
	Where results make sense

Topic: Hyperuricemia

Related Topics

Gout

Uric acid

Thiazide

Purine

Hydrochlorothiazide

EC number

Excretion

In the News (Sat 14 Nov 09)

Northern Trust

Marvin Harrison

Peter Chernin

Gary Locke

Match Play

Penelope Cruz

Mickey Rourke

AR Rahman

Danny Boyle

Hugh Jackman

	Health Reports - Evanston Northwestern Healthcare (Site not responding. Last check: 2007-10-29)
		The process leading to hyperuricemia and gout begins with the metabolism of purines, which are nitrogen-containing compounds that are important for energy.
		Even if hyperuricemia is present, it is very common in the population and does not necessarily indicate the presence of gout.
		Hyperuricemia is caused by an identifiable inborn metabolic deficiency.
	www.enh.org /healthandwellness/encyclopedia/wellconnected/000093.asp (9310 words)

	Progress in Transplantation: Treating gout in kidney transplant recipients
		Hyperuricemia is defined as serum urate concentrations greater than 416 µml/L (7 mg/dL) with no symptoms of uric acid deposits.4 Uric acid is the end product of purine metabolism and is filtered in the glomeruli before being reabsorbed in the proximal tubule, where it is then excreted distally into the urine.
		Gout is defined as hyperuricemia of intra-articular monosodium urate crystals with symptomatic occurrences including inflammation at joints, erythema, and decreased range of motion often associated with severe pain or discomfort.4,7 Following initial gout attacks, patients are susceptible to future acute flares unless the underlying cause is remedied and risks factors are modified.
		Hyperuricemia is a common manifestation in patients with renal dysfunction, as uric acid tends to accumulate.
	www.findarticles.com /p/articles/mi_qa4117/is_200406/ai_n9423714 (1108 words)

	Gout
		Hyperuricemia in primary gout arises or is presumed to arise from a genetic or other inborn disorders that cause metabolic problem resulting in overproduction of uric acid or reduced excretion of uric acid.
		Because asymptomatic hyperuricemia usually does not lead to gout or other health problems, and would have to be treated with drugs that present certain risks and can be expensive, treatment to prevent a first attack of gout in hyperuricemic patients is considered inadvisable.
		Long-term treatment of hyperuricemia is recommended for tophi prevention and when the patient has suffered several acute attacks of gout over a number of years, when the attacks are unusually severe or affect more than one joint, or when hyperuricemia is caused by an identifiable inborn metabolic deficiency.
	www.podlink.com /pathology/gout.htm (6050 words)

	Overview of the Evaluation and Management of Gout and Hyperuricemia
		Therefore, treatment of asymptomatic hyperuricemia to prevent gout is not recommended, because it is not usually needed and may be associated with side effects from therapy.
		Primary hyperuricemia and gout (genetic rarely or idiopathic commonly) account for most cases of gout and are most often (>90%) related to relative uric acid underexcretion leading to and maintaining a higher than normal serum urate concentration.
		Treatment of hyperuricemia is undertaken when recurrent gouty attacks are not prevented by colchicine or NSAID prophylaxis, recurrent attacks are frequent (3-4/year), or polyarticular gout or tophi are present (in subcutaneous tissues or on radiographs).
	www.rheumatology.org /publications/primarycare/number4/hrh0021498.asp (3933 words)

	UpToDate Hyperuricemia and gout in renal transplant recipients
		The incidence of hyperuricemia in one study of renal transplant recipients was 84 percent in those treated with cyclosporine versus 30 percent in patients treated with azathioprine and prednisone[1].
		Despite persistent hyperuricemia, patients with previous gouty arthritis note a marked reduction in symptomatic episodes, and de novo gout is a rare event [5].
		The hyperuricemia induced by cyclosporine is not restricted to renal transplant recipients but is also frequent in heart or heart-lung transplant patients [7].
	patients.uptodate.com /topic.asp?file=renltran/10039 (619 words)

	Magnetic therapy, gout
		Hyperuricemia also may result when a person eats too many high-purine foods, such as liver, dried beans and peas, anchovies, and gravies.
		Hyperuricemia is not a disease and by itself is not dangerous.
		Although most people with gout have hyperuricemia at some time during the course of their disease, it may not be present during an acute attack.
	www.worldofmagnets.co.uk /health_info/gout.htm (1465 words)

	Gout
		Hyperuricemia occurs in between 30% and 85% of people who have kidney transplants and who receive immunosuppressive and diuretic drugs.
		Many experts believe, however, that chronic hyperuricemia is unlikely to be a common cause of kidney disease, and that, in most cases, the kidney abnormalities come first and cause high concentrations of uric acid.
		Hyperuricemia has also been associated with a higher risk of death from heart and circulatory diseases, although it is unknown whether hyperuricemia is a risk factor independent of the high-risk conditions it often accompanies.
	www.bethesdaclinic.com /gout.htm (6903 words)

	American Family Physician: Gout and Hyperuricemia
		Asymptomatic hyperuricemia is the term for an abnormally high serum urate level, without gouty arthritis or nephrolithiasis.
		Although gouty arthritis characteristically occurs in patients with hyperuricemia, it is incorrect to equate hyperuricemia with clinical gout.
		Hyperuricemia predisposes patients to both gout and nephrolithiasis, but therapy is generally not warranted in the asymptomatic patient.
	www.findarticles.com /p/articles/mi_m3225/is_1999_Feb_15/ai_54113328 (1179 words)

	[No title]
		Gout is a syndrome caused by an inflammatory response to the formation of monosodium urate monohydrate crystals which develop secondary to hyperuricemia.
		Hyperuricemia may be due to environmental and/or genetic factors.
		Hyperuricemia is clearly a risk factor for the development of gout, the risk increasing with a higher urate concentration.
	www.arthritis.co.za /gout.html (1279 words)

	eMedicine - Nephropathy, Uric Acid : Article by Mark Fahlen, MD
		Hyperuricemia is an important finding, with urate levels in the plasma often exceeding 15 mg/dL and peaks as high as 50 mg/dL.
		In some instances, hyperuricemia and acute uric acid nephropathy cannot be avoided because of a large tumor burden, aggressive chemotherapy, and the inability to delay chemotherapy until allopurinol has lowered the serum uric acid concentration.
		Because of the lack of evidence that hyperuricemia in itself causes chronic nephropathy (except in the rare enzyme deficiencies previously mentioned), the current trend is to not treat hyperuricemia for the prevention of chronic nephropathy alone.
	www.emedicine.com /med/topic1610.htm (4148 words)

	DG DISPATCH - ACR: Allopurinol, Benziodarone Treat Hyperuricemia In Renal-transplant Patients
		The term "hyperuricemia" refers to an excess of urates (uric acid) in the blood.
		Hyperuricemia usually precedes the development of gout, and may lead to renal disease.
		The researchers concluded that both drugs were efficacious in controlling hyperuricemia in renal-transplant patients, although benziodarone was more useful in those with low renal function.
	www.docguide.com /dg.nsf/PrintPrint/748B9A4E31C224228525698C006D97FB (400 words)

	Elitek™ Treatment of Choice for Hyperuricemia in Aggressive Non-Hodgkin’s Lymphoma
		Hyperuricemia refers to excess uric acid in the blood.
		Treatment for hyperuricemia may include intravenous administration of fluids, diuretics to promote excretion of uric acid in the urine, an agent such as Elitek® (rasburicase) or allopurinol to reduce the formation or uric acid and the alkalinization of urine.
		Efficacy and safety of rasburicase (recombinant urate oxidase) for the prevention and treatment of hyperuricemia during induction chemotherapy of aggressive non-Hodgkin’s lymphoma: results of the GRAALI1 (Group d’Etude des lymphomas de l’Adulte trial on rasburicase activity in adult lymphoma) study.
	patient.cancerconsultants.com /nhl_cancer_news.aspx?id=18327 (629 words)

	eMedicine - Hyperuricemia : Article by Yasir Qazi, MD
		For years, hyperuricemia has been identified with or thought to be the same as gout, but uric acid has now been identified as a marker for a number of metabolic and hemodynamic abnormalities.
		In patients with hyperuricemia, the history involves determining whether the patient is symptomatic or asymptomatic and identifying causative etiologies and comorbid conditions.
		Johnson RJ, Kivlighn SD, Kim YG, et al: Reappraisal of the pathogenesis and consequences of hyperuricemia in hypertension, cardiovascular disease, and renal disease.
	www.emedicine.com /med/topic1112.htm (5341 words)

	The Analyst - Internet Health Report: Condition: Gout / Hyperuricemia
		The explanation for this phenomenon may be that they have not incurred sustained hyperuricemia levels long enough to develop gout.
		Hyperuricemia is caused by a variety of means, one of which is abnormal kidney function.
		Among the more common predisposing factors to hyperuricemia are kidney failure from any cause, diuretic use, dehydration, hormonal diseases, alcohol consumption and using low doses of aspirin.
	www.digitalnaturopath.com /cond/c142857.html (2920 words)

	Gout
		Although hyperuricemia is not a requirement for the diagnosis of gout and its presence in a patient with arthritis does not necessarily imply that diagnosis, the risk of gout increases with the degree and the duration of hyperuricemia.
		Sustained hyperuricemia is a risk factor for acute gouty arthritis, tophaceous gout and uric acid nephrolithiasis.
		However, most patients with hyperuricemia will never have an attack of gout, and no treatment is required although it is prudent to determine the cause of hyperuricemia and correct them if possible.
	clevelandclinicmeded.com /diseasemanagement/rheumatology/gout/gout.htm (2242 words)

	Diagnose-Me: Condition: Gout / Hyperuricemia
		The four phases of gout include elevated uric acid levels without symptoms, acute gouty arthritis, multiple attacks with intervals between attacks, and chronic tophaceous gout, in which nodular masses of uric acid crystals (tophi) are deposited in different soft tissue areas of the body.
		Gout is strongly associated with obesity, hypertension, hyperlipidemia and diabetes.
		Among the more common predisposing factors for hyperuricemia are kidney failure from any cause, diuretics, dehydration, hormonal diseases, alcohol consumption and using low doses of aspirin.
	www.diagnose-me.com /cond/C143018.html (3038 words)

	Drug-induced hyperuricemia.
		Diuretic-induced hyperuricemia is probably the single most common form of hyperuricemia seen in clinical practice.
		Laine J, Holmberg C. Mechanisms of hyperuricemia in cyclosporine-treated renal transplanted children.
		Furosemide-induced hyperuricemia, hyperglycemia, hypertension and arterial lesions in nonarteriosclerotic and arteriosclerotic rats.
	www.globalrph.com /uricacid.htm (215 words)

	The Analyst - Internet Health Report: Condition: Gout / Hyperuricemia
		Known as "the disease of kings and the king of diseases", gout has been studied by physicians and has caused suffering in countless humans since at least the days of Hippocrates.
		The four phases of gout include elevated uric acid levels without symptoms, acute gouty arthritis, multiple attacks with intervals between attacks, and chronic tophaceous (nodular masses of uric acid crystals (tophi) deposited in different soft tissue areas of the body) gout.
		Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle.
	www.digitalnaturopath.com /cond/C142857.html (2920 words)

	Hyperuricemia and urate nephropathy in urate oxidase-deficient mice. (Site not responding. Last check: 2007-10-29)
		Hyperuricemia and urate nephropathy in urate oxidase-deficient mice.
		The loss of urate oxidase in the human during primate evolution predisposes man to hyperuricemia, a metabolic disturbance that can lead to gouty arthritis and renal stones.
		To create a mouse model for hyperuricemia and gout, and to address the question of whether urate oxidase is essential in lower mammalian species, we have disrupted the urate oxidase gene in the mouse by homologous recombination in embryonic stem cells.
	www.bioscience.org /knockout/ref/wu.htm (199 words)

	Gout
		Gout is an arthritic condition (inflammation of the joints) that mostly affects men age 40 and older.
		In both types of gout, between 70% and 95% of hyperuricemia cases are the result of under-excretion of uric acid, rather than uric acid over-production.
		Hyperuricemia, in fact, has been associated with a higher risk of death from these conditions.
	www.mercydesmoines.org /ADAM/WellConnected/articles/000093.asp (8912 words)

	Hyperuricemia - Cause of High Uric Acid Level (Site not responding. Last check: 2007-10-29)
		Hyperuricemia is an excess of uric acid in the blood.
		Causes of high uric acid levels (hyperuricemia) can be primary (increased uric acid levels due to purine), and secondary (high uric acid levels due to another disease or condition).
		If your blood uric acid levels are significantly elevated, and you are undergoing chemotherapy for leukemia or lymphoma, you may have symptoms kidney problems, or gouty arthritis from high uric acid levels in your blood.
	www.chemocare.com /managing/fullstory.sps?iNewsid=24583 (1200 words)

	Johns Hopkins Arthritis article on Gout
		Causes of hyperuricemia can be divided into two major categories: decreased clearance of uric acid from the kidney and increased synthesis of uric acid.
		Although 90% of patients with hyperuricemia have decreased clearance of uric acid, many have poor renal function.
		Hyperuricemia increases risk for both calcium and uric acid renal stones.
	www.hopkins-arthritis.som.jhmi.edu /other/gout.html (1998 words)

	Renal Transplant-Associated Hyperuricemia and Gout -- CLIVE 11 (5): 974 -- Journal of the American Society of Nephrology
		Prevalence of hyperuricemia and gout in renal transplant patients
		it is invariably preceded by a period of hyperuricemia.
		Hyperuricemia and gout are common problems among renal transplant recipients.
	jasn.asnjournals.org /cgi/content/full/11/5/974 (3585 words)

	Final Diagnosis -- Case 205 (Site not responding. Last check: 2007-10-29)
		Although hyperuricemia is a sin qua non for the development of gout, it is not the sole determinant.
		The various conditions producing hyperuricemia and gout are divided into those that produce primary gout in which the basic metabolic defect is unknown or gout is the main manifestation of a known defect and secondary gout in which the cause of hyperuricemia is known or gout is not the main clinical dysfunction.
		The documented incidence of CyA induced hyperuricemia is upto 80% and that of gout is 5 to 24% in renal transplant patients.
	path.upmc.edu /cases/case205/dx.html (432 words)

	Full Text: Editorial
		In the majority of patients with primary gout, hyperuricemia results from relative renal urate underexcretion ("relative urate underexcretors"), while in about 10% of subjects, hyperuricemia is due to endogenous overproduction of uric acid ("urate overproducers")
		Hyperuricemia was also found to be a significant correlate of alcohol abuse in an unselected group of male patients admitted to a general hospital
		In light of its clinical and therapeutic implications, it is important to recognize the strong association of IRS (abdominal obesity, dyslipidemia, raised serum insulin levels, and glucose intolerance) with hyperuricemia and gout.
	www.jrheum.com /subscribers/02/07/1350.html (3775 words)

	Postgraduate Medicine: RHEUMATIC DISEASES: A practical approach to gout
		The two main mechanisms of hyperuricemia are uric acid overproduction (in 10% to 15% of patients with primary gout) and impaired renal clearance of uric acid (in the remainder of patients).
		Indications: Hyperuricemia associated with overproduction, urinary uric acid excretion >700 mg/24 hr, nephrolithiasis, prophylaxis before chemotherapy, hyperuricemia associated with enzyme defects, intolerance to uricosuric agents, inability to lower uric acid level to <7 mg/dL with uricosuric drugs
		Asymptomatic hyperuricemia does not usually produce adverse effects before the development of gout and, therefore, does not require treatment (11-13).
	www.postgradmed.com /issues/1999/10_01_99/davis.htm (2757 words)

Try your search on: Qwika (all wikis)