Uric acid is a poorly soluble end product of purine metabolism in humans.
Human beings have higher levels of uric acid, in part, because of a deficiency of the hepatic enzyme uricase, and a lower rate of excretion of uric acid. Approximately two thirds of total body urate is produced endogenously, (within the body) while the remaining one third is accounted for by dietary purines.
Approximately 70% of the urate produced daily is excreted by the kidneys, while the rest is eliminated by the intestines.
Dietary purines are found particularly in organ meats and seafood. Thus all protein rich foods DO NOT elevate uric acid.
Uric acid in the blood is saturated at 6.4-6.8 mg/dL at ambient conditions, with the upper limit of solubility placed at 7 mg/dL.
Contributing factors:
- Certain medications e.g., niacin, beta blockers, aspirin, TB drugs.
- Diabetes
- Cancer therapy
- Alcoholism
- Disturbed kidney function
- Genetic enzyme defect that
- Ketosis (in some subjects)
- Obesity
Most patients with asymptomatic hyperuricemia never develop gout or stones. Pharmacologic treatment for asymptomatic hyperuricemia carries some risk, is not considered beneficial or cost-effective, and generally is not recommended. However, these patients can be advised on lifestyle changes such as changes in diet, reduction in alcohol intake, and exercise, which may lower uric acid levels.
Medication:
Allopurinol continues to be the mainstay for the treatment of patients who are overproducers (where production exceeds normal excretion), but febuxostat has become an established alternative to allopurinol**.
**Kindly consult your physician for the drug of choice based on current levels, contributing factors and risk of progression to gout/stones.
Guest Article, Dietician Shwetha Bhatia