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PubMed1992

Hyperuricemia induced by fructose load in liver cirrhosis.

The intravenous administration of fructose in healthy subjects may induce an increase of blood uric acid and the urinary excretion of urate and xanthine as a result of hepatic adenosine triphosphate (ATP) breakdown. These changes are partially reversed by ATP resynthesis. We studied the effect of fructose load (0.5 g/kg body weight) on the products of ATP metabolism, and the interference of fructose on the galactose test in 10 patients with well compensated cirrhosis compared with 10 healthy controls. The fructose and the fructose/galactose loads induced a significantly greater increase of plasma uric acid in cirrhotics than in controls, with a 60 minute peak in the cirrhotics. Urinary excretion of urate and xanthines was significantly increased (p less than 0.001) only in the cirrhotics after the fructose/galactose load. As expected, the galactose elimination capacity (GEC) calculated with the galactose test, was lower in these patients than in controls. Fructose infusion before galactose did not significantly modify the GEC in either of the two groups compared. The higher uric acid increase induced by fructose in the blood of cirrhotic patients seems to be a good marker of the energy crisis of the diseased liver whereby it is unable to efficiently resynthesize ATP from its breakdown products.

Adult↗
PubMed1992

[Long lasting normalization of uric acid after combination therapy with 300 mg allopurinol and 60 mg benzbromarone in patients with gout and hyperuricemia].

Lasting normalisation of uric acid levels after treatment of patients with gout and hyperuricaemia with a combination of 300 mg allopurinol and 60 mg benzbromarone A total of 210 patients (163 men, 47 women) with gout and hyperuricaemia was treated for three months with daily doses of 300 mg allopurinol and 60 mg benzbromarone. During the course of treatment, the uric acid levels decreased to 4.3 +/- 1.3 mg/dl in male, and 4.4 +/- 1.3 mg/dl in female patients. Both of these levels differ significantly from the initial levels (p less than 0.001). Three months after discontinuation of treatment, uric acid levels were 5.7 +/- 1.2 mg/dl in women, and 5.9 +/- 1.4 mg/dl in men, levels that again differed significantly from the initial levels (p less than 0.001); both levels were, however, within the therapeutic range of below 6.4 mg/dl.

Allopurinol↗
PubMed1991

[Physiopathological aspects of secondary hyperuricemia].

Secondary hyperuricaemia expresses a heterogeneous group of clinical conditions generally classified according to the pathogenetic criteria. Hyperuricaemia can depend on an increased production, reduced renal excretion or on the combination of both. Myelo and lymphoproliferative diseases are clinically prevalent among the conditions accompanying this overproduction. The most frequent causes of reduced uric acid excretion are chronic renal failure and diuretic treatment. In recent years, several conditions of hyperuricaemia with mixed pathogenesis have revealed a common mechanism connected to the ATP cellular depletion.

Acute Disease↗