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At least 811 records · Page 45Linked to original sources
PubMed1988

[Acute fatty liver of pregnancy. Diagnostic value of hyperuricemia in the pre-jaundice stage].

Acute fatty liver of pregnancy, with a case history where an early diagnosis could have been made, and a review of the French literature. Acute fatty liver of pregnancy, or Sheehan's syndrome is a rare but very serious complication of pregnancy. The disease is demonstrated by vomiting, abdominal pain and a high level of uric acid in the blood before jaundice is noted. Within a few days the triad of jaundice, pruritus and encephalopathy occur. These are often associated with toxaemia of pregnancy and with polyuria and polydipsia. A raised white blood count and a high level of bilirubinemia are almost always present. The outlook is very serious when haemorrhage appears. This malignant form of the disease is characterised by liver and kidney failure. Liver biopsy confirms the diagnosis. The prognosis is related to an early diagnosis and is good when labour is induced or caesarean section performed. Acute fatty liver of pregnancy is an emergency from the diagnostic as well as the therapeutic angles.

Acute Disease↗
PubMed1977

[Treatment of hyperuricemia using daily doses of 50 and 25mg of benzbromarone].

By treating 16 hyperuricemic patients each with 25 and 50 mg of Benzbromarone a significant decrease of the uric acid concentration in the serum into the normal range is achieved. On the 5th and 6th day after beginning the treatment the dosage of 25 mg of Benzbromarone renders a morning value of 5,3 +/- 1,0 and an evening value of 5,0 +/- 0,9 mg/100 ml. After administration of 50 mg of Benzbromarone there is also prevailing a steady-state behaviour on the 5th and 6th day for the uric acid concentration in the serum. Thereby the morning value is 3,7 +/- 0,8 mg/100 ml and th evening value 3,4 +/- 0,9 mg/100 ml. After both dosages an increased urate elimination occurs initially during the 1st, 2nd and 3rd day after beginning of the therapy. However, after having achieved therapeutically reduced uric acid levels, the uric acid elimination from the 4th, 5th and 6th day partially ranges below those values existing before beginning of the therapy. During a chronic treatment no hyperuraturia can be observed on account of the therapeutically reduced serum concentrations. Consequently an increased risk towards a formation of urate calculi is not given under the long-term treatment.

Benzbromarone↗
PubMed1987

[Evaluation of hyperuricemia caused by fructose in a status of altered uric acid metabolism].

It's reported that oral administration of fructose in normal and gouty patients causes a rise in serum uric acid (see "References": Stirpe et al.). The changes in serum uric acid after administration of fructose to gouty patients and to children of gouty patients were significantly different from the changes observed in normal subjects, both for the extent and for the duration of hyperuricaemia. In this study the authors verify if the fructose-induced hyperuricaemia can help to identify gouty patients from people with different metabolic alteration of serum uric acid levels (i.e. chronic leukaemias and some neoplastic diseases).

Adult↗
PubMed1987

[Mechanism of exercise-induced hyperuricemia].

This study was designed to make clear why increases and decreases in serum uric acid levels after vigorous exercise were delayed. Eight healthy male subjects who were given allopurinol before exercise participated in this study. We performed exhaustive exercise test on bicycle ergometer, and investigated the changes in purine metabolites levels in blood and urine. Results were summarized as follow; 1) Serum uric acid concentrations did not change significantly. Urinary excretions of uric acid decreased from 30 minutes to 1 hour after exercise, and recovered thereafter. 2) Plasma oxypurines concentrations exhibited the maximum level at 1 hour after exercise, and maintained the higher levels until 7 hours after exercise. Urinary oxypurines excretions exhibited the maximum level at 1 hour after exercise, and maintained the higher levels until 24 hours after exercise. 3) Plasma inosine concentrations increased only in one subject. Plasma hypoxanthine concentrations increased significantly in all subjects. Plasma xanthine concentrations did not change. 4) Blood ammonia concentrations exhibited the maximum level at 5 minutes after exercise, and returned to basal levels at 2 hours after exercise. These observations suggest that the delays of increases and decreases in serum uric acid levels are due to that the prolonged release of hypoxanthine from skeletal muscle lead to the prolonged production of uric acid in liver.

Adult↗