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)

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 effect of fructose on liver metabolism in patients with hereditary fructose intolerance (HFI) and in heterozygotes for HFI was studied by 31P magnetic resonance spectroscopy (31P-MRS). In patients with HFI (n = 5) ingestion of small amounts of fructose was followed by an increase in sugar phosphates and decrease in inorganic phosphate (Pi) in the liver that could be detected by 31P-MRS. 31P-MRS could be used to diagnose fructose intolerance and to monitor the patients' compliance with a fructose-restricted diet. In heterozygotes (n = 8) 50 g fructose given orally led to accumulation of sugar phosphates and depletion of Pi in the liver. Fructose also induced a larger increase in plasma urate in heterozygotes than in control subjects. The effect of fructose on liver Pi and plasma urate was most pronounced in heterozygotes with gout (n = 3). Heterozygosity for HFI may predispose to hyperuricaemia.
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PMID:Study of hereditary fructose intolerance by use of 31P magnetic resonance spectroscopy. 288 61

We report an asymptomatic man found to have simultaneous renal transport defects for magnesium and phosphate. Associated findings include gout, high frequency hearing loss, chronic elevations of SGOT and SGPT, metabolic bone disease, and hyperparathyroidism. The clinical expression of hyperparathyroidism was masked for 5 years by hypomagnesemia, and the patient became hypercalcemic only when magnesium levels were normalized by intravenous infusion. Both the phosphate and magnesium transport abnormalities persisted after parathyroidectomy. The many unique features of this case distinguish it from previously described disorders of magnesium or phosphate wasting.
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PMID:Renal wasting of magnesium and phosphate. 344 Nov 43

Osteoarthritis or 'Joint Failure' is a multi-factorial disease with a final common pathway of cartilage degeneration and bone eburnation. The association of arthritic disease and joint degeneration with the deposition of sodium urate crystals in gout and calcium pyrophosphate crystals in pseudogout (chondrocalcinosis) is clinically well established. Electron microscopy coupled with electron probe analysis has revealed the presence of various other calcium phosphate crystals in joint tissues and fluids. We have found three new morphological types of apatite crystals in human articular cartilage which are too small to be detected by X-rays of human joints or even by light microscopy of joint tissues. Two morphologically distinct types of apatite crystals in articular cartilage are associated with extracellular matrix vesicles formed from the cell processes of chondrocytes. 'Cuboid' crystals, which are found in the pericellular regions near the surface zone of articular cartilage, appear to be a variant of apatite and may even be 'Whitlockite' because there are traces of magnesium present. There are increased numbers of these microscopic 'cuboid' crystals (Type II) and Mineral Nodules (Type I) in arthritic cartilage and this is coupled with increased numbers of matrix vesicles and alkaline phosphatase activity. Clusters of fine needle-shaped apatite crystals (Type III) found on the surface of articular cartilage are not associated with matrix vesicles. Thus some forms of osteoarthritis are closely associated with apatite type crystal deposition and may imply abnormal mineral formation in articular cartilage as a pathogenic mechanism.
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PMID:Apatite-type crystal deposition in arthritic cartilage. 409 1

A simple, rapid screening method using alizarin red S stain and ordinary light microscopy to detect microcrystalline or noncrystalline calcium phosphate salts was used on wet drop preparations of synovial fluids. This proved to be helpful in detecting apatite crystal clumps and small calcium pyrophosphate dihydrate (CPPD) crystals missed by polarized light. The staining was positive in 100% of synovial fluids from patients later proven to have apatite and/or CPPD deposition diseases. Apatite and CPPD crystals were commonly found together in the same fluids. In addition, some synovial fluids from patients with osteoarthritis, renal failure dialysis, rheumatoid arthritis, and gout also exhibited positive staining. The correlation of positive alizarin red S staining with radiologic evidence of osteoarthritis suggests that apatite crystals might be related to articular cartilage degeneration in different rheumatic diseases.
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PMID:Alizarin red S staining as a screening test to detect calcium compounds in synovial fluid. 618 60

Superactivity of phosphoribosylpyrophosphate (PRPP) synthetase is one of several hereditary enzyme abnormalities associated with gout and excessive uric acid excretion. Although measurement of PRPP synthetase activities in erythrocyte lysates should provide a practical means to detect abnormalities of the enzyme, reported values for normal individuals have varied considerably. We describe a radioisotopic procedure for measurement of PRPP synthetase activities in dialyzed hemolysates under a variety of conditions permitting evaluation of enzyme catalytic function and responsiveness to inhibitors and activators. Utilizing this procedure, enzyme activities for normal individuals were higher than generally reported, a difference attributable in part to the following measures undertaken to assure accuracy in activity determinations: precise control of pH of reaction mixtures, provision of verified excesses of the auxiliary enzyme adenine phosphoribosyltransferase, and measurement of all of the radiolabeled products of the assay. Under each condition of measurement, enzyme activities in 44 normal individuals, 13 patients with gout and normal uric acid excretion, and 10 patients with gout and uric acid overproduction were indistinguishable. In four additional individuals with uric acid overproduction, however, excessive enzyme activities were identifiable at all inorganic phosphate concentrations, but responses to purine nucleotide inhibitors were normal. In hemolysates from a patient with an inhibitor-resistant PRPP synthetase, an altered pattern of inorganic phosphate activation and diminished nucleotide inhibitor response was demonstrated. Our studies confirm the ability of the assay procedure to detect kinetically distinct variant forms of PRPP synthetase. Application of this procedure should aid in evaluation of the prevalence of derangements of PRPP synthetase among patients with gout and uric acid overproduction.
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PMID:Diagnostic evaluation of phosphoribosylpyrophosphate synthetase activities in hemolysates. 632 65

An outbreak of urolithiasis that doubled the annual mortality rate of chickens in a large flock of table-egg-layers is described. Despite the presence of a large unilateral urolith and/or severe renal atrophy, the layers often maintained active egg production and apparent homeostasis until a small urolith blocked the ureteral flow from the contralateral kidney. This terminal episode appeared to produce acute obstructive renal failure, rapidly developing visceral gout (visceral urate deposition), uremia, and death. The atrophy observed appeared to be acquired and progressive. Histologic features in the kidneys were acute to chronic glomerulonephritis, interstitial nephritis, and pyelonephritis. Epizootiologic and microbiologic studies indicated that a combination of infectious and noninfectious mechanisms may have been involved. Causative roles for calcium-phosphate imbalance, infectious bronchitis (IB), Newcastle disease (ND), and adenovirus or reovirus infections could be neither excluded nor confirmed. Contributory factors may have been spray ND-IB and other vaccinations of 15-week-old ND-IB-susceptible pullets, water deprivation, shipping stress, Mycoplasma synoviae infection, immune complex disease, and mycotoxins.
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PMID:Epizootiology, pathology, and microbiology of an outbreak of urolithiasis in chickens. 672 98

1. Variables that affect the measurement of purine synthesis de novo in human lymphocytes were studied and a reliable method of measurement of purine synthetic activity in these cells was established. 2. Purine synthesis de novo was measured as the rate of incorporation of [14C] formate into alpha-N-formylglycinamide ribonucleotide when further steps in the biosynthetic pathway had been blocked by azaserine. Incubation was carried out in a synthetic medium with a high phosphate concentration (25 mmol/l). 3. Purine synthesis de novo was measured in lymphocytes obtained on several occasions both from control subjects and from patients with gout, particularly those who tended to overproduce urate as suggested by high values of urinary urate. 4. Lymphocytes obtained from each individual on different occasions showed considerable variations in purine biosynthetic activity. This variation was such that there was no difference between the mean values obtained for the gouty subjects and the control subjects. 5. No correlation was obtained between the mean purine synthetic activity de novo in lymphocytes and either the serum urate concentration or the 24 h urinary urate excretion on a purine-free diet. 6 Apart from those with recognized enzyme mutations, no subgroup of the gouty population has been demonstrated in whom isolated lymphocytes demonstrate an intrinsic abnormality of purine synthesis de novo.
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PMID:Purine synthesis de novo in lymphocytes from patients with gout. 711 83

Of 264 patients with urolithiasis those with pure uric acid or urate stones were compared to those with other types of calculi for differences in epidemiologic factors and uric acid, calcium and phosphate metabolism. Patients with uric acid stones were predominantly older men. These patients had comparatively lower incomes and spent less money on food but consumed more alcohol. The urinary pH was lower than in the other groups. The absence of abnormally elevated serum uric acid levels and elevated 24-hour urinary uric acid excretion suggests this variety of uric acid lithiasis to be idiopathic in nature. This finding is supported by the results of standardized oral purine loading, which showed no post-loading differences in serum levels and revealed urinary concentrations in 12 patients with pure uric acid stones and 10 normal subjects. However, there is evidence to suggest that this condition may be a precursor of primary gout. Hereditary mechanisms are absent and the relapse rate is the same as in patients with other stones. Therefore, our results suggest the existence of an idiopathic variety of uric acid lithiasis that, at least in central Europe, occurs more frequently than previously assumed. The condition is not inherited, alcohol consumption is a major etiologic factor and there is no evidence of a causative role of abnormalities in purine metabolism.
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PMID:Idiopathic uric acid lithiasis: epidemiologic and metabolic aspects. 715 74

A high-performance liquid chromatographic method was developed for the determination of plasma purine nucleoside phosphorylase activity. In this method, the reaction mixture consisted of 15 microliters of plasma and 285 microliters of 50 mM phosphate buffer (pH 7.4) containing 3.8 mM inosine and 0.15 mM 2-(3-cyano-4-isobutoxyphenyl)-4-methyl-5-thiazolecarboxylic acid (strong xanthine oxidase inhibitor). After the reaction, the hypoxanthine produced was monitored to express plasma purine nucleoside phosphorylase activity. By this method, the activity of purine nucleoside phosphorylase was easily determined even with a small-volume plasma sample and despite its low activity in plasma. In addition, plasma purine nucleoside phosphorylase activity can be accurately determined even if the plasma is turbid. As a result, we were able to measure plasma purine nucleoside phosphorylase activity in patients with gout or asthma and healthy subjects, whereby it was demonstrated that plasma purine nucleoside phosphorylase activity was higher in patients with asthma than in either healthy subjects or patients with gout.
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PMID:Determination of plasma purine nucleoside phosphorylase activity by high-performance liquid chromatography. 766 72


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