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Of gout

Information on the toxic effects of molybdenum in humans is scarce. A high incidence of gout was reported in a locale in Armenia where the soil contained exceptionally high levels of both molybdenum and copper (15). However, the significance of the suggested correlation is questionable because of the lack of information on the study population and the absence of a control group. [Pg.463]

The active principle of the autumn crocus (Colchicum autumnale), colchicine (48), is one of the very few drugs that have remained in reputable medical use since ancient times. This drug was the only useful treatment available for the excruciating pain associated with crystallization of uric acid in the joints characteristic of gout until the advent of allopurinol. Although the precise mechanism by which colchicine gives this dramatic relief remains undefined, the antimitotic activity of this agent is... [Pg.152]

Replacement of the methyl ketone moiety in 78 by a phenyl sulfoxide, interestingly, leads to a relatively potent uricosuric agent with diminished antiinflammatory action. This effect in lowering serum levels or uric acid leads to the use of this drug in the treatment of gout. Alkylation of diethyl malonate with the chlorosulfide, 79, gives the intermediate, 80. The pyrazolodione (81) is prepared in the usual way by condensation with hydrazobenzene. Careful oxidation of the sulfide with one equiv-... [Pg.237]

In addition, the alkaloid colchicine (from Colchicum autumnale) blocks tubulin polymerization by binding to heterodimeric (3-tubulin between amino acids 239 and 254. Since it inhibits the MT-dependent migration of granulocytes into areas of inflammation and their MT-dependent release of proinflammatory agents, it is used to treat attacks of gout. Its antimitotic effect in the gastrointestinal system induces diarrhoea. Nocodazole competes for the binding site of colchicine and has similar effects on heterodimeric (3-tubulin. [Pg.416]

Gout is a form of arthritis in which uric acid accumulates in increased amounts in the blood and often is deposited in the joints. The deposit or collection of urate crystals in the joints causes the symptoms (pain, redness, swelling, joint deformity) of gout. [Pg.187]

In those with gout, the serum uric acid level is usually elevated. Sulfinpyrazone increases the excretion of uric acid by the kidneys, which lowers serum uric acid levels and consequently retards the deposit of urate crystals in the joints. Probenecid (Benemid) works in the same manner and may be given alone or with colchicine as combination therapy when there are frequent, recurrent attacks of gout. Probenecid also has been used to prolong the plasma levels of the penicillins and cephalosporins. [Pg.187]

Drugp indicated for treatment of gout may be used to manage acute attacks of gout or in preventing acute attacks of gout (prophylaxis). [Pg.187]

When allopurinol (Zyloprim) is used for the treatment of gout, the nurse ... [Pg.198]

Humans catabolize purines to uric acid (pA 5.8), present as the relatively insoluble acid at acidic pH or as its more soluble sodium urate salt at a pH near neutrality. Urate crystals are diagnostic of gout. Other disorders of purine catabolism include Lesch-Nyhan syndrome, von Gierke s disease, and hypo-uricemias. [Pg.301]

Long-term consequences of gout and hyperuricemia include joint destruction, tophi, and nephrolithiasis. [Pg.891]

Treatment of gout involves (1) acute relief of a gouty arthritis attack and (2) in some patients long-term maintenance treatment to prevent future attacks. [Pg.891]

The risk of gout increases as the serum uric acid concentration increases, and approximately 30% of patients with levels greater than 10 mg/dL (greater than 595 pmol/L) develop symptoms of gout within 5 years. However, most patients with hyperuricemia are asymptomatic. Other risk factors for gout include obesity, ethanol use, and dyslipidemia. Gout is seen frequently in patients with type 2 diabetes mellitus and coronary artery disease, but a causal relationship has not been established. [Pg.892]

Some drugs can cause hyperuricemia and gout, such as thiazide diuretics, niacin, pyrazinamide, cyclosporine, and occasionally, low-dose aspirin. In most cases, these drugs block uric acid secretion in the kidney. Long-term consequences of gout and hyperuricemia include joint destruction, tophi, and nephrolithiasis. [Pg.892]

Radiographs of affected joints may have characteristic appearances of gout, including cystic changes, punched-out lytic lesions with overhanging bony edges, and soft-tissue calcified masses. These signs may appear in other arthropathies as well. [Pg.892]

If the diagnosis of gout has not been confirmed previously, consider aspiration of an affected joint to identify uric acid crystals. [Pg.897]

Bardin T. Current management of gout in patients unresponsive or allergic to allopurinol. Joint Bone Spine 2004 71 481-485. [Pg.898]

Conaghan PG, Day RO. Risks and benefits of drugs used in the management and prevention of gout. Drug Safety 1994 11 252-258. [Pg.898]

Mikuls TR, Farrar JT, Bilker WB, et al. Suboptimal physician adherence to quality indicators for the management of gout and... [Pg.898]

Monosodium urate A crystallized form of uric acid that can deposit in joints leading to an inflammatory reaction and the symptoms of gout. [Pg.1571]

Colchicine (a drug used in treatment of gout) and vinblastine (a cancer chemotherapy agent) may decrease liver uptake of americium. In rats that received an intraperitoneal injection of either colchicine and vinblastine prior to an intravenous or intramuscular injection of americium citrate, liver uptake of americium was lower, relative to controls, and kidney and skeletal americium uptake were higher (Seidel 1984, 1985). The effect is thought to involve disruption of hepatic microtubule formation, which is critical to the formation and intracellular processing of lysosomes, the initial site of accumulation of americium in the liver. [Pg.114]

Anti-inflammatory. Elder flowers help soothe an inflamed respiratory tract irritated by hay fever and sinusitis. Elder has even been used to calm the agony of gout. Cool, strained elder flower tea makes an excellent application to inflamed eyes. Elderberries taken internally as a tea, tincture or syrup help to soothe irritated bowels or colitis. Topical applications are also helpful for glandular swellings. Parts used flowers, berries. [Pg.27]

It is important to note that the gout patients with high mobilizable lead and renal impairment had blood lead levels and ZPP concentrations that were no different from the rest of the group, indicating that there was no indication of lead overexposure in these individuals until the EDTA lead mobilization test was administered. Based on these results, it may be concluded that more extracellular lead accumulates in the renal impairment associated with some forms of gout. [Pg.70]

An interesting study related to these findings has been reported by Dryhurst and De 83> who examined the adsorption of uric acid an the PGE and the effect of allopurinol (4-oxypyrazolo [3,4-d] pyrimidine) on this adsorption. Allopurinol is a drug that is widely used for the treatment of gout 84>... [Pg.85]


See other pages where Of gout is mentioned: [Pg.365]    [Pg.546]    [Pg.656]    [Pg.538]    [Pg.135]    [Pg.134]    [Pg.135]    [Pg.135]    [Pg.135]    [Pg.136]    [Pg.136]    [Pg.139]    [Pg.755]    [Pg.187]    [Pg.189]    [Pg.189]    [Pg.189]    [Pg.451]    [Pg.171]    [Pg.299]    [Pg.252]    [Pg.185]    [Pg.894]    [Pg.70]    [Pg.502]    [Pg.218]    [Pg.696]   
See also in sourсe #XX -- [ Pg.1710 ]




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