Institute of Myology, Paris, France.
Neuromuscul Disord. 2010 Aug;20(8):548-58. doi: 10.1016/j.nmd.2010.06.011.
Debranching enzyme deficiency (Glycogen storage disease (GSD) type III) causes progressive muscle wasting myopathy. A comprehensive nuclear magnetic resonance study involving spectroscopy (NMRS) and imaging (NMRI) evaluated status and function of calf muscles in 18 GSDIII patients. At rest, (31)P NMRS showed elevated pH and accumulation of anomalous phosphomonoesters, (13)C NMRS quantified excess glycogen accumulation and NMRI demonstrated progressive fat replacement that paralleled muscle weakness. Multi-parametric functional NMR, performed at recovery from a single bout of aerobic exercise, simultaneously assessed oxidative phosphorylation from (31)P NMRS, muscle perfusion and BOLD, a marker of blood oxygenation, from arterial spin labeled NMRI, and oxygen uptake from deoxymyoglobin proton NMRS. While blocked glycogenolysis caused inadequate substrate supply to the mitochondria, combined measurements suggested that altered perfusion was also responsible for impaired post-exercise phosphocreatine recovery and could contribute to exercise intolerance in GSDIII. These non-invasive investigations provide new indices to quantify the progression of GSDIII.
去分支酶缺乏症(糖原贮积病 III 型)可导致进行性肌肉消耗性肌病。一项涉及光谱学(NMR 光谱)和成像(NMRI)的综合磁共振研究评估了 18 例 GSDIII 患者小腿肌肉的状态和功能。在休息时,(31)P NMR 显示 pH 值升高和异常磷单酯的积累,(13)C NMR 定量了过量的糖原积累,NMRI 显示进行性脂肪替代,与肌肉无力平行。多参数功能 NMR 在单次有氧运动恢复后进行,同时评估(31)P NMR 的氧化磷酸化、动脉自旋标记 NMR 的肌肉灌注和血氧的 BOLD 标志物,以及脱氧肌红蛋白质子 NMR 的摄氧量。虽然糖原分解受阻导致线粒体底物供应不足,但联合测量表明,灌注改变也是导致运动后磷酸肌酸恢复受损的原因,并可能导致 GSDIII 运动不耐受。这些非侵入性研究提供了新的指标来量化 GSDIII 的进展。