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Biomedical subjects

W Gröbner

Publications and source records attributed to W Gröbner.

At least 19 recordsLinked to original sources
PubMed1988

A study of dose-response relationships of allopurinol in the presence of low or high purine turnover.

Effects of allopurinol (125-500 mg/m2 body surface) were studied in normal subjects during periods of 18 days both during a purine-free, isoenergetic liquid formula diet and additional intake of ribonucleic acid, 4 g/day. Plasma uric acid and renal excretion of uric acid, oxypurines (hypoxanthine plus xanthine) and orotic acid were measured and total purine excretion calculated. Effects of allopurinol were evaluated by comparison of the results obtained in the steady state during diet alone (average of days 7-10) with those during allopurinol administration (days 16-18). During the purine-free diet, plasma uric acid was lowered more than urinary uric acid by allopurinol on doses of 250-500 mg/m2 (44%-54% of control values on 500 mg/m2), demonstrating an increase in renal clearance. At the same dose, the uric acid lowering effect of allopurinol was more pronounced with than without purine loads (plasma 41%, urine 32% of control on 500 mg/m2 during purine intake), while renal uric acid clearance was decreased. The more pronounced reduction of uric acid excretion during purine administration was balanced to the greater part by a more pronounced increase in oxypurine excretion. Total purine excretion was reduced by about 20% during the purine-free diet irrespective of dose. The size of this purine deficit was doubled, but was also independent of dose during addition of purines. Orotic acid excretion increased with dose during allopurinol treatment and was reduced by addition of purines.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Gout and uric acid nephropathy: some new aspects in diagnosis and treatment.

It has been recognized that primary disorders of uric acid metabolism result from impaired renal excretion or increased endogenous production of uric acid. It has also been found that these two mechanisms do not comprise two distinct syndromes, but may each constitute a group of syndromes. Contrary to earlier as well as currently published reports we conclude from our clinical and experimental experience that the fraction of so-called over-producers is less than 1% of all patients with primary hyperuricaemia and gout. A procedure for the diagnosis of uric acid overproduction is suggested. The manifestation of hyperuricaemia and gout mainly depends on renal uric acid clearance and is greatly influenced by dietary habits in most of the patients. An impaired renal uric acid excretion results in an increased intestinal excretion; this partly compensates for the defect. Normalization of serum uric acid should be achieved by dietary regimens with or without additional drug treatment, but not by drug treatment alone. With drug treatment xanthine oxidase inhibitors are preferable to uricosurics; no other xanthine oxidase inhibitor besides Allopurinol has been in clinical trial, however. Due to the enhancement of uric acid clearance with uricosurics, there are groups of patients who should not be treated with these drugs. Fixed combinations of Allopurinol and uricosurics should not be used. Drugs which have uricosuric as well as other pharmacologic properties are under investigation. So far they have not reached general clinical application.

Adult↗
PubMed1983

[The effect of dietary purines and pyrimidines on human pyrimidine biosynthesis].

Young healthy volunteers received a purine-free, isoenergetic formula diet over a period of 28 to 32 days. After a short time under formula diet alone 400 mg allopurinol were administered daily. After a further 10 days each volunteer received daily, in addition, either 4 g RNA, 4 g RNA-hydrolysate, 1 g guanosine-5-monophosphate (GMP), 1 or 3 g adenosine-5-monophosphate (AMP), uridine-5-monophosphate (UMP), cytidine-5-monophosphate (CMP) or adenosine, guanosine, uridine, cytidine, guanine, hypoxanthine, xanthine, cytosine and uracil. Finally the allopurinol was omitted. The renal excretion of total orotic acid (orotic acid and orotidine), uric acid and creatinine was determined daily; serum uric acid concentrations and the enzyme activities of orotidine-5-phosphate-decarboxylase (ODCase) and hypoxanthine-guanine-phosphoribosyltransferase (HGPRTase) from erythrocytes were determined every other day. The results show that RNA, RNA-hydrolysate, purine- and pyrimidine-nucleotides and -nucleotides as well as hypoxanthine, and to a lesser extent adenine, diminish allopurinol-induced orotaciduria. This is compatible with an influence of dietary purines and pyrimidines on human pyrimidine biosynthesis.

Adenosine Monophosphate↗
PubMed1983

[Uric acid-lowering effect of a combination of benzbromarone and allopurinol--studies under standardized dietary conditions].

The effects of a fixed combination of 100 mg allopurinol and 20 mg benzbromarone (Acifugan) on plasma and urinary uric acid were compared with those of 300 mg allopurinol alone during standardized dietary conditions (purine-free, isoenergetic formula diet with addition of 2 g ribonucleic acid per day). In addition, the components of the fixed combination were given separately. Diet and ribonucleic acid were taken by healthy volunteers for periods of 14 days, drugs were added from day 8 to day 14. Steady state uric acid values before and during drug ingestion were compared intraindividually to calculate drug effects. The fall of plasma uric acid was not significantly different during treatment with 300 mg allopurinol as compared with combined low dose treatment. Renal uric acid excretion was decreased by 56 and 23%, respectively. Comparing combined low dose treatment with the cumulative effects of its constituents it was found that combined treatment was less effective. With combined low dose treatment there is no need to observe prophylactic measures concerning complications at the site of the urinary tract. Compared with monotherapy with 300 mg allopurinol there is no advantage. However, the frequencies of side effects, which are not dose-dependent, will be cumulative with combined treatment, which is probably a major disadvantage. Combined treatment should not be used therefore with the exception of proven inefficiency of monotherapy.

Adult↗
PubMed1982

[Carpal tunnel syndrome and gout (author's transl)].

Bilateral carpal tunnel syndrome was observed in a 39-year-old female with gout. Until now carpal tunnel syndrome caused by gout has not been observed in females. Due to marked clinical symptoms neurolysis on the right side had to be performed. The course of the left hand affection was observed while on conservative treatment with a xanthine oxidase inhibitor. As such therapy is possible and successful, it is mandatory to diagnose carpal tunnel syndrome early in gout. Histology showed the cause of carpal tunnel syndrome to be uric acid tendovaginitis.

Adult↗