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静脉注射果糖和1,6 - 二磷酸果糖的负荷量:对非酒精性肝病患者血尿酸的影响

Intravenous load of fructose and fructose 1,6-diphosphate: effects on uricemia in patients with nonalcoholic liver disease.

作者信息

Loguercio C, Nardone G, Sicolo P, Cuomo R, Del Vecchio C, Budillon G

机构信息

Cattedra di Gastroenterologia, II Università degli Studi di Napoli, Italy.

出版信息

Am J Gastroenterol. 1996 Mar;91(3):559-64.

PMID:8633509
Abstract

OBJECTIVES

The i.v. load of fructose causes a significantly higher adenosine triphosphate (ATP) degradation and uric acid production in cirrhotic patients than in healthy controls. Resynthesis of ATP from adenosine diphosphate (ADP) may be facilitated by the phosphorylated compound fructose 1,6-diphosphate, which is used as energy support in parenteral nutrition. The aim of our research was to evaluate: 1) The 1-h uricemic effect of i.v. fructose (0.5 g/kg body weight) in 10 healthy controls and in 78 patients with differenct stages of non-alcoholic chronic liver damage associated or not with malnutrition or hepatocellular carcinoma; and 2) the effect of fructose 1,6-diphosphate (5 g/50 ml) administered i.v. after fructose infusion on the induced uricemia in a subgroup of 13 patients with well compensated cirrhosis.

RESULTS AND CONCLUSIONS

The increase of uricemia above the basal level after fructose infusion was significantly higher (p < 0.01) in cirrhotics (3 mg/dl) than in controls (1.2 mg/dl) and in patients with chronic hepatitis (1.9 mg/dl) and was completely reversed by fructose 1,6-diphosphate in the patients tested. Neither Child-Pugh classes of cirrhosis nor malnutrition (present in about 50% of the patients) or hepatocarcinoma significantly affected the fructose-induced uricemia. Therefore, the fructose test efficiently differentiates cirrhotics from chronic hepatitis patients and healthy subjects, but it does not distinguish the various stages of the progression of cirrhosis or its complications.

摘要

目的

与健康对照相比,静脉输注果糖负荷量会使肝硬化患者的三磷酸腺苷(ATP)降解和尿酸生成显著增加。二磷酸腺苷(ADP)重新合成ATP可能会受到磷酸化化合物1,6 -二磷酸果糖的促进,该化合物在肠外营养中用作能量支持。我们研究的目的是评估:1)静脉输注果糖(0.5 g/kg体重)对10名健康对照以及78名不同阶段非酒精性慢性肝损伤患者(无论是否伴有营养不良或肝细胞癌)1小时的尿酸血症影响;2)在13名代偿良好的肝硬化患者亚组中,果糖输注后静脉注射1,6 -二磷酸果糖(5 g/50 ml)对诱导的尿酸血症的影响。

结果与结论

输注果糖后,肝硬化患者(3 mg/dl)尿酸血症高于基础水平的升高幅度显著高于对照组(1.2 mg/dl)和慢性肝炎患者(1.9 mg/dl)(p < 0.01),且在受试患者中被1,6 -二磷酸果糖完全逆转。肝硬化的Child - Pugh分级、营养不良(约50%的患者存在)或肝癌均未显著影响果糖诱导的尿酸血症。因此,果糖试验能有效区分肝硬化患者与慢性肝炎患者及健康受试者,但无法区分肝硬化进展的不同阶段或其并发症。

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