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)

A 25-year-old white man with gout and nephropathy and with a previous reaction to allopurinol was given a trial dose of oxypurinol. He developed malaise, a generalized erythematous reaction with edema, pruritus, and emesis; this was clinically identical to the reaction he experienced with allopurinol. When the patient's lymphocytes were exposed in vitro to oxypurinol and allopurinol, increased DNA synthesis was observed, suggesting an immunologic basis for the reaction. This patient indicates that clinical cross reactivity to allopurinol and oxypurinol does occur and may be of an immunologic basis. There is a need for additional xanthine oxidase inhibitors for such patients.
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PMID:Allergic reaction to allopurinol with cross-reactivity to oxypurinol. 13 55

Multicentric reticulohistiocytosis is a special form of an erosive, destructive arthropathy. It can be distinguished from other forms of erosive polyarthropathies by the characteristic x-ray appearances, although the final proof of the diagnosis is histological in association with the clinical features and the presence of nodular skin lesions. A case of multicentric reticulohistiocytosis is described. The typical radiological appearances are discussed and the differential diagnosis from other forms of chronic polyarthritis, such as gout, psoariatic arthropathy, Reiter's disease and erosive osteoarthritis is considered.
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PMID:[Multicentric reticulohistiocytosis as a cause of an erosive, destructive arthropathy (author's transl)]. 15 71

Recent studies have shown elevated inorganic pyrophosphate (PPi) levels in most knee joint fluid supernates from patients with pseudogout (PG) or osteoarthritis (OA) and more modestly elevated levels in some supernates from patients with gout or rheumatoid arthritis (RA) relative to PPi levels found in the venous blood plasma of normal or arthritic subjects. We measured the intraarticular PPi pool and its rate of turnover to better understand the significance of the joint fluid-plasma PPi gradient. Preliminary studies in rabbits showed that (32-P)PPi passed from joint space to blood and vice versa without detectable hydrolysis. Incubation of natural or synthetic calcium pyrophosphate dihydrate (CPPD) microcrystals with synovial fluid in vitro in the presence of (32P)PPi tracer showed no change in PPi specific activity in the supernate over a 19-h period so that exchange of PPi in solution with that in CPPD microcrystals could be ignored. Clearance rates of (32P)PPi and of (33P)Pi, as determined by serially sampling the catheterized knee joints of volunteers with various types of arthritis over a 3-h period, were nearly identical. The (32P)PPi/(32P)Pi was determined in each sample. A mixture of a large excess of cold PPi did not influence the clearance rate of either nuclide. The quantity of PPi turned over per hous was calculated from the pool size as determined by isotope dilution and the turnover rate. The residual joint fluid nuclide was shown to be (32P)PPi. The PPi pool was generally smaller and the rate of turnover was greater in clinically inflamed joints. The mean plus or minus SEM pool size (mu-moles) and turnover rate (percent/hour) in PG knees was 0.23 plus or minus 0.07 and 117 plus or minus 11.9, hydrolysis rate (%/h) to Pi was 27.7 plus or minus 13.2; in OA knees: 0.45 plus or minus 0.26 and 72 plus or minus 9.2, hydrolysis 6.9 plus or minus 0.9; in gouty knees: 0.8 plus or minus 0.41 and 50 plus or minus 11.6, hydrolysis 9.8 plus or minus 2.8; and in RA knees: 0.14 plus or minus 0.14 and 114 plus or minus 35.8, hydrolysis 236 plus or minus 116. PPi turnover (mumoles/hour) correlated with the degree of OA change present in the joint as graded by radiologic criteria irrespective of the clinical diagnosis. Mean PPi turnover in joints with advanced OA was greater than in those with mild or moderate changes (P smaller than 0.001), but the mild and moderate groups showed no significant difference. We conclude that synovial PPi turnover and elevated PPi fluid concentrations are not specific for PG patients, and that these factors alone cannot be the only determinants of CPPD crystal deposition.
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PMID:Inorganic pyrophosphate pool size and turnover rate in arthritic joints. 16 95

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

Colchicine, given locally, inhibits urate-crystal- and CaPPD-crystal-induced inflammation. Since this inflammation is known to be mediated in part by PGE1 these observations indicate colchicine acts as an anti-PG agent. Colchicine counteracts the phlogistic action of exogenous PGE1 in both urate- and CaPPD-crystal-induced inflammation. With use of large excesses of colchicine, its anti-inflammatory action appears limited to its anti-PGE1 activity. In turn, PGE1 counteracts the antiphlogistic action of colchicine. Colchicine is less effective in reducing swelling due to CaPPD-crystals than that due to urate-crystals, a finding similar to the clinical observations that colchicine is more effective therapy for gout than for pseudogout. Some relationships are reviewed to suggest that CaPPD-crystal inflammation is a more severe membrane disorder than is urate-crystal inflammation.
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PMID:Anti-prostaglandin action of colchicine. 16 97

Crystal identification is made with a polarizing, color-compensated light microscope. Most microscopes can be easily and inexpensively adapted for crystal identification. The color compensator allows differentiation between the monosodium urate crystals of gout and the crystals of pseudogout, or calcium pyrophosphate deposition disease. All synovial fluid specimens should be examined. The observation of phagocytosis of crystals establishes that they are the etiologic agent responsible for an ongoing acute attack of arthritis.
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PMID:An office technique for identifying crystal in synovial fluid. 16 59

Patients with hepatic glucose-6-phosphatase deficiency usually have a striking clinical syndrome during childhood and are readily diagnosed by the pediatrician. An adult patient had childhood manifestations of glucose-6-phosphatase deficiency that were mild and unrecognized; symptoms of tophaceous gout, urate nephropathy and characteristic blood chemical studies suggested the diagnosis at age 39. Subsequent epinephrine and galactose tolerance tests were characteristic of hepatic glucose-6-phosphatase deficiency and direct assay of hepatic glucose-6-phosphatase confirmed a partial deficiency of the enzyme. The case emphasized that patients with this deficiency may escape diagnosis during childhood and that internists should consider the diagnosis in adolescents or young adults with acute gouty arthritis or tophaceous gout.
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PMID:Partial deficiency of hepatic glucose-6-phosphatase in an adult patient. 16 24

The clinical and biochemical features of eleven patients with Type V hyperlipoproteinaemia have been reviewed. All patients were male, and there was a high incidence in the group of obesity, vascular disease, acute abdominal pain, gout, diabetes mellitus and alcoholism. Plasma cholesterol concentrations ranged from 212 to 1512 mg/100ml and triglycerides from 708 to 7670 mg/100 ml. Lipaemia was associated with significant hyponatraemia, and also interfered with the determination of plasma glucose and serum amylase. Chylomicronaemia and hyperprebetalipoproteinaemia were accompanied by reduction in the pools of beta and alpha lipoproteins. All lipoprotein classes were relatively depleted of cholesterol compared to triglyceride. There was a variable pattern of treatment response. In some patients alcohol withdrawal produced a rapid improvement in plasma lipids. In diabetes mellitus there were two types of response: a rapid one in chronic insulin deficiency, and secondly, a more gradual one in mild diabetes associated with hyperinsulinaemia. In other patients there was a rapid response to carbohydrate-calorie restriction but the respective contributions of each of the steps remained unclear.
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PMID:Type V hyperlipoproteinaemia re-visted: findings in a sydney population. 16 79

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


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