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.
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 hepatitispatients and healthy subjects, but it does not distinguish the various stages of the progression of cirrhosis or its complications.