Salti I S, Kattuah N, Alam S, Wehby V, Frayha R
J Rheumatol. 1976 Jun;3(2):201-4.
In a patient with xanthine urolithiasis secondary to hereditary xanthinuria (xanthine oxidase deficiency), allopurinol administration resulted in a 20 per cent increase in oxypurine excretion and an elevation of the urinary xanthine/hypoxanthine ratio from 4.08 to 6.53. The rise in this ratio suggests that residual xanthine oxidase activity may have been present. It is possible that the excessive re-utilization of hypoxanthine and xanthine in this disease prevents the allopurinol-induced inhibition of de novo purine biosynthesis that is seen in normal subjects.
在一名继发于遗传性黄嘌呤尿症(黄嘌呤氧化酶缺乏)的黄嘌呤尿路结石患者中,给予别嘌呤醇后,氧嘌呤排泄增加了20%,尿中黄嘌呤/次黄嘌呤比值从4.08升高至6.53。该比值的升高表明可能存在残余的黄嘌呤氧化酶活性。在这种疾病中,次黄嘌呤和黄嘌呤的过度再利用可能会阻止别嘌呤醇对正常受试者中从头嘌呤生物合成的抑制作用。