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)

Serum levels of carrier proteins, transferrin, ceruloplasmin and albumin were determined in patients with rheumatic disorders, along with serum levels of acute phase proteins, ceruloplasmin, alpha 1-acid glycoprotein and alpha 1-antitrypsin. Depressed levels of transferrin occurred in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Albumin was reduced in SLE and RA men. Acute phase reactants which are protective in inflammation were elevated in RA, osteoarthritis (OA), gout, pseudogout (PsG), and SLE. All of these rheumatic disorders show biochemical changes compatible with systemic inflammatory disease including gout and PsG which are considered local disorders and OA which is considered noninflammatory arthritis.
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PMID:Serum proteins--transferrin, ceruloplasmin, albumin, alpha 1-acid glycoprotein, alpha 1-antitrypsin--in rheumatic disorders. 31 26

Protein binding of urate may have some pertinence to the pathogenesis of gout. However, binding studies have been hampered by problems with in vitro methodology and by the problem of relating the results of in vitro studies to the physiological situation. In the present study urate binding was determined by an ultrafiltration procedure. All manipulations were performed anaerobically and at 37 degrees in order to maintain the sample under physiological conditions. Normal urate bound was 15 +/- 7.5% in males and 10 +/- 6.6% in females. Urate binding did not correlate significantly with either the albumin or total urate concentration. It is suggested that the interaction between protein and urate is influenced by a number of factors other than the concentrations of free urate and binding protein. Some possible ones are discussed. The techniques described might usefully be applied to a study of urate binding in various pathological states.
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PMID:The binding of urate by plasma proteins. 47 69

The interactions between sodium urate monohydrate (MSU) crystals and human serum albumin (HSA) were investigated in vitro in relation to the disease of gout. It was found that HSA accelerates (by up to ten times or even more) the nucleation of MSU crystals at a pH of more than 7.5, but only to a much lesser extent (1.2 times) at pH 7.0. Protein denaturation, as well as blocking exposed carboxylate groups on the protein, substantially reduced the nucleating effect. By use of immunofluorescence, immunogold labelling and crystal morphology studies, albumin was shown to interact preferentially with the (110) faces of MSU crystals. Taking these results into consideration, a mechanism is proposed whereby albumin stabilizes MSU crystal nuclei by interaction of structured carboxylate-containing protein domains with planes of the incipient crystal exposing sodium cation layers.
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PMID:A structural approach to pathological crystallizations. Gout: the possible role of albumin in sodium urate crystallization. 290 44

The amount of the initiating complement component (Clq) in the classical pathway and the first essential component (C3) in the alternative complement pathway were measured with a single radial immunodiffusion (SRID). A high ionic strength was used corresponding to that of 0 . 25 M NaCl and 0 . 01 M EDTA to avoid nonspecific binding of Clq with immune aggregates. Measurements were made on sera and/or synovial fluids from 165 patients with various bone and joint diseases. Values of Clq and C3 in synovial fluids were also expressed as ratios to that of albumin in the same specimens to avoid the influence of differences in volume of synovial fluid in various diseases, and this appeared to provide a reliable index reflecting pathological conditions. Both serum Clq and C3 levels were raised highly in rheumatoid arthritis, gout, and osteomyelitis, but the extent of the elevation of C3 was less conspicuous. Values of Clq and C3 in synovial fluids also markedly increased in rheumatoid arthritis.
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PMID:Immunochemical quantitation of complement components of Clq and C3 in sera and synovial fluids of patients with bone and joint diseases. 677 72

A review of the clinical applications and of the disposition of probenecid in man, including drug interactions, is presented. Probenecid is the classical competitive inhibitor of organic acid transport in the kidney and other organs. There are 2 primary clinical uses for probenecid: as a uricosuric agent in the treatment of chronic gout and as an adjunct to enhance blood levels of antibiotics (such as penicillins and cephalosporins). Adsorption of probenecid is essentially complete following oral administration. The drug is extensively metabolised by glucuronide conjugation and by oxidation of the alkyl side chains; oxidation of the aromatic ring does not occur. The half-life of probenecid in plasma (4 to 12 hours) is dose-dependent. Renal excretion is the major route of elimination of the metabolites; excretion of the parent drug is minimal and is dependent on urinary pH. Probenecid and its oxidised metabolites are extensively bound to plasma proteins, mainly to albumin. Tissue concentrations (based on animal studies) are generally lower than plasma concentrations. Most of the drug-drug interactions involving probenecid are due to an effect on the kidney-block of transport of acidic drugs. Similarly probenecid affects the tubular secretion of a number of acidic endogenous substances by the kidney. Probenecid is also involved in the block of transport of acidic metabolites of catecholamines, for example homovanillic and hydroxyindoleacetic acids, in the brain. There are a number of analytical procedures for the assay of probenecid. These are based on spectrophotometry, spectrofluorometry, gas and liquid chromatography and radioimmunoassay.
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PMID:Clinical pharmacokinetics of probenecid. 701 57

Turkey poults were fed diets containing oosporein at concentrations of 0, 500, 1,000, and 1,500 micrograms/g from hatching until three weeks of age. Low feed consumption resulted in poor growth rates at every dietary level of oosporein; however, a dose-related increase in water consumption was observed. The most significant effect of dietary oosporein was severe visceral and articular gout, with death ensuing in 24 and 52% of the poults at the 1,000 and 1,500 micrograms/g levels, respectively. Gout and mortality were absent at 0 and 500 micrograms/g. In addition to tissue urate deposition, necropsies revealed dehydration, swollen pale kidneys, hemorrhagic proventriculitis with mucosal necrosis, gizzard enlargement and lining discoloration, an increase in gall bladder size, and focal hepatic necrosis. The relative weights of the kidney, liver, proventriculus, gizzard, and pancreas were increased in a dose-related fashion; spleen and bursa weights were unaffected. Among plasma constituents, uric acid, urea, and the activities of glutamic-oxalacetic transaminase and lactic dehydrogenase were elevated in response to dietary oosporein; albumin, potassium, phosphorus, and calcium were decreased. The toxin had no effect on plasma total protein, sodium, glucose, cholesterol, triglycerides, alkaline phosphatase, or creatine phosphokinase. These data substantiate the original classification of oosporein as a nephrotoxin and etiologic agent of gout in avian species.
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PMID:Oosporein-toxicosis in the turkey poult. 709 45

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

Low levels of oestrogen, FSH and LH in serum have been reported in patients with gout. The mechanism by which sex hormones affect the development of gout is unknown, but some investigators believe that it is related to the influence of oestrogens on serum uric acid levels. We studied the relationship between serum uric acid and 17 beta oestradiol (ES) levels in asymptomatic hyperuricaemic (ASH) men in order to test the hypothesis that low ES levels are associated with hyperuricaemia. Thirty-eight men with asymptomatic hyperuricaemia (ASH) were selected from a population of healthy individuals undergoing periodical multiphasic health examinations. After adjusting for the differences in albumin levels between the two groups, no significant difference in serum ES level was found. The serum testosterone levels were similar in both groups. These findings suggest that there is no difference in the sex hormone profiles between asymptomatic hyperuricaemic and normouricaemic men.
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PMID:Serum 17-beta-estradiol and testosterone levels in asymptomatic hyperuricaemic men. 808 62

The self-limiting response to urate crystals allows the exploration of events involved in both the onset and resolution of gout. Using i.v. injected radiolabelled anti-E-selectin monoclonal antibody 1.2b6 together with differentially radiolabelled neutrophils, mononuclear cells and albumin, we have characterized the expression of E-selectin in relation to leucocyte traffic, microvascular permeability and clinical sequelae following intracutaneous injection of monosodium urate crystals. We found that the inflammatory response in this model involved several distinct phases. First, E-selectin expression increased over 2-6 h in the context of increases in neutrophil and mononuclear cell accumulation, and albumin leakage. Secondly, leucocyte accumulation rapidly declined despite persisting E-selectin expression. Thirdly, E-selectin expression peaked at approximately 8 h and then fell despite an increase in clinically detectable erythema and induration. Lastly, these clinical manifestations of inflammation resolved despite the continued presence of urate crystals in the tissues. The further dissection of mechanisms regulating these phases will lead to a better understanding of events in both the pathogenesis and resolution of gout. Of broader significance, this inflammatory model may yield information about the protective events that underly resolution of inflammation, and provide insights into factors which determine chronicity.
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PMID:Characterization of E-selectin expression, leucocyte traffic and clinical sequelae in urate crystal-induced inflammation: an insight into gout. 862 35

To assess the physiologic effects of cherry consumption, we measured plasma urate, antioxidant and inflammatory markers in 10 healthy women who consumed Bing sweet cherries. The women, age 22-40 y, consumed two servings (280 g) of cherries after an overnight fast. Blood and urine samples were taken before the cherry dose, and at 1.5, 3 and 5 h postdose. Plasma urate decreased 5 h postdose, mean +/- SEM = 183 +/- 15 micro mol/L compared with predose baseline of 214 +/- 13 micro mol/L (P < 0.05). Urinary urate increased postdose, with peak excretion of 350 +/- 33 micro mol/mmol creatinine 3 h postdose compared with 202 +/- 13 at baseline (P < 0.01). Plasma C-reactive protein (CRP) and nitric oxide (NO) concentrations had decreased marginally 3 h postdose (P < 0.1), whereas plasma albumin and tumor necrosis factor-alpha were unchanged. The vitamin C content of the cherries was solely as dehydroascorbic acid, but postdose increases in plasma ascorbic acid indicated that dehydroascorbic acid in fruits is bioavailable as vitamin C. The decrease in plasma urate after cherry consumption supports the reputed anti-gout efficacy of cherries. The trend toward decreased inflammatory indices (CRP and NO) adds to the in vitro evidence that compounds in cherries may inhibit inflammatory pathways.
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PMID:Consumption of cherries lowers plasma urate in healthy women. 1277 24


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