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

In order to clarify the mechanism of hyperuricemia and hyperuricosuria resulting from rapid infusion of fructose in man, the effects of an intravenous infusion of 125-200 g of fructose given over 3-4 hr on the rate of purine synthesis de novo was measured in one individual with osteoarthritis and four patients with gout. The incorporation of 1-minus 14C glycine into urinary uric acid was measured, and the pool size and turnover of urate were assessed by renal excretion of simultaneously administered 15-N urate. Fructose caused an expansion of body urate pool in all subjects, while urate turnover was increased in four. The rate of incorporation of 14-C glycine into urinary uric acid corrected for extrarenal disposal was increased in all cases (21%-430%). In two patients, rates of incorporation of 14-C glycine into urinary creatinine were increased by 10% and 11%, while rates of incorporation into uric acid were increased 84% and 159%, respectively, as a result of fructose infusion. Specific enhancement of the rate of purine synthesis de novo was suggested by these findings. The rate of infusion appeared more important than total dose in determining the magnitude of this effect. Whether the increased rate of purine synthesis was a result of direct stimulation by a fructose metabolite or was secondary to fructose-induced purine nucleotide depletion is uncertain, since the kinetics of glycine incorporation were consistent with either mechanism. Erythrocyte PP-ribose-P concentrations, however, were diminished during infusion rather than increased as might be expected if fructose infusion stimulated purine synthesis by increasing availability of this regulatory substrate.
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PMID:Stimulation of human purine synthesis de novo by fructose infusion. 16 70

It is reported of 726 patients incidentally elected and mainly with life-shortening risk factors. 341 (47.1p.c.) showed an increased concentration of neutral fats and/or total cholesterol in the serum. Type IV (49.8 p.c.) according to Fredrickson was observed most frequently, followed by type IIb (31.1 p.c.) and by type IIa (19.1 p.c.). Most of the patients with hyperlipoproteinemia were overweight (53.1 p.c.), 33.6 p.c. suffered from arterial hypertension, 25.3 p.c. from diseases of the liver, 10.9 p.c. from coronary heart diseases, and 8.7 p.c. from manifest diabetes mellitus. The distribution of different types of hyperlipoproteinemia among the various diseases deviates from that of the total number of patients observed in this study. Cases of hyperlipoproteinemia were observed most frequently in diseases of the kidney with arterial hypertension (62.7 p.c.), coronary heart diseases (60.8 p.c.), manifest gout (60.0 p.c.), manifest diabetes mellitus (58.7 p.c.), and hyperuricemia without symptoms (55.8 p.c.). Type-IV-hyperlipoproteinemia was observed most frequently within the different groups of patients with life-shortening risk factors. An exception was the group of patients suffering from malignancies. Type IIb was found most frequently within the group of patients suffering from malignancies.
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PMID:[Frequency and distribution of types of hyperlipoproteinemia with life-shortening risk factors among ambulant patients (author's transl)]. 17 Apr 97

The idea that, in view of potent drugs, the dietary treatment of a metabolic disease must be reserved for a small group of particularly susceptible patients or even for a minority of neurotically structured patients who would alone be capable of bearing the hardship of a consequent change of accustomed feeding habits needs correction. Considerably greater importance must be attached to dietetics in disorders of uric acid metabolism than formerly, particularly with a view to the status already gained by the dietary treatment of diabetes mellitus a long time ago. Dietetic therapy of familial hyperuricemia and its later clinical manifestation, gout, is a basic therapy of a preventive character. Because today, superiority is increasingly conceded to prophylaxis rather than to the treatment of late sequelae.
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PMID:[Diet in hyperuricemia (author's transl)]. 17 May 14

Work is continuing in the attempt to increase knowledge of the regulation of the rate of purine synthesis in man by means of an analysis of biochemical alterations leading to purine overproduction among patients with gout. The authors are now assessing the frequency of kinetic mutations in enzymes whose alterations already have been associated with increased purine synthesis. Efforts in this regard have been rewarded by the identification of a new form of alteration leading to partial deficiency of HGPRT and a kinetic variant of PRPP synthetase with increased affinity for ribose-5-phosphate. In order to identify new forms of enzyme abnormalities associated with excessive purine synthesis, the value of a proposed classification scheme requiring measurement of PRPP and ribose-5-phosphate concentration and generation is being assessed in cultured fibroblasts. It is hoped that the results of these measurements will lead to the identification of additional kinetic variants of presently known enzyme abnormalities and will help to identify new classes of mutants in the regulation of human purine metabolism. The excessive purine synthesis that underlies the hyperuricemia of a substantial number of patients with gouty arthritis reflects alterations in the normal mechanism regulating the rate of purine nucleotide synthesis. The study of such purine "overproducers" has provided insight into the nature of this regulatory mechanism and has underscored the diversity of specific genetic and biochemical aberrations affecting it. Despite these advances, however, less than 10% of all patients with gout and excessive purine production can presently be accounted for by known enzyme abnormalities (1). Recognition that current knowledge of the regulation of the rate of purine nucleotide synthesis in man is incomplete has provided the authors impetus leading to the studies described here, which are preceded by a brief review of background.
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PMID:Recent advances in the identification of enzyme abnormalities underlying excessive purine synthesis in man. 17 46

Type V hyperlipemia is not very common. The series of 54 cases descrubed here is the largest reported to date. Our observations were recorded when lipidograms showed the presence of chylomicrons and a large pre-beta-lipoprotein spot in the serum of fasting subjects. Type V hyperlipemia was often combined with other metabolic syndromes such as diabetes, hyperuricemia or gout, or obesity. Chronic alcoholism was also noted in half our subjects, in whom hyperlipemia quickly regressed after alcohol consumption ceased. Ischemic arterial complications, chiefly coronary, were found in one third of our cases, and the vascular risks accompanying this type of hyperlipemia rose considerably in patients with high blood pressure. Various type of treatment were administered, but all subjects were put on a special diet, comprising either the elimination of alcoholic drinks only, or, in addition to this, reduced carbohydrate or calorie intake. As a rule, these measures resulted in a distinct regression of lipid anomalies. Clofibrate or derivatives proved effective in cases where hyperlipemia failed to respond to dietary measures.
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PMID:[Type V hyperlipemia. 54 cases (author's transl)]. 22 80

We carefully selected 30 men with primary gout, rendered asymptomatic by therapy, to examine the frequency and type of hyperlipidemia and hyperlipoproteinemia, with the objective of determining whether serum uric acid, alcohol intake, liver function, kidney function, and (or) drugs were participating in the secondary lipid disorder. Sixty-one age- and sex-matched men were used as controls. About 73% of the gout patients had hypertriglyceridemia, 1.6-fold the frequency found in the control group. Types IV and IIb lipoprotein electrophoretic patterns were most prevalent in the gout group. Neither alcohol intake nor hyperuricemia, per se, seems to be the cause of the lipid and lipoprotein disorder and cannot be related to liver or kidney dysfunctions. Obesity was the major underlying factor associated with the lipidemia. The study suggests that diet and, possibly, defective clearance of triglycerides may be etiologic factors associated with the abnormal serum triacylglycerol (triglyceride) and lipoprotein concentrations in these individuals.
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PMID:Secondary hypertriglyceridemia and hyperlipoproteinemia in patients with primary asymptomatic gout. 26 76

Diagnosis of gout by crystal identification in synovial fluid is simple and definitive. To treat gout effectively, the physician must determine whether overproduction or underexcretion of uric acid is the underlying mechanism. The acute attack is treated initially with antiinflammatory agents. After the acute phase is controlled, lifelong definitive therapy for hyperuricemia is begun.
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PMID:Hyperuricemia and gout. A modern approach to diagnosis and treatment. 42 48

A family is reported where four males have developed hyperuricemia, renal damage and, except for the youngest person affected, gout at an early age. The disease appears to be inherited as an X-linked recessive metabolic error. Clinically the patients have developed classical, tophaceous gout before the age of 25 and have suffered repeated attacks of renal colic. Renal tubular damage with decreased ability to concentrate and acidify urine was seen in a family member of only 16 years of age. Progressive renal failure seems to develop slowly. None in the family has shown neurologic symptoms, and two of the four affected men are apparently of at least average intelligence, two slightly below average. One female carrier has repeatedly passed uric acid stones. Studies of the red blood cell lysate have shown a normal activity of enzyme hypoxanthine phosphoribosyltransferase, and an increased level of adenine phosphoribosyltransferase. Skin fibroblasts from affected family members grew normally in the presence of 8-azaguanine. Administration of azathioprine to the patients did not decrease their serum uric acid levels. This is the first family described with this type of disorder of the purine metabolism.
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PMID:Recessive X-linked hyperuricemia with gout and renal damage, normal activity of hypoxanthine phosphoribosyltransferase and resistance to azaguanine. 42 44

The diagnosis of gout depends on showing urate crystals in synovial effusions or, with less certainty, recognizing a characteristic clinical presentation. The management of gout has four phases: control of inflammation, diagnostic evaluation, education of the patient, and treatment for the hyperuricemia. Sound logical principles guide each aspect. Careful attention to these four phases of management should lead to highly satisfactory control of the syndrome of gout.
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PMID:Management of gout. 43 90

Complex segregation analysis supports the polygenic hypothesis of Hauge and Harvald and Neel et al, according to which hyperuricemia ascertained through gout is rarely due to a major gene, evidence for which is not significant in two studies that were considered to favor a major locus.
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PMID:Genetics of hyperuricemia in families with gout. 49 48


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