Gout Information

The presence of certain diseases

Any disease in which there is a rapid breakdown and turnover of bodily cells will raise levels of uric acid in the blood. In severe psoriasis, for example, the turnover of skin cells is much faster than normal. This has an effect on the degradation of purines, on the levels of uric acid produced and on the elimination of uric acid by the kidneys. Increased turnover of the bone marrow, in leukaemia and glandular fever for example, can also raise levels of uric acid.

Overweight diabetics with insulin resistance are at risk of developing hypertriglyceridemia and hyperuricemia because their uric acid is not effectively excreted by the kidneys. (Insulin resistance means the cells have difficulty converting glucose to energy. In an effort to compensate, the pancreas produces more insulin, which creates higher circulating levels of insulin than normal.) The result is often abnormal cholesterol and lipid levels, as well as weight gain. Raised levels of uric acid can also result from hypothyroidism (abnormally low activity of the thyroid gland) and disorders of the parathyroid glands (four small glands located behind the thyroid gland).

The use of certain medications

Diuretics (water tablets) prescribed for high blood pressure can lead to hyperuricemia. Also, chemotherapy drugs used to treat cancer often promote hyperuricemia due to the cell destruction they cause. Aspirin, in low doses, has the effect of reducing the excretion of uric acid, but in high doses it increases elimination. Aspirin should, therefore, be avoided if you suffer from gout. Because some other medications can cause hyperuricemia, check with your doctor to see if they can be the cause of your gout. An alternative medication may be available. If gout is the result of diuretic medication, stopping the diuretic may be possible and all that is required to return uric acid levels to normal.

Inheritance of certain genes

The genes a person inherits can promote either the overproduction or underproduction of uric acid. Small structural defects in the genetic code can affect the control mechanisms for the formation of uric acid, meaning the body produces an abnormally large amount of purine, the precursor to uric acid. The defective gene is located on the X chromosome, which relates to the male. As a result, only males suffer this particular defect, but it can be passed down by a female carrier who herself will either be mildly affected by hyperuricemia or completely normal. Alternatively, the genetic defect can arise spontaneously and there may be no other family members affected.

The ability of the kidneys to eliminate uric acid can also be passed down through families. The average rate of uric acid clearance is 10 ml per minute, the range being between 5 and 15 ml per minute. Those who inherit a clearance rate of only 5 or 6 ml per minute will obviously have much more difficulty eliminating a uric acid load than those who inherit a rate of 14 to 15 ml per minute. Apart from an inherited poor ability to excrete uric acid, the kidney is likely to be normal in all other respects.

The Arthritis Research Campaign (ARC) is sponsoring research to find out more about the underlying chemical and genetic processes that cause gout and also to search for more effective drugs to treat the disease. Much other research is under way.