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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The responses of cultured rabbit synovial fibroblasts to amorphous and microcrystalline calcium oxalate were compared with responses to MSUM. Like urate crystals, crystalline calcium oxalate (but not amorphous oxalate) caused marked stimulation of secretion of latent collagenase and PGE2 after 3 days of culture without significant change in cell protein or gross cellular morphology. Collagenase rose from undetectable levels in control cultures to 32.4 +/- 6.0 and 27.4 +/- 7.9 U/mg of cell protein for crystalline calcium oxalate and MSUM, respectively. PGE2 rose from a control level of 0.24 +/- 0.14 to 19.47 +/- 5.15 and 23 +/- 4.84 micrograms/mg of cell protein for crystalline calcium oxalate and sodium urate compared to 1.22 +/- 0.48 microgram for amorphous calcium oxalate. Although the crystalline species studied caused LDH in the media to increase threefold, this was minimal. Cell stimulation by amorphous oxalate and the crystals did not correlate with membranolytic potential as measured with an erythrocyte lysis assay. Stimulation of resident synovial cells by crystalline calcium oxalate and sodium urate may contribute to the chronic inflammation and destruction of joint tissues that occurs in oxalosis and gout.
J Lab Clin Med 1982 Dec
PMID:Stimulation of synovial fibroblasts by calcium oxalate and monosodium urate monohydrate. A mechanism of connective tissue degradation in oxalosis and gout. 629 14

The enzymic activities of erythrocyte phosphoribosyl pyrophosphate synthetase (EC 2.7.6.1) and glutathione reductase (EC 1.6.4.2) have been measured in 54 primary gout patients, 35 individuals having hyperuricaemia and 51 healthy controls. Statistical analyses have shown a significant increase (p less than 0.01) in the enzymic activity of erythrocyte PRPP synthetase in both the hyperuricaemic and gout groups compared with the controls. No correlation between activity and age was found in any of the three clinical groups. A significant decrease (p congruent to 0.01) was found in the enzymic activity of red cell glutathione reductase in the gout group compared with the other two groups. The biochemical significance of the changes in enzymic activities of the two enzymes in primary gout is discussed.
Clin Chim Acta 1982 Dec 23
PMID:Phosphoribosyl pyrophosphate synthetase and glutathione reductase in erythrocytes from hyperuricaemic and gout patients. 629 64

A patient with gout had a peripheral neuropathy that improved with the lowering of the serum uric acid level. He had a relapse when hyperuricemia recurred, suggesting that the hyperuricemia of gout may produce a treatable form of peripheral neuropathy.
Arch Neurol 1983 Dec
PMID:Gouty neuropathy. 631 47

A patient with lead nephropathy and gout was treated with three months of edetic acid chelation. The therapy resulted in normalization of a previously abnormal result of edetic acid lead mobilization test. Nevertheless, progressive renal insufficiency occurred. At autopsy, an increased bone lead content was documented, suggesting that the edetic acid lead mobilization test may underestimate total body lead stores and that chelation therapy may not be effective in reversing advanced lead nephropathy. Alternatively, a longer period of therapy may be necessary to remove lead stores. More studies are needed to determine the relationship between the results of the edetic acid test and bone lead stores. Methods other than the edetic acid lead mobilization test should be considered to monitor the adequacy of treatment in lead nephropathy.
Arch Intern Med 1984 Dec
PMID:Failure of chelation therapy in lead nephropathy. 643 41

Crystals can be identified in synovial fluids (SF) in the absence of acute inflammation as well as during acute gouty arthritis. We examined gouty joint effusions to evaluate whether observable properties of the crystals correlate with the clinically detectable inflammation. Higher SF leukocyte counts and more crystal phagocytosis were confirmed during more severe arthritis. We found no differences between crystal sizes, numbers of shapes in severe versus mild inflammation. Some patients with severe acute gout had few crystals or only punctate birefringent fragments. Factors other than those we examined must affect the severity of the inflammatory response in gouty arthritis.
J Rheumatol 1984 Dec
PMID:Prospective study of morphology and phagocytosis of synovial fluid monosodium urate crystals in gouty arthritis. 652 Aug 27

We describe 2 adult patients with cyanotic congenital heart disease whom, as a complication of their cardiopathy, had 2 different rheumatic syndromes: gout and hypertrophic osteoarthropathy. The coexistence of these arthropathies in the same patient, to our knowledge, has not been previously reported. We discuss the possible pathogenic mechanisms that may link these syndromes to cyanotic heart disease.
J Rheumatol 1984 Dec
PMID:Coexistent gout and hypertrophic osteoarthropathy in patients with cyanotic heart disease. 652 Aug 38

Four patients with a simultaneous occurrence of psoriasis and gout are described. These cases were selected out of a group of 108 gouty in-patients. Clinical and laboratory findings in the reported patients are briefly outlined and this association of diseases is described from the viewpoint of differential diagnosis.
Clin Rheumatol 1983 Dec
PMID:Psoriasis and gout: report of 4 cases. 667 3

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.
Klin Wochenschr 1983 Dec 15
PMID:Gout and uric acid nephropathy: some new aspects in diagnosis and treatment. 668 51

Gout may be a primary or a secondary disorder. In both types of gout, overproduction or underexcretion of uric acid, or a combination of these abnormalities, may be the underlying mechanism. Controversy exists over the need for treatment of asymptomatic hyperuricemia. Treatment of tophi requires use of both uricosurics and allopurinol. A xanthine oxidase inhibitor is the drug of choice for patients with uric acid stones and for those with renal insufficiency.
Am Fam Physician 1981 Dec
PMID:Hyperuricemia and gout: an update. 689 39

A rapid and selective reversed-phase high-performance liquid chromatographic method for the simultaneous determination of hypoxanthine and xanthine in biological fluids was developed. The identification of hypoxanthine and xanthine was confirmed by xanthine oxidase reaction. This method was applied to the investigation of purine metabolism in subjects with xanthine oxidase deficiency or gout. Hypoxanthine concentrations three to ten times higher than those determined in plasma were found in erythrocyte samples from normal subjects and from patients with xanthine oxidase deficiency or hyperuricemia under allopurinol therapy.
J Chromatogr 1982 Dec 10
PMID:High-performance liquid chromatographic determination of hypoxanthine and xanthine in biological fluids. 689 51


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