Hays A P, Hallett M, Delfs J, Morris J, Sotrel A, Shevchuk M M, DiMauro S
Neurology. 1981 Sep;31(9):1077-86. doi: 10.1212/wnl.31.9.1077.
A 61-year-old woman with muscle phosphofructokinase (PFK) deficiency had mild limb weakness all her life but no cramps or myoglobinuria. For 5 years the limb weakness progressed. In muscle, PFK activity was 1% of normal and glycogen concentration was elevated (2.13%). By light microscopy, a minor component of the accumulated glycogen appeared as PAS-positive, diastase-resistant inclusions in 10% of muscle fibers. The inclusions had a filamentous fine structure that resembled the abnormal long-chain glycogen of brancher enzyme deficiency. Iodine absorption spectra of both the inclusions and a diastase-resistant fraction of isolated glycogen resembled amylopectin. The abnormal polysaccharide in PFK deficiency may be related to greatly elevated concentration of muscle glucose-6-phosphate, an activator of the chain-elongating enzyme glycogen synthase.
一名61岁的女性患肌肉磷酸果糖激酶(PFK)缺乏症,一生都有轻度肢体无力,但无痉挛或肌红蛋白尿。5年来肢体无力逐渐加重。肌肉中,PFK活性为正常的1%,糖原浓度升高(2.13%)。光镜下,10%的肌纤维中,累积糖原的一小部分表现为PAS阳性、淀粉酶抵抗性包涵体。这些包涵体具有丝状精细结构,类似于分支酶缺乏症的异常长链糖原。包涵体和分离糖原的淀粉酶抵抗部分的碘吸收光谱类似于支链淀粉。PFK缺乏症中的异常多糖可能与肌肉葡萄糖-6-磷酸浓度大幅升高有关,葡萄糖-6-磷酸是链延长酶糖原合酶的激活剂。