Thomson W H, Smith I
Metabolism. 1978 Feb;27(2):151-63. doi: 10.1016/0026-0495(78)90161-0.
Data are presented which suggest that Duchenne muscular dystrophy (DMD) may have some origin in a severe deficiency of total muscle adenine nucleotides. Using double-blind techniques, this possibility was tested in 16 DMD patients by giving oral allopurinol, a synthetic inhibitor of the purine catabolic enzyme xanthine oxidase. Sublingual procaine adenylate was also briefly tested. Instances of clinical improvement quickly occurred which were statistically significant; they were accompanied by a significant increase in physical strength. These improvements have been maintained for more than 6 mo by administration of a small amount of allopurinol daily. Procaine adenylate had little effect. These results support the above view of DMD and seem to indicate that existing purines, retained and recycled after allopurinol, can sustain such improvement, and that additional adenylate is unnecessary.
所呈现的数据表明，杜兴氏肌营养不良症（DMD）可能源于总肌肉腺嘌呤核苷酸的严重缺乏。采用双盲技术，通过给16名DMD患者口服嘌呤分解代谢酶黄嘌呤氧化酶的合成抑制剂别嘌呤醇，对这一可能性进行了测试。还对舌下注射的普鲁卡因腺苷酸进行了简短测试。临床上很快出现了具有统计学意义的改善情况；同时体力也显著增强。通过每天服用少量别嘌呤醇，这些改善情况已持续了6个多月。普鲁卡因腺苷酸几乎没有效果。这些结果支持了上述关于DMD的观点，似乎表明在服用别嘌呤醇后保留和循环利用的现有嘌呤可以维持这种改善，并且不需要额外的腺苷酸。
