Dahan N, Baussan C, Moatti N, Lemonnier A
Laboratoire de Biochimie Appliquée, Centre pharmaceutique de Châtenay-Malabry.
J Inherit Metab Dis. 1988;11(3):253-60. doi: 10.1007/BF01800366.
We determined glycogen concentration and phosphorylase 'a+b' and phosphorylase a activities in platelets, mononuclear and polymorphonuclear cells from control subjects and patients with phosphorylase kinase deficiency (glycogen storage disease IX) and liver phosphorylase deficiency (glycogen storage disease VI). Variations according to cellular type and to subjects' age (1-40 years) were established. Variable glycogen overloading was found in all our patients. Glycogen storage disease (GSD) VI was characterized by a diminished total phosphorylase activity with a low or normal a/(a+b) ratio of phosphorylase activity. GSD IX was characterized by a very low residual activity of phosphorylase a with an 'a+b' activity low or normal.
我们测定了对照组受试者以及磷酸化酶激酶缺乏症(糖原贮积病IX型)和肝磷酸化酶缺乏症(糖原贮积病VI型)患者血小板、单核细胞和多形核细胞中的糖原浓度、磷酸化酶“a+b”及磷酸化酶a活性。确定了细胞类型和受试者年龄(1至40岁)的变化情况。在我们所有患者中均发现了不同程度的糖原超载。糖原贮积病(GSD)VI型的特征是总磷酸化酶活性降低,磷酸化酶活性的a/(a+b)比值较低或正常。GSD IX型的特征是磷酸化酶a的残余活性非常低,“a+b”活性较低或正常。