Kogut M D, Roe T F, Ng W, Nonnel G N
Pediatr Res. 1975 Oct;9(10):774-8. doi: 10.1203/00006450-197510000-00005.
After the infusion of fructose, 0.25 g/kg body wt, the mean peak plasma uric acid level was 5.4 +/- 0.7 (SEM) mg/100 ml in six normal children and was not significantly increased compared with that of the mean basal value of 4.1 +/- 0.5 mg/100 ml. The mean blood inorganic phosphate (Pi) levels were significantly less than the mean fasting value after fructose. Blood glucose, lactic acid, and fructose levels were significantly increased after fructose, but serum magnesium levels did not change. In two patients with hereditary fructose intolerance (HFI) the peak blood uric acid levels were 12.1 and 7.6 mg/100 ml, respectively, after fructose. In both patients the blood glucose concentrations decreased 69 and 26 mg/100 ml below the fasting levels after fructose. The serum Pi level decreased 2.3 and 1.2 mg/100 ml below fasting values, decrements greater than the mean decrement in serum Pi of 0.8 +/- 0.2 mg/100 ml which occurred in six normal children. The mean uric acid excretion, expressed as milligrams per mg urinary creatinine, was 0.6 +/- 0.1 (SEM) before fructose in the normal children and increased significantly to 1.0 +/- mg/mg creatinine after fructose. In two patients with HFI the uric acid excretion increased four- to fivefold after fructose administration; the increased uric acid excretion in HFI exceeded that of normal children. In three patients with galactosemia, increases in blood uric acid levels after galactose ingestion were similar to those in normal children after fructose, but less than those in patients with HFI after fructose. The serum Pi levels decreased less in galactosemic patients after galactose administration than in patients with HFI after fructose infusion. These studies support the hypothesis that fructose-induced hyperuricemia results from degradation of adenosine monophosphate. This effect appears to be specific for fructose. The lack of hyperruricemia in galactosemia patients after galactose ingestion may be explained by the observation that galactose is phosphorylated more slowly than fructose.
给六名正常儿童输注0.25g/kg体重的果糖后，血浆尿酸平均峰值水平为5.4±0.7（标准误）mg/100ml，与平均基础值4.1±0.5mg/100ml相比无显著升高。果糖输注后，血液无机磷酸盐（Pi）平均水平显著低于空腹值。果糖输注后血糖、乳酸和果糖水平显著升高，但血清镁水平未改变。两名遗传性果糖不耐受（HFI）患者在输注果糖后，血尿酸峰值水平分别为12.1和7.6mg/100ml。两名患者的血糖浓度在输注果糖后分别比空腹水平降低了69和26mg/100ml。血清Pi水平分别比空腹值降低了2.3和1.2mg/100ml，降幅大于六名正常儿童血清Pi平均降幅0.8±0.2mg/100ml。正常儿童在输注果糖前，以每毫克尿肌酐中尿酸毫克数表示的平均尿酸排泄量为0.6±0.1（标准误），输注果糖后显著增加至1.0±mg/肌酐。两名HFI患者在输注果糖后尿酸排泄增加了四至五倍；HFI患者尿酸排泄的增加超过了正常儿童。三名半乳糖血症患者在摄入半乳糖后血尿酸水平的升高与正常儿童输注果糖后相似，但低于HFI患者输注果糖后的升高幅度。半乳糖血症患者在摄入半乳糖后血清Pi水平的降低幅度小于HFI患者输注果糖后的降低幅度。这些研究支持了果糖诱导的高尿酸血症是由一磷酸腺苷降解引起的这一假说。这种作用似乎对果糖具有特异性。半乳糖血症患者摄入半乳糖后未出现高尿酸血症，这可能是因为观察到半乳糖磷酸化的速度比果糖慢。
