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Urate deposition

Tophi (urate deposits) are uncommon in gouty subjects and are a late complication of hyperuricemia. The most common sites of tophaceous deposits in patients with recurrent acute gouty arthritis are the base of the great toe, helix of the ear, olecranon bursae, Achilles tendon, knees, wrists, and hands. [Pg.15]

Allopurinol, a xanthine-oxidase inhibitor, may decrease tissue urate deposits in patients who are overproducers of uric acid, i.e. patients with primary hypemricaemia, in myeloproliferative neoplastic diseases and in hyperuricaemia resulting from tissue breakdown after cancer chemotherapy or radiation therapy. Allopurinol may also be recommended, in certain circumstances, in undersecre-tors of uric acid. [Pg.443]

Oosporein, which is produced primarily by Oospora colo-rans and Caetomium trilaterale, is observed in feed stuffs, cereals and peanuts. It has been reported to be toxic in poultry resulting in nephrotoxicity, and visceral and articular gout. The pathological observations in oosporein toxicity include necrosis of the tubular epithelial cells in the proximal tubules with basophilic casts, hyaline casts in the distal tubules with fibrosis and interstitial pyogranuloma-tous inflammation, urate deposits in various tissues, and proventricular enlargement with mucosal necrosis (Pegram and Wyatt, 1981 Brown et al, 1987). [Pg.570]

A uricosuric and renal tubular-blocking agent, probenecid inhibits the tubular resorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum uric-acid levels. Effective uricosuria reduces the miscible urate pool, retards urate deposition, and promotes resorption of urate deposits. [Pg.589]

It must be underlined however, that the daily de-novo-synthetized (not absolute) concentration of uric acid is responsible for the acid load. In the presence of tophi, one must further take into account that the monosodium urate, deposited in tophi (20), has been formed by leaving behind in extracellular fluid an equivalent amount of hydrogen ions. [Pg.26]

The patients had a much greater frequence of nephrolithiasis, crystalline urate deposits in synovial punch biopsies and were somewhat more tophaceous than expected.The severity of their gout was confirmed by the high incidence of radiographic finding of bone erosions and by the high number of joints involved for each patient. [Pg.116]

Case Sex Age Urate deposit Other diseases Drugs Plasma Creatinine urate clearance pmols/l mis/min ... [Pg.134]

CONCENTRATION OF URATE BY DIFFERENTIAL DIFFUSION A HYPOTHESIS FOR INITIAL URATE DEPOSITION... [Pg.184]

After three weeks on the diet containing oxonic acid and uric acid the following biochemical features were detected. There is clearly a statistically significant hyperuricemia, increased urinary urate concentration and increased tissue urate deposition. [Pg.189]

This experimental model provides opportunities for many novel experiments. Studies on the early evolution of the inflammatory response to renal urate deposition are possible. Conversely, the long-term sequelae of hyperuricemia and tissue urate deposition can be observed and correlated with renal function. Moreover, the modifying effect of the anti-inflammatory agents on the renal med-... [Pg.189]

Although the etiologic role of microcrystalline monosodium urate monohydrate in the pathogenesis of acute gouty arthritis has been well established, the mechanism by which urate precipitates in joints, soft tissues and the kidneys remains unclear. Some studies have suggested that the solubility of urate is the key factor and that when the solubility of urate in blood synovial fluid and urine is exceeded, urate then precipitates. The question is more complex than this, however, since only approximately 25 per cent of patients with hyperuricemia develop acute gouty arthritis. Furthermore, there is poor correlation between uric acid concentration and the frequency of acute gouty attacks. This has led to speculation that there are factors in serum which are partially responsible for solubilization of urate and that alterations in these factors could be responsible for urate deposition. [Pg.193]

Sodium urate deposits in the fibrous tissues near the joints or in the cartilage of the external ear present in gout. [Pg.1024]


See other pages where Urate deposition is mentioned: [Pg.193]    [Pg.2]    [Pg.48]    [Pg.2693]    [Pg.181]    [Pg.1498]    [Pg.221]    [Pg.221]    [Pg.133]    [Pg.135]    [Pg.159]    [Pg.183]    [Pg.129]   


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Urate Deposits without Gouty Arthritis

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