to be both clinically and genetically rather homogeneous; decrease of alpha-glucosidase activity is the final common pathway leading to destruction of muscle fibers and progression of muscle weakness over a period of years.
我们对来自11个家庭的16例成年起病的酸性麦芽糖酶缺乏症患者进行了临床、生化和遗传学研究。所有患者均为复合杂合子,一个等位基因携带IVS1(-13T→G)颠换;第二个等位基因要么在外显子2的525位缺失一个T(7例先证者,64%),要么缺失外显子18(1例先证者,9%)。残疾程度的恶化与年龄有关,肺活量的下降与症状期的持续时间有关。呼吸功能不全从未是首发表现。血清肌酸激酶以及外周血细胞或肌肉中α-葡萄糖苷酶的活性水平有助于诊断,但无预后价值。成年型酸性麦芽糖酶缺乏症在临床和遗传上似乎都相当一致;α-葡萄糖苷酶活性的降低是导致肌肉纤维破坏和肌肉无力在数年内进展的最终共同途径。