Hyperuricemia
From Wikipedia, the free encyclopedia
| ICD-10 | E79.0 |
|---|---|
| ICD-9 | 790.6 |
| DiseasesDB | 5375 |
| eMedicine | med/1112 |
Hyperuricemia is the presence of high levels of uric acid in the blood. The upper end of the normal range is 360 micromol/L (6 mg/dL) for women and and 400 micromol/L (6.8 mg/dL) for men. [1] Hyperuricemia is caused either by accelerated generation of uric acid through purine metabolism or by impaired excretion in the kidney, or by high levels of fructose in the diet.[2][3]
Consumption of purine-rich diets is one of the main causes of hyperuricemia. Other dietary causes are ingestion of high protein and fat and starvation. Purine bases composition of foods varies. Foods with higher content of purine bases adenine and hypoxanthine are suggested to be more potent in exacerbating hyperuricemia[1].
Humans lack urate oxidase, an enzyme which degrades uric acid. Increased levels predispose for gout and (if very high) renal failure. Apart from normal variation (with a genetic component), tumor lysis syndrome produces extreme levels of uric acid, mainly leading to renal failure. The Lesch-Nyhan syndrome is also associated with extremely high levels of uric acid. The Metabolic syndrome often presents with hyperuricemia, while a hyperuricemic syndrome is also common in Dalmatian dogs.
[edit] See also
[edit] External links
 |
This medical sign article is a stub. You can help Wikipedia by expanding it. |
[edit] References
- ^ Brule, D. Sarwar, G. and Savoie (1992). "Changes in Serum Uric Acid Levels in Normal Human Subjects Fed Purine-Rich Foods Containing Different Amounts of Adenine and Hypoxanthine". Journal of American College of Nutrition 11 (3): 353-358.
- Michael A. Becker, M.D., H. Ralph Schumacher, Jr., M.D., Robert L. Wortmann, M.D., Patricia A. MacDonald, B.S.N., N.P., Denise Eustace, B.A., William A. Palo, M.S., Janet Streit, M.S., and Nancy Joseph-Ridge, M.D. "Febuxostat Compared with Allopurinol in Patients with Hyperuricemia and Gout" The New England Journal of Medicine. Boston: Dec 8, 2005. Vol. 353, Iss. 23; pg. 2450 - 2461
