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  • Book
    Harris, Harry; Hirschhorn, Kurt.
    Print Access Request
    Location
    Version
    Call Number
    Items
    Periodicals (Downstairs)
    v. 1-22, 1970-94.
    22
  • Article
    Thomson WH, Smith I.
    Metabolism. 1978 Feb;27(2):151-63.
    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.
    Digital Access Access Options