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)

Effect of a non-steroidal anti-inflammatory drug, pranoprofen (PPF), on sodium urate crystal-induced inflammation was investigated in comparison with standard drugs for treating acute gout in experimental animals. PPF inhibited sodium urate crystal-induced paw edema in both rats (1-10 mg/kg, p.o.) and mice (5-25 mg/kg, p.o.) in a dose-dependent manner. On rat sodium urate crystal-induced paw edema, PPF was found to be almost equally active as indomethacin (IM) and colchicine. In addition, PPF (2.5-10 mg/kg, p.o.) inhibited the accumulation of exudate and decreased the leucocyte numbers and the amount of prostaglandin E2 (PGE2)-like substance in sodium urate crystal-induced pleurisy in rats dose-dependently, with a potency slightly greater than that of IM. The specific anti-gout agent colchicine (5 mg/kg, p.o.) also suppressed the accumulation of exudate and decreased the leucocyte numbers, without affecting the amount of PGE2-like substance. Moreover, in mouse peritonitis, PPF (1-10 mg/kg, p.o.) suppressed the sodium urate crystal-induced increase in vascular permeability in a dose-dependent manner. Furthermore, in experimental models of articular gout, PPF inhibited the pain response (abnormal gait) of sodium urate crystal-induced arthritis in both rats (0.25 and 1 mg/kg, p.o.) and dogs (3 mg/kg, p.o.), with a potency greater than that of IM and phenylbutazone, respectively. These results indicate that as an anti-gout agent, PPF is at least as effective as other standard drugs, so that it should have good clinical potential.
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PMID:[Effect of pranoprofen on sodium urate crystal-induced inflammation]. 358 35

A 37-year-old man presented with panniculitis of the legs that, on biopsy, showed aggregates of crystals whose appearance suggested sodium urate. Based on this finding, a uric acid level was obtained which proved to be markedly elevated. The patient subsequently developed gouty arthritis. Gout should be added to the differential diagnosis of causes of panniculitis, and biopsy specimens of panniculitis should be carefully examined for crystals.
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PMID:Gout presenting as lobular panniculitis. 363 56

Gout is a disease linked to altered uric acid metabolism with increased uric acid concentration in the blood, the deposition of sodium urate crystals in certain tissues and abscesses. Uric acid derives from ex novo purinogenesis and the catabolism of cellular and alimentary nucleic acids. It is eliminated by uricolysis mainly in the intestines and renal excretion. The restriction of dietary protein purines, fats and calories reduces uricemia and explains the relationship between gout and diet. In Europe 5-18% of adult males suffer from uricemia with gout occurring in 0.5-1%. The incidence among females is much lower. The clinical picture presents an acute phase with a gouty abscess linked to the swollen joints caused by sodium urate crystals and a chronic phase characterised by gouty tophi and chronic gouty arthropathy. Treatment of the acute phase in which ample use is made of colchicine must be followed by medical and dietary treatment of the chronic condition.
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PMID:[Arthropathies and nutrition: gout]. 372 25

A typical gouty tophus with birefringent, dichroic, needle shaped crystals was found in a resected calcified aortic valve on routine histological examination. The patient, an elderly man, had a long history of gout. X-ray diffraction confirmed the presence of sodium acid urate monohydrate and identified hydroxyapatite and whitlockite in the accompanying dystrophic calcification of the aortic valves. Previous reports indicate that gouty tophi of the cardiac valves are rare: of the nine cases reported, eight occurred in the mitral valve.
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PMID:Aortic valvular tophus: identification by X-ray diffraction of urate and calcium phosphates. 403 Oct 99

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

We have previously described a 14-yr-old boy with hyperuricemia, renal failure, and accelerated purine production resistant in vivo and in vitro to purine analogs. This patient demonstrated normal red cell hypoxanthine-guanine phosphoribosyltransferase (HPRT) heat stability, electrophoresis at high pH, and activity at standard substrate levels. In the present report an abnormal HPRT enzyme was demonstrated by enzyme kinetic study with phosphoribosylpyrophosphate (PRPP) as the variable substrate and inhibitory studies with sodium fluoride. Apparently normal HPRT activity in a patient with hyperuricemia and gout does not exclude a functionally significant HPRT mutation.
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PMID:Hypoxanthine-guanine phosphoribosyltransferase variant associated with accelerated purine synthesis. 435 74

The responses of cultured rabbit synovial fibroblasts to amorphous and microcrystalline calcium oxalate were compared with responses to MSUM. Like urate crystals, crystalline calcium oxalate (but not amorphous oxalate) caused marked stimulation of secretion of latent collagenase and PGE2 after 3 days of culture without significant change in cell protein or gross cellular morphology. Collagenase rose from undetectable levels in control cultures to 32.4 +/- 6.0 and 27.4 +/- 7.9 U/mg of cell protein for crystalline calcium oxalate and MSUM, respectively. PGE2 rose from a control level of 0.24 +/- 0.14 to 19.47 +/- 5.15 and 23 +/- 4.84 micrograms/mg of cell protein for crystalline calcium oxalate and sodium urate compared to 1.22 +/- 0.48 microgram for amorphous calcium oxalate. Although the crystalline species studied caused LDH in the media to increase threefold, this was minimal. Cell stimulation by amorphous oxalate and the crystals did not correlate with membranolytic potential as measured with an erythrocyte lysis assay. Stimulation of resident synovial cells by crystalline calcium oxalate and sodium urate may contribute to the chronic inflammation and destruction of joint tissues that occurs in oxalosis and gout.
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PMID:Stimulation of synovial fibroblasts by calcium oxalate and monosodium urate monohydrate. A mechanism of connective tissue degradation in oxalosis and gout. 629 14

20 patients with an attack of acute gout participated in this double-blind study, ten patients received N-(2,6-dichloro-m-tolyl)anthranilic acid, sodium salt (meclofenamate sodium, Meclomen) and ten indometacin. The median time interval between onset of attack and onset of treatment was 11 h in the meclofenamate sodium group and 14 h in the indometacin group; medication was started with a dose of 200 mg meclofenamate sodium or 25 mg indometacin followed by 100 mg meclofenamate sodium or 25 mg indometacin every 4 h for the first 24 h. Thereafter patients received 100 mg meclofenamate sodium or 50 mg indometacin at 8-h intervals for 6 days. Similar improvement of intensity of spontaneous pain, swelling, tenderness of touch and degree of limitation of function was noted in patients of both treatment groups. This improvement could already be noted after 24 h of treatment and was sustained throughout the medication period and follow-up period. Adverse reactions were reported by 2 patients in the meclofenamate sodium group and by 5 patients in the indometacin group. The results of this double-blind study indicate that meclofenamate sodium in the dose administered was equally effective in relieving pain and inflammation and restoring restricted function in patients with acute gout as indometacin when used in the generally recommended dose for this indication. Meclofenamate sodium, even at these high dosage levels, was better tolerated than indometacin.
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PMID:Meclofenamate sodium in the treatment of acute gout. Results of a double-blind study. 634 48

An appreciation of the physiology of fasting is essential to the understanding of therapeutic dietary interventions and the effect of food deprivation in various diseases. The practice of prolonged fasting for political or religious purposes is increasing, and a physician is likely to encounter such circumstances. Early in fasting weight loss is rapid, averaging 0.9 kg per day during the first week and slowing to 0.3 kg per day by the third week; early rapid weight loss is primarily due to negative sodium balance. Metabolically, early fasting is characterized by a high rate of gluconeogenesis with amino acids as the primary substrates. As fasting continues, progressive ketosis develops due to the mobilization and oxidation of fatty acids. As ketone levels rise they replace glucose as the primary energy source in the central nervous system, thereby decreasing the need for gluconeogenesis and sparing protein catabolism. Several hormonal changes occur during fasting, including a fall in insulin and T(3) levels and a rise in glucagon and reverse T(3) levels. Most studies of fasting have used obese persons and results may not always apply to lean persons. Medical complications seen in fasting include gout and urate nephrolithiasis, postural hypotension and cardiac arrhythmias.
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PMID:Fasting: the history, pathophysiology and complications. 675 55

The necropsy of an 84-year-old woman with painful polyarticular gout showed a severe erosion of the L2 vertebral body due to sodium urate deposition. The radiological signs of this tophus had existed for many years; it had caused recurrent pain but no neurological complications. A small tophus and a Schmorl's node on 2 neighbouring thoracic vertebrae permitted the differentiation between vertebral plate erosion in the first, which was of bone origin, and vertebral plate remodelling in the second, which originated in the cartilaginous tissue of the disc.
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PMID:Spondylodiscal erosions due to gout: anatomico-radiological study of a case. 685 68


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