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Hyperuricemia and

Uric acid is the endproduct of purine metabolism in man. Uric acid has a lower solubility than its progenitor metabolites, hypoxanthine and xanthine. Impaired uric acid elimination and/or increased uric acid production result in hyperuricemia and increase the risk of gouty arthritis. At physiological pH, 99% of the uric acid molecules are actually in the form of the urate salt. A decrease in pH increases the fraction of uric acid molecules relative to urate molecules. Uric acid possesses lower solubility than urate. [Pg.1267]

Some drugs can cause hyperuricemia and gout, such as thiazide diuretics, niacin, pyrazinamide, cyclosporine, and occasionally, low-dose aspirin. [Pg.891]

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]

The major adverse effect of niacin treatment is intense cutaneous flushing (vasodilation), which manifests as an uncomfortable burning sensation and itchiness of the face and upper body, thereby limiting patient compliance to therapy [13]. Moreover, a short half-life, dyspepsia, hyperuricemia, and modest hyperglycemia were also reported [14-16]. [Pg.74]

A patient develops hyperglycemia, hyperuricemia, and hypomagnesemia on which of the following diuretic agents ... [Pg.210]

Wu, X., Wakamiya, M., Vaishnav, S. et al. Hyperuricemia and urate nephropathy in urate oxidase-deficient mice Proa Natl Acad. Sci. U.S.A. 91 742-746,1994. [Pg.307]

About two-thirds of the uric acid produced each day is excreted in the urine. The remainder is eliminated through the GI tract after enzymatic degradation by colonic bacteria. A decline in the urinary excretion of uric acid to a level below the rate of production leads to hyperuricemia and an increased miscible pool of sodium urate. [Pg.15]

Potentially important laboratory abnormalities occurring with niacin therapy include elevated liver function tests, hyperuricemia, and hyperglycemia. Niacin-associated hepatitis is more common with sustained-release preparations, and their use should be restricted to patients intolerant of regular-release products. Niacin is contraindicated in patients with active liver disease, and it may exacerbate preexisting gout and diabetes. [Pg.119]

Salvi e enzymes recycle normally about 90% of these purines, and 10% are converted to tuic acid and excreted in urine. When purine catabcdism is increased significantly, a person is at risk for developing hyperuricemia and potentialty gout. [Pg.269]

AHopurinol inhibits xanthine oxidase and also can reduce purine synthesis by inhibiting PRPP amidotransferase (provided HPRT is active). Hyperuricemia and gout often accompany the following conditions ... [Pg.270]

The anticancer drug 6-mercaptopurine is deactivated by the enzyme xanthine oxidase. A cancer patient being treated with 6-meicaptopurine develops hyperuricemia, and the physician decides to give the patient allopurinoL... [Pg.274]

Most cases of hyperuricemia are due to disturbed uric acid excretion via the kidneys (1). A high-purine diet (e.g., meat) may also have unfavorable effects (2). A rare hereditary disease, Lesch-Nyhan syndrome, results from a defect in hypoxanthine phosphoribosyl-transferase (A, enzyme [1]). The impaired recycling of the purine bases caused by this leads to hyperuricemia and severe neurological disorders. [Pg.186]

Adverse reactions occurring in 3% or more of patients receiving rifapentine combination therapy include the following Rash pyuria proteinuria hematuria urinary casts neutropenia lymphopenia hyperuricemia and an increase in ALT and AST. [Pg.1736]

Hyperuricemia and chronic or episodic joint pain due to deposition of sodium urate crystals and consequent inflammation (gouty arthritis) are the hallmarks of gout. [Pg.146]

The excess purines are degraded to uric acid causing increased biood ieveis of this metaboiite (hyperuricemia) and deposition of sodium urate crystais in the Joints and kidneys. [Pg.147]

Becker M, Schumacher H, Wortmann R, MacDonald P, Eustace D, Palo W et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med 2005 353(23) 2450-61. [Pg.444]

Hepatotoxicity is the major concern in 15% of pyrazinamide recipients. It also can inhibit excretion of urates, resulting in hyperuricemia. Nearly all patients taking pyrazinamide develop hyperuricemia and possibly acute gouty arthritis. Other adverse effects include nausea, vomiting, anorexia, drug fever, and malaise. Pyrazinamide is not recommended for use during pregnancy. [Pg.560]

C. Pyrazinamide is known to cause hyperuricemia and precipitate gouty arthritis. Pyrazinamide-induced gouty arthritis does not respond to uricosuric therapy with probenecid but may respond to acetylsalicylic acid. Cycloserine (A) can cause headaches, confusion, tremors, and seizures, possibly secondary to low levels of magnesium in the cerebrospinal fluid cycloserine should be avoided in patients with epilepsy and mental depression. It is not associated with hyperuricemia. Thiacetazone (B) is an antibiotic that is rarely used in tuberculosis. The most common adverse reactions are general rashes and GI intolerance. Its use is not associated with hy-... [Pg.565]

The pyrazolo[3,4- pyrimidines 425 and 426 are claimed to be useful as pharmaceuticals for treatment of hyperuricemia and prevention of gout. [Pg.650]

Loop diuretics can cause hyperuricemia and precipitate attacks of gout. This is caused by hypovolemia-associated enhancement of uric acid reabsorption in the proximal tubule. It may be prevented by using lower doses to avoid development of hypovolemia. [Pg.331]

In long-term treatment, the thiazides may produce hypokalemia, hyperglycemia hyperuricemia, and a 5% increase in plasma cholesterol indapamide has been shown not to increase plasma cholesterol or lipids at therapeuLic doses. Thiazides can cause hyponatremia in patients with large Water intake while on the drug hyponatremia may be associated with nausea, vomiting, and headaches. [Pg.505]

There has been an anecdotal report of hyperuricemia and acute gout in a patient taking etacrynic acid (387). [Pg.601]

Burack DA, Griffith BP, Thompson ME, Kahl LE. Hyperuricemia and gout among heart transplant recipients receiving cyclosporine. Am J Med 1992 92(2) 141-6. [Pg.666]

Ben Hmida M, Hachicha J, Bahloul Z, Kaddour N, Kharrat M, Jarraya F, Jarraya A. Cyclosporine-induced hyperuricemia and gout in renal transplants. Transplant Proc 1995 27(5) 2722 1. [Pg.666]

Harper, M., C.G. Hatjis, R.G. Appel, and W.E. Austin. 1987. Vasopressin-resistant diabetes insipidus, liver dysfunction, hyperuricemia and decreased renal function. A case report. /. Reprod. Med. 32 862-865. [Pg.239]

Correct answer = D. Among black patients, diuretic and calcium channel blockers are more effective than ACE inhibitors or p-blockers. Diuretics are effective among the elderly. Thiazide diuretics cause hyperuricemia and can precipitate a gout attack in susceptible individuals. Thiazide diuretics increase LDL cholesterol and may increase the risk of atherosclerosis in patients with hyperlipidemia. Patients with evidence of elevated catecholamines are best treated with p-blockers. Thiazides cannot promote sodium excretion when renal function is severely impaired. The loop diuretics, such as furosemide, are used in patients with impaired renal function. [Pg.203]

A classic example of essential metal deficiency resulting from nonessential metal exposure is Itai itai disease. Cadmium pollution in the Jinzu River basin in Japan resulted in severe nephrotoxicity in approximately 184 people. Renal tubule damage caused excessive loss of electrolytes and small proteins from the urine. In severe cases, urinary Ca loss was so severe that bone Ca was mobilized, resulting in osteomalacia. Renal tubular defects persisted for life and induced hypophosphatemia, hyperuricemia, and hyperchloremia, which are characteristic biochemical features of Itai-itai disease (see Section 21.6.1). [Pg.419]


See other pages where Hyperuricemia and is mentioned: [Pg.135]    [Pg.135]    [Pg.135]    [Pg.559]    [Pg.474]    [Pg.307]    [Pg.270]    [Pg.441]    [Pg.445]    [Pg.665]    [Pg.86]    [Pg.282]    [Pg.222]    [Pg.135]    [Pg.135]    [Pg.135]    [Pg.559]   
See also in sourсe #XX -- [ Pg.1710 ]




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