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

Sumo is an ancient sport in Japan and there are at present over 800 professional sumo wrestlers (rikishis). After entrance into the wrestler society a wrestler takes strenuous daily training together with a very high calorie diet (more than 5,000 cal). Frequency of food intake is twice a day. The average diet of Japanese people contains of 2,279 calories and the meal frequency is generally three times a day. In 96 wrestlers average actual body weight and modified Broca index was 100.4 kg and 143.5%, respectively. In this group the prevalence of overweight with obesity, overweight without obesity, nonoverweight with obesity, and nonoverweight without obesity was 53.4, 39.1, 1.0, and 6.5%, respectively. Also mean serum levels of triglyceride, phospholipid, uric acid, and total protein were significantly higher than those obtained in 89 age-matched healthy males. The incidence of diabetes mellitus, gout, and hypertension in wrestlers was 5.2, 6.3, and 8.3%, respectively, all values being considerably higher than in controls. Weight correlated significantly with skinfold thickness, diastolic blood pressure, total cholesterol, and uric acid in each group. Multiple regression analyses were made treating weight or uric acid as dependent variables in both groups. Obesity, hyperlipidemia, and hyperuricemia in wrestlers were presumed to be caused chiefly by the high calorie diet and partially by the infrequent meal intake.
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PMID:Some factors related to obesity in the Japanese sumo wrestler. 97 5

Several points may be stressed. (1)When in doubt, perform joint aspiration and look for crystals of micro-organisms. A joint tap is nearly always indicated. (2)Do not rely on a coincidental elevated serum uric acid level. Question the patient regarding drug therapy and other causes of secondary hyperuricemia. (3)Examine all of the patient, looking for tophi (gout), skin lesions (gonococcal infection, psoriasis), erythema nodosum (allergic reactions, fungal infections), and other clues. (4)Monoarticular rheumatoid arthritis is a rare cause of a single hot joint, but it is much more common that the real rarities (e.g., pigmented willondular synovitis). (5)Anky-losing spondylitis and Reiter's syndrome are common, yet frequently overlooked. (6)Radiologic examination is usually not helpful. (7)Having ruled out infection, crystal synovitis, and hemorrhage, it is sufficient to introduce symptomatic treatment and await the natural development of the joint disease. Follow-up in four to six weeks and simple blood studies often reveal the definitive diagnosis. Most of the time, natural healing processes are effective , and reward the patience of the conservative physician. Blind management must always be avoided.
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PMID:The single hot joint. 97 58

Haloperidol, a dopamine receptor blocking agent, is the most effective therapy for Tourette's syndrome. In five patients with Tourette's syndrome, we found in the CSF an elevated probenecid-induced accumulation of HVA, the major metabolite of dopamine. This supports the hypothesis that Tourette symptoms are related to an increased firing of dopaminergic neurons in the central nervous system; haloperidol relieves these symptoms by blocking dopamine receptors. Some similarities of Tourette's syndrome to Lesch-Nyhan's syndrome prompted us to compare these two disorders, obtaining data from a large number of Tourette patients. In a questionnaire completed by 114 patients with Tourette's syndrome, the incidence of self-destructive behavior was 43%, a family history of gout or hyperuricemia was present in 27%, and 11% had a family history of Tourette's syndrome or tics. We propose that Tourette's syndrome could be a genetic disorder of purine metabolism which may result in neurotransmitter abnormalities such as an increased brain dopamine turnover.
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PMID:Gilles de la Tourette's syndrome: biochemical approaches. 107 64

The effectiveness of naproxen in the management of acute gouty arthritis was assessed in an open study of 20 patients. These patients were selected on the basis of their clinical presentation of characteristic acute arthritis associated in 19 with concomitant hyperuricemia. There were 17 men and three women varying in age from 35 to 89 years. The first 12 patients were treated with 600 mg naproxen initially, followed by 300 mg every 8 hours for the first 48 hours and then tapered or discontinued depending upon their clinical response. The last eight patients received a loading dose of 750 mg naproxen, followed by 250 mg every 8 hours for a duration of 72 hours before tapering the drug. The response of 15 of the 20 was either excellent or good, while the response was fair in three and poor in two. Poor responders had been failures in other regimens or were treated late in the course of their attack. The higher loading dose was associated with more rapid and satisfactory remission. No significant undesirable side effects were observed. On the basis of this study, naproxen was found effective in alleviating the inflammation of acute gout.
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PMID:The treatment of acute gout with naproxen. 109 30

Historical evidence suggests that the Maori people of New Zealand were virtually untroubled by gout or obesity at a time when these disorders, along with other elements of the gouty diathesis, were rife in the best fed and hardest drinking sections of the Northern European population. By the mid 20th century, however, the apparent decline of the gout in Europe and North America and the breakup of the gouty diathesis in those lands had been more than compensated by their large-scale reappearance in the Maori and in other indigenous inhabitants of the Pacific Basin who, at first sight, appeared to have become one large gouty family. Half the Polynesian population of New Zealand, Rarotonga, Puka Puka, and the Tokelau Islands proved to be hyperuricemic by accepted European and North American standards, the associated gout rate reaching 10.2% in Maori males aged 20 and over. The trends towards hyperuricemia and gout, on the one hand, and towards obesity, diabetes mellitus, hypertension, and associated degenerative vascular disorders, on the other hand, which manifest themselves separately in some Polynesian Pacific Islanders, run together in the Maori and Samoan people, presenting a combined problem of considerable importance to the public health. The appearance of these traits under conditions of plenty in the descendants of hardy and wide-ranging Polynesian voyagers, suggests the emergence of a formerly favorable ancestral polygenic variation through selection for survival under harder conditions. This may now have lost its primitive survival value with a paradoxic shift towards increased prevalence of obesity and the gouty diathesis in more affluent environmental conditions. This may now constitute a genetic load, with recent environmentally determined increase in morbidity and mortality rates from degenerative vascular disorders. There is no satisfactory evidence that overproduction of uric acid differs in mechanism from its European counterparts, although more work remains to be done to determine whether there is any difficulty in renal handling of an increased uric acid load. A high Maori morbidity rate from gout and morbidity and mortality rates from associated components of the gouty diathesis in the face of readily available skilled medical advice and care, indicate the need for greater future attention to help education and health care delivery, at least while conditions of plenty continue. Continuation of previous epidemiologic surveillance may then be required in order to provide a continuing index of the effectiveness of these measures, as well as an opportunity for further research into the interrelationships of these associated disorders.
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PMID:Gout in Maoris. 110 93

Seven young adults with uric acid overproduction due to sickle cell anemia were normouricemic with a mean serum uric acid level of 4.9 mg/100 ml. Urate clearance was greater in these patients than in normal subjects or in patients with primary hyperuricemia due to uric acid overproduction. The increase in urate clearance was entirely accounted for by increased pyrazinamide suppressible urate clearance. Pyrazinamide administration abolished the uricosuric response to ribonucleic acid (RNA) feeding in these patients with sickle cell anemia, and maximal uricosuric response to the administration of probenecid was similar in the patients with sickle cell anemia and in normal subjects suggesting that reabsorption of both filtered and secreted urate was not impaired in sickle cell disease. Pyrazinamide suppressible urate clearance at maximal uricosuric response to probenecid was increased in patients with sickle cell disease suggesting increased tubular secretion of urate. This increase in urate secretion permits most young adults with urate overproduction due to sickle cell anemia to remain normouricemic and may account for the low frequency of secondary gout in this disease.
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PMID:Hyperuricosuria and increased tubular secretion of urate in sickle cell anemia. 110 19

In vitro binding studies on antiinflammatory and uricosuric acidic anions performed under "physiologic" conditions have demonstrated that these substances displace urate from its protein bond. The property of urate displacement appears to be a useful marker for potential uricosuric activity in vivo, and thereby a means to detect novel uricosuric drugs. One such drug, halofenate, was indeed a safe and effective uricosuric (comparable to probenecid) when used to treat hyperuricemia/gout over the long term; it did result in a modest and variable fall in serum lipid concentrations. However, used as a single fixed dose, halofenate did not produce a marked and consistent effect on the elevated serum triglyceride concentrations so commonly present in gouty patients.
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PMID:Halofenate. Its selection and trial as a primary uricosuric agent. 110 34

The etiology of hyperuricemia following myocardial infarction was investigated by uric acid kinetic studies carried out on seven male patients following myocardial infarction and on two control subjects. The patients selected had uncomplicated myocardial infarction and were maintained on a low-purine diet. Measurements of uric acid pool size and turnover rates using 2-C14 uric acid were made, commencing on days 2-5 following myocardial infarction. Initial concentration of serum uric acid ranged from 2.9 to 9.8 mg/100 ml. Uric acid pool size was elevated in six of seven patients. Five had a pool size of from 36.9 to 79.6 mg/kg, while the single gouty subject demonstrated 104 mg/kg compared with 12.6 and 16.8 mg/kg for the control subjects. Turnover rates were also increased, ranging from 1036 to 2772 mg/day (controls, 612 and 872 mg/day). Twenty-four-hour urine uric acid excretions ranged from 358 to 623 mg/24 hr. Serum lactic acid concentration was normal (1.03 plus or minus 0.17 muM/ml), and endogenous creatinine clearance in all cases was 77.9 ml/min or greater. These data suggest that following myocardial infarction there is an expansion of the uric acid pool with an increased uric acid turnover rate. Only the patient with a previous history of gout had uric acid excretion outside the normal range.
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PMID:Uric acid kinetic studies in the immediate post-myocardial-infarction period. 111 39

The origin of uric acid, metabolic pathways of purine metabolism and the disposition of uric acid in normal man are reviewed. Two thirds of the uric acid is normally excreted through the kidney while one third gains entrance to the gut where it undergoes uricolysis. The pathogenesis of hyperuricemia in primary and secondary gout is discussed. Increased production or decreased excretion of uric acid are the two principal mechanisms of hyperuricemia. The known biochemical defects associated with primary overproduction gout are outlined. Extrarenal uricolysis assumes a greater role when the renal excretion of uric acid is compromised.
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PMID:Origin and extrarenal elimination of uric acid in man. 112 37

Since approximately two thirds of daily urate production is normally excreted by the kidney, intrinsic renal disease resulting in abnormalities of urate excretion may have a profound effect upon urate homeostasis. Alterations in the pattern of urate excretion encountered in chronic renal failure are reviewed in depth, with a description of adaptive mechanisms for urate excretion which develop in residual nephrons, as exemplified by the remaining normal kidney of transplant donors. In addition, abnormalities in urate excretion in the presence of a normal complement of nephrons are described. Diminished urate excretion per nephron appears to be responsible for hyperuricemia in some patients with gout, while a variety of tubular defects resulting in excessive renal urate excretion have been documented as the basis for some cases of hypouricemia.
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PMID:Intrinsic renal disease leading to abnormal urate excretion. 112 38


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