|
Hyperuricemia (American English), or hyperuricaemia (British English), 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 400 micromol/L (6.8 mg/dL) for men. [1]
Causes
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]. A common fructose found in processed food is high-fructose corn syrup (HFCS), which is the dominant ingredient in soft drinks, candy, fruit preserves, jam, and jelly [4].
Consumption of purine-rich diets is one of the main causes of hyperuricemia. Other dietary causes are ingestion of high protein and fat [citation needed], and starvation. Starvation results in the body metabolizing its own muscle mass for energy, in the process releasing purines into the bloodstream. 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.[5]
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.
Treatment
- Aquaretics
- Allopurinol (200-300mg by mouth once daily) use is controversial. By reducing uric acid production in the body, uric acid stores in the body could be mobilized leading to nephrolithiasis or gout.[citation needed]
- Alkalinizing the urine with sodium bicarbonate, Stohl's Solution, or Acetazolamide.
- Low purine diet (see gout).
- Febuxostat has been investigated.[6]
- Benemid (Probenecid) is an uricosuric that promotes uric acid excretion in the kidneys, lowering uric acid levels in blood. Following LeChatelier's principle, if the patient has suffered from chronic gout episodes, uric acid crystals in joints will be mobilized and will dissolve into blood as uric acid levels in blood keep decreasing while it is being excreted through the kidneys.
See also
External links
References
- ^ Chizynski K, Rózycka M (2005). "Hyperuricemia" (in Polish). Pol. Merkur. Lekarski 19 (113): 693–6. PMID 16498814.
- ^ Nakagawa T, Hu H, Zharikov S, et al (2006). "A causal role for uric acid in fructose-induced metabolic syndrome". Am. J. Physiol. Renal Physiol. 290 (3): F625–31. doi:10.1152/ajprenal.00140.2005. PMID 16234313.
- ^ Mayes PA (1993). "Intermediary metabolism of fructose". Am. J. Clin. Nutr. 58 (5 Suppl): 754S–765S. PMID 8213607.
- ^ Johnson, Richard Joseph; Timothy Gower (2008). The Sugar Fix : The High-Fructose Fallout That is Making You Fat and Sick. US: Rodale, 304. ISBN 10 1-59486-665-1.
- ^ Brulé D, Sarwar G, Savoie L (1992). "Changes in serum and urinary uric acid levels in normal human subjects fed purine-rich foods containing different amounts of adenine and hypoxanthine". J Am Coll Nutr 11 (3): 353–8. PMID 1619189.
- ^ Becker MA, Schumacher HR, Wortmann RL, et al (2005). "Febuxostat compared with allopurinol in patients with hyperuricemia and gout". N. Engl. J. Med. 353 (23): 2450–61. doi:10.1056/NEJMoa050373. PMID 16339094.
| |
