Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Gout and uric acid nephropathy: some new aspects in diagnosis and treatment. 668 51

In a metabolic ward study of five patients, azapropazone lowered plasma uric acid but exerted only a modest and variable uricosuric effect without altering urinary xanthine and hypoxanthine levels. An alternative mechanism other than uricosuria or xanthine oxidase inhibition must account for some of the hypouricaemic action of this drug. During the first day of treatment urine volume and pH declined sharply. In a separate investigation, 22 patients were given azapropazone and 18 were given allopurinol combined with colchicine for 3 months. Allopurinol reduced plasma uric acid more quickly but at the end of the study there was little difference in the hypouricaemic results achieved by both drugs. Recurrent gout occurred more frequently with allopurinol but side-effects were confined to those taking azapropazone. A slight rise in blood urea and creatinine and a fall in haemoglobin were also features of long-term azapropazone treatment.
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PMID:Azapropazone--a treatment for hyperuricaemia and gout? 669 72

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.
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PMID:Hyperuricemia and gout: an update. 689 39

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.
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PMID:[Carpal tunnel syndrome and gout (author's transl)]. 689 2

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.
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PMID:High-performance liquid chromatographic determination of hypoxanthine and xanthine in biological fluids. 689 51

Of 29 524 hospitalised medical patients monitored in a drug surveillance programme 1835 (6.2%) received the xanthine oxidase inhibitor allopurinol. After the exclusion of skin reactions adverse effects were attributed to this drug in 33 (1.8%) patients, the most frequent being haematological abnormalities (11 patients, 0.6%) and diarrhoea and drug fever (5 each, 0.3%). Adverse effects were dose-related. Reactions were unrelated to age, weight, reason for therapy, admission blood urea, or albumin concentrations. Acute exacerbation of gout was troublesome in 3 patients (1 in 600 exposed).
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PMID:Acute adverse reactions attributed to allopurinol in hospitalised patients. 724 70

Diploptene(1), beta-sitosterol(2), a mixture of 6'-O-(E-P-coumaroyl)-alpha-glucopyranose and 6'-O-(E-P-coumaroyl)-beta-glucopyranose(3), a mixture of 6'-O-(E-P-caffeoyl)-alpha-glucopyranose and 6'-O-(E-P-caffeoyl)-beta-glucopyranose(4), caffeic acid(5) and astragalin(6) were isolated from an ethanolic extract of the leaves of Alsophila spinulosa Hook Tryon (Cyatheaceae). The plant has been used in folk medicine for hepatitis, gout, rheumatism, and tumor and these compounds were tested for their inhibitory effect on xanthine oxidase. Caffeic acid was the most potent constituent (IC50 = 39.21 microM; Ki = 28.2 microM) and was an uncompetitive inhibitor of the enzyme with respect to the substrate xanthine.
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PMID:Xanthine oxidase inhibitors from the leaves of Alsophila spinulosa (Hook) Tryon. 753 70

Caffeic acid has been reported to have activity on xanthine oxidase inhibition which is related to several diseases, e.g. gout, hepatitis and tumors. Based on this study, the alpha, beta-unsaturated COOH moiety in the molecule of caffeic acid plays a very important role on the xanthine oxidase inhibition because hydrocaffeic acid was inactive and the activities of coniferyl aldehyde and coniferyl alcohol were reduced as compared with ferulic acid. Moreover, chlorogenic acid showed a weaker activity than caffeic acid. On the other hand, the phenolic OH group present in the molecule of caffeic acid makes an important contribution to the activity, e.g. transcinnamic acid in which the absence of the phenolic OH group in the structure reduced its activity as compared with caffeic acid. Ferulic acid, isoferulic acid and 3,4-dimethoxy cinnamic acid also had reduced activity due to the methoxy groups replacing the phenolic OH group in the structures. However, m-coumaric acid displayed the strongest activity (IC50 = 63.31 microM) and induced uncompetitive inhibition with respect to the substrate xanthine (Ki = 21.568 microM). Caffeic acid (IC50 = 74.6 microM) showed the second strongest activity, followed by p-coumaric acid (IC50 = 111.09 microM).
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PMID:Structure-activity relationship of caffeic acid analogues on xanthine oxidase inhibition. 764 46

A high-performance liquid chromatographic method was developed for the determination of plasma purine nucleoside phosphorylase activity. In this method, the reaction mixture consisted of 15 microliters of plasma and 285 microliters of 50 mM phosphate buffer (pH 7.4) containing 3.8 mM inosine and 0.15 mM 2-(3-cyano-4-isobutoxyphenyl)-4-methyl-5-thiazolecarboxylic acid (strong xanthine oxidase inhibitor). After the reaction, the hypoxanthine produced was monitored to express plasma purine nucleoside phosphorylase activity. By this method, the activity of purine nucleoside phosphorylase was easily determined even with a small-volume plasma sample and despite its low activity in plasma. In addition, plasma purine nucleoside phosphorylase activity can be accurately determined even if the plasma is turbid. As a result, we were able to measure plasma purine nucleoside phosphorylase activity in patients with gout or asthma and healthy subjects, whereby it was demonstrated that plasma purine nucleoside phosphorylase activity was higher in patients with asthma than in either healthy subjects or patients with gout.
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PMID:Determination of plasma purine nucleoside phosphorylase activity by high-performance liquid chromatography. 766 72

Gout is a common disease with a worldwide distribution. The major risk factor for the development of gout is sustained asymptomatic hyperuricaemia. Although pharmacological therapy of asymptomatic hyperuricaemia is not recommended, primary prevention of gout can be achieved through lifestyle changes including weight loss, restricting protein and calorie intake, limiting alcohol consumption, avoiding the use of diuretics in the treatment of hypertension, and avoiding occupational exposure to lead. The arthritis of gout can be readily managed with the use of nonsteroidal anti-inflammatory drugs (NSAIDs); systemic steroids or corticotrophin (adrenocorticotrophic hormone; ACTH) should be used in patients with contraindications to NSAIDs, or who are intolerant of them. Because of potential toxicity, colchicine should not be used to treat acute gout, but should be used in low dosage (0.6 to 1.2 mg/day) for prophylaxis of recurrent attacks of gout. The other cornerstone of prevention of recurrent gouty attacks is control of hyperuricaemia, which can be effectively accomplished with antihyperuricaemic therapy. The choice of agents, either uricosuric drugs or xanthine oxidase inhibitors, is based on the level of urinary uric acid excretion, renal function, age of patient, history of renal calculi and presence of tophi. Treatment and prevention of gout are exceedingly effective and patients can usually be managed by their primary care physician.
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PMID:Prevention and management of gout. 768 72


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