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Biomedical subjects

W Gröbner

Publications and source records attributed to W Gröbner.

At least 37 records · Page 2Linked to original sources
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↗
PubMed1982

Influence of dietary purines on pool size, turnover, and excretion of uric acid during balance conditions. Isotope studies using 15N-uric acid.

Pool size, turnover, and excretion of uric acid were investigated in three normal subjects both during purine-free, isoenergetic liquid formula diet and during additional purine administration by use of isotope dilution techniques. The fractional turnover of the uric acid pool was increased during dietary purine administration suggesting an increased total body uric acid clearance as a result of the increase in renal clearance. Fractional turnover increased more in the female subject than in males, while pool size was increased less. It can be calculated from the results obtained that endogenous uric acid synthesis is not inhibited by dietary purines.

Adenosine Monophosphate↗
PubMed1981

Pseudohypoparathyroidism and hypocalcemic "myopathy". A case report.

A patient with the clinical features of pseudohypoparathyroidism and elevated concentrations of serum CK and LDH, which normalized after successful therapy, is described. Clinical signs of myopathy did not exist. The bioptical material from the m. tibialis anterior was microscopically normal. The biochemical analysis revealed a reduced phosphorylase-a-activity with the total phosphorylase-activity (a and b) being within the normal range. The significance of these findings as well as possible pathogenetic mechanisms are discussed.

Adolescent↗
PubMed1981

Sonography of polypoid gastric lesions by the fluid-filled stomach method.

The fluid-filled stomach allows visualization of the gastric wall on real-time ultrasonic examination. In four cases with small focal gastric wall lesions (two cases with hyperplastic polyps, one with pseudopolypoid lesions, and one with polypoid infiltration of the gastric mucosa by malignant lymphoma), typical ultrasonic pictures were demonstrated. The polypoid lesions were located on the anterior and posterior gastric walls and at the gastric fundus, respectively. All who use the gastric sonic window for imaging the pancreas or the left upper abdomen should be aware that focal gastric lesions are also observable.

Adult↗
PubMed1979

[Properties of hypoxanthineguanine-phosphoribosyltransferase (HGPRTase) in a gout patient with partial deficiency of this enzyme (author's transl)].

Some physicochemical properties of HGPRTase were studied in hemolysates and fibroblasts of a gout patient with partial deficiency of this enzyme. In comparison to normal HGPRTase the mutant enzyme from erythrocytes was found to have an elevated apparent Km-value for hypoxanthine and guanine and a lower Km-value for PRPP. The patient's enzyme from erythrocytes is more stable at +4 degrees C and +80 degrees C, the enzyme from fibroblasts more labile than that of controls. The inhibition of the mutant enzyme by some purine nucleosides and -nucleotides differed from that found in controls. No evidence was shown for an inhibitor of the patient's HGPRTase from erythrocytes. Ultracentrifugation of hemolysate in a saccharose gradient revealed no difference in the sedimentation coefficient.

Adenine Phosphoribosyltransferase↗
PubMed1979

Uricosuric therapy and urate solubility in blood and urine.

In most patients with primary gout hyperuricaemia results from a renal defect in tubular uric acid secretion. An increased endogenous purine biosynthesis is observed in only 2% of all patients with gout. Secondary hyperuricaemai results either from an increased breakdown of endogenous nucleic acids as in polycythaemia or from a decreased renal excretion of uric acid due to drug treatment, renal insufficiency or metabolic disturbances. Hyperuricaemia may be defined either in statistical terms from epidemiological studies of normal and gouty populations or from physicochemical properties of urate. Monosodium urate and uric acid are soluble in water to the extent of 6.32 mmol/l and 0.39 mmol/l respectively. In human plasma saturation of monosodium urate occurs at a concentration of about 0.42 mmol/l. The solubility of uric acid and urate in urine is more complicated as it is affected by changes in pH and salt concentration. Uricosuric drugs decrease serum uric acid concentration by enhancing the renal excretion of uric acid. Effects and side effects of uricosuric therapy are discussed.

Gout↗