Pastoris O, Dossena M, Vercesi L, Scelsi R, Torcetta F, Savasta S, Bianchi E
Institute of Pharmacology, Faculty of Science, University of Pavia, Italy.
Childs Nerv Syst. 1992 Jun;8(4):237-41. doi: 10.1007/BF00262858.
Muscle phosphofructokinase (PFK) deficiency in man is responsible for at least two forms of myopathy; one is characterized by painful contractures of muscles and typically occurs in adults, whereas the other is often disabling and typically occurs in childhood, with psychomotor and growth retardation. In this investigation, a young myopathic patient with severe mental retardation and aplasia of the cerebellar vermis presented with muscular hypotrophy of the limbs, generalized hypotonia, convergent strabismus and marked pain during passive movement. Biopsy of quadriceps femoris muscle showed variation in the fiber size with sarcoplasmic areas positive for periodic acid-Schiff stain. Histochemical qualitative reaction for PFK showed no staining of muscle fibers; ultrastructural studies showed abnormal accumulation of glycogen granules in both intermyofibrillar and subsarcolemmal areas. While some enzyme activities in the muscular crude extract were significantly lower than in controls, direct assay of PFK revealed no activity, thus demonstrating that the child's myopathy was due to the lack of PFK activity.
人类肌肉磷酸果糖激酶(PFK)缺乏至少会导致两种形式的肌病;一种以肌肉疼痛性挛缩为特征,通常发生在成年人中,而另一种往往会导致残疾,通常发生在儿童期,伴有精神运动发育迟缓和生长发育迟缓。在这项研究中,一名患有严重智力发育迟缓且小脑蚓部发育不全的年轻肌病患者出现四肢肌肉萎缩、全身肌张力减退、共同性斜视以及被动运动时明显疼痛。股四头肌活检显示肌纤维大小不一,肌浆区域过碘酸-希夫染色呈阳性。PFK的组织化学定性反应显示肌纤维无染色;超微结构研究显示肌原纤维间和肌膜下区域均有糖原颗粒异常积聚。虽然肌肉粗提物中的一些酶活性显著低于对照组,但PFK的直接测定显示无活性,从而证明该儿童的肌病是由于缺乏PFK活性所致。