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)

Sally Chesson and Sarah Redfern give an overview of the signs, symptoms and nursing care of individuals suffering from gout. Principally a disease affecting men, this condition, extremely painful in the acute stages, is definitively diagnosed by the detection of crystals in joint aspirate. Pain results from the deposition of crystalline sodium urate in the synovial joint but nursing care also requires consideration of associated immobility, anxiety and irritability which the patient may experience.
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PMID:Gout: nursing and medical actions. 212 52

Sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS PAGE) and western blot techniques were used to analyze proteins adsorbed in vitro to synthetic monosodium urate crystals (MSUC) from a variety of gouty biologic fluids. Distinct differences in adsorbed proteins were found in comparing synovial fluid (SF) with serum or plasma, particularly at 220 kD and below 19 kD. Further studies should consider the importance of the synovial milieu. Patterns of proteins adsorbed to MSUC from the SF of all 12 patients with gout were similar. A considerable number of polypeptides appeared to be selectively adsorbed. Of these, polypeptides associated with fibronectin, C1q and IgM were identified by immunotransblotting. The experiments also demonstrated that the overall polypeptide patterns obtained by SDS PAGE of eluates from MSUC exposed to SF were unaffected by heating MSUC to 180 degrees C, as well as by the volume of SF in the incubation mixture.
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PMID:Binding of synovial fluid proteins to monosodium urate crystals in vitro. 234 33

The calcium antagonists are effective and safe agents for the treatment of arterial hypertension. They are well tolerated by the patients. In contrast to other types of antihypertensive agents, they cause few metabolic disturbances. They can be combined with diuretics, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors. They can be safely prescribed to patients with hypertension and concomitant diseases such as diabetes mellitus, chronic obstructive lung disease, congestive heart failure, gout, renal failure, peripheral atherosclerotic disease, or Raynaud's phenomenon. Dietary sodium restriction during antihypertensive therapy with calcium antagonists is not required for optimal antihypertensive efficacy. The second generation of calcium antagonists especially the dihydropyridine analogues that have greater potency and vascular selectivity, and a longer duration of action, will optimize the treatment of hypertension. Their antiatherosclerotic, antiplatelet, and "antitrophic" effects in experimental models for atherogenesis and hypertension hold great promise for the future since, so far, there has been no major success in reducing the incidence of coronary death by the treatment of hypertension.
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PMID:Calcium antagonists in hypertension. 265 29

A case of a 23 year-old-man with a history of polyarthritis and chronic tophaceous gout is reported. He developed a crural paraparesis caused by sodium urate deposits in the spinal canal. Decompressive laminectomy and removal of urate-laden ligamentum flavum was performed without improvement. According to the literature there are nine cases previously reported.
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PMID:[Paraparesis due to gout]. 269 12

During a study of clinical and laboratory features in 83 patients with sickle cell disease in the Netherlands, serum creatinine, sodium, potassium, uric acid and osmolality were determined and reported for 65: 39 with homozygous sickle cell (SS) disease, 5 with beta degrees thalassaemia (S beta degrees thal), with sickle cell beta + thalassaemia (S beta degrees + thal) and 17 with sickle cell haemoglobin C (SC) disease. Data on history of hyposthenuria was unreliable. Haematuria was reported in 6 (7%) of the 83 patients. Four of the six patients with a history of haematuria, two of whom had elevated creatinine levels, had SS disease. Lower mean levels of serum sodium and higher levels of serum potassium were observed in SS's than in the other genotypes (p less than 0.001). Hyperkalaemia of greater than 5 mmol/l was seen in 50% of SS disease cases and in 33% of paediatric SC disease cases. Some high potassium levels must be ascribed to in vitro haemolysis. The rate of hyperuricaemia ranged from 24% to 40% among the various genotypes. Clinical gout was not observed.
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PMID:Renal and electrolyte profile in steady state sickle cell disease: observations in patients with sickle cell disease in The Netherlands. 276 58

The activity of the plasma membrane Na+/K+-ATPase and cellular sodium (Nai) and potassium (Ki) content were analysed in RBCs from 15 rheumatoid arthritis (RA) and 30 reference subjects (11 healthy controls, 12 osteoarthritis and 7 gouty patients). Na+/K+-ATPase activity was determined by measuring the inorganic phosphate (Pi) released by incubation in a reaction medium in the presence and absence of K ions or ouabain. Nai and Ki were measured with an ion-selective electrode analyser on the hemolysates, after washing the RBCs in 110 mM MgCl2. The Na/K-ATPase activity was significantly lower in RA patients than in both healthy controls and patients with osteoarthritis or gout. A slight but significant increase in Nai was observed in rheumatoid subjects. It is hypothesized that the decrease in the Na+/K+-ATPase activity in RA may be the result of a defective expression of membrane proteins, which is probably related to the altered cell sensitivity observed.
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PMID:Decreased NA+, K+-ATPase activity in erythrocyte membrane from rheumatoid arthritis patients. 282 52

The influence of a once daily dose of 200 mg celiprolol alone and in combination with 12.5 mg chlorthalidone on uric acid and electrolyte metabolism was investigated in 22 hypertensive patients with gout in a randomized trial. All patients were treated with allopurinol and diet. A four weeks treatment with celiprolol (11 patients) showed no influence on uric acid metabolism, electrolytes, blood glucose, cholesterol and triglycerides. Under treatment with celiprolol plus chlorthalidone (11 patients) only a small rise in serum uric acid was observed after four weeks but at the same time uric acid clearance and excretion increased significantly. There was no obvious change in serum electrolytes but an increase in sodium, potassium and chloride urine excretion. Serum uric acid, uric acid clearance and excretion decreased during a 6 months treatment period. A small decrease in cholesterol and triglycerides was observed. Blood pressure decreased in both treatment groups but there was only a small change in heart rate.
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PMID:[Uricosuric action of a new beta receptor blocker-diuretic drug combination]. 287 73

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

Monosodium urate crystals are clearly related to acute attacks of gout and to the hard tissue destruction of chronic tophaceous gout. Fortunately, the acute attacks are readily treated with anti-inflammatory drugs, and destructive changes due to tophi may be prevented or reversed, at least in part, by the intelligent control of serum urate levels. Control of gout is one of the premier success stories of modern medicine. In contrast, the number of patients who have arthritis associated with crystals that contain calcium appears to be rising--perhaps a function of better recognition, perhaps related to the aging of the population. CPPD and BCP crystals can be associated with acute or subacute inflammation, but as in acute gout, it is easily controlled with anti-inflammatory drugs or by local injections of corticosteroids. A direct relationship of BCP and CPPD crystals to the associated destructive arthropathies has been hypothesized and is supported by clinical observations, animal studies, and in vivo experiments. Unlike gout, which is usually associated with a systemic metabolic abnormality (i.e., hyperuricemia), calcium crystals deposition seem to be a localized phenomenon, although numerous local sites in several joints are often involved in a given patient. Tissue degeneration in gout clearly follows (tophaceous) crystal deposition. Calcium crystal deposition may follow, rather than precede, destructive joint changes. Alternatively, both destructive changes and crystal deposition may derive independently from a common, still obscure, biochemical abnormality of joint tissues. P. A. Dieppe and colleagues believe that calcium crystal deposition follows either primary or secondary tissue degeneration but that the crystals exert a positive feedback effect (amplification loop) that accelerates degeneration. Each of those formulations of a pathogenetic role for crystals may be true in a given case, analogous to the etiology of primary and secondary forms of hyperuricemia and to sodium urate crystal deposition coexistent with osteoarthritis (tophus formation in Heberden's nodes). Conclusive proof of a significant role for BCP or CPPD crystals in the pathogenesis of human joint tissue damage depends on interrupting the postulated disease mechanism and showing that this prevents joint deterioration and leads to significant repair of existing damage. Our current position is somewhat analogous to that of our colleagues who had to contend with management of gouty arthritis before the advent of effective drugs for control of hyperuricemia.
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PMID:Arthropathies associated with calcium-containing crystals. 302 71

Indices of past lead absorption were measured and compared in patients with chronic renal failure from many causes, including some with chronic lead nephropathy. X-ray fluorescence (XRF) yielded finger bone lead concentrations by a new in vivo method. These correlated significantly with excess urinary lead following calcium di-sodium EDTA (ethylenediamine tetra-acetate) and erythrocyte lead concentration. Discriminant function analysis demonstrated that the patients in the study could be separated into two groups without any reference to the EDTA lead excretion test using the following variables, all of which contributed significantly to the discrimination. In order of importance, these were: a childhood history of acute lead poisoning, a history of gout, a family history of gout and detectable XRF finger bone lead. Although the XRF finger bone lead measurement is convenient and non-invasive, its lack of sensitivity (48%) limits its usefulness as a screening test for chronic lead nephropathy.
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PMID:Chronic lead nephropathy in Queensland: alternative methods of diagnosis. 308 47


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