Hyperuricemia

7. Hyperuricemia is the presence of high levels of uric acid in the blood. The normal range for men is 6.8 mg / dL, and 6 mg / dL for women.

8. Humans do not produce urate oxidase, an enzyme that degrades uric acid. High levels of this substance can lead to gout (disease) and, in some cases, impaired renal function (urate nephrolithiasis).

9. Causes and epidemiology

10. Uric acid levels in plasma above 6 mg% in women and 7 mg% in men occur in 10 &ndsh; 15% of the population over 40 years. Usually asymptomatic, is related to other diseases, such as diabetes mellitus, hyperthyroidism, prolonged use of diuretics, alcohol intake and obesity. Hyperuricemia may occur due to overproduction or reduced renal and intestinal excretion of uric acid.

11. Most often occurs in men after puberty, with the highest incidence from 30 &ndsh; 40 years and in women at menopause. Hyperuricemia may be of two categories: Primary, when uric acid in the blood is high, regardless of concomitant diseases or drugs that alter the production and excretion of urate. Secondary, when the increase is due to diseases existing diets and drugs that alter the production and excretion of uric acid. Hyperuricemia in 75% of patients are asymptomatic. In 25%, symptoms such as: gout, arthritis, nephrolithiasis (kidney stones), kidney disease (nephritis) and formation of uric acid deposits in tissues (tophi). The asymptomatic hyperuricemia often occurs frequently with alcohol abuse, obesity and chronic use of drugs that inhibit the excretion of uric acid as anti-inflammatory - acetylsalicylic acid (aspirin) - and diuretics. The presence of hyperuricemia is associated with risk factors such as hypertension, hyperlipidemia, diabetes and coronary vascular alterations.

12. The widespread consumption of foods high in purines is recognized as one of the causes of hyperuricemia, despite being demonstrably a minor factor compared to the protein metabolism of endogenous origin. The composition of purine bases in foods varies, but studies suggest that diets rich in adenine and hypoxanthine are more effective in increasing hyperuricemia.

13. In addition, it can also be caused by genetic defects that alter the cycle of urate formation.

Treatment

Given that hyperuricemia is a risk factor for cardiovascular disease should maintain normal plasma uric acid. For this it is necessary that physicians educate their treatment. In the treatment of hyperuricemia is necessary: ​​to prevent an acute attack of arthritis uric acid (gout), using anti-inflammatory drugs in pain crises; hipouriceminates or uricosuric use in patients (according to their clinical conditions, the decision to be taken by the physician); make prophylaxis of recurrent arthritis, nephrolithiasis, nephritis and gout; reduce predisposing factors such as alcohol, improper diet and medications that reduce uric acid excretion by the kidney, preventing and reversing the deposition of urate crystals in the joints, bones and tissues; extend long enough for the treatment to be demobilized urate tissue and bone and the plasma uric acid value returns to normal.

The diet is an item of treatment of uric acid, but not the only (or necessarily important.) Foods not recommended for patients with hiperuricemias are rich in purines, such as meats and kids in general (liver, heart, tongue and kidneys), small fish, sardines, trout, anchovies, seafood like mussels, shrimp and fish eggs. Stews and broths should be avoided because uric acid is very soluble in water and when the meat is cooked in water, uric acid diffuses in the liquid. Certain grains such as beans, chickpeas, peas, lentils and whole grains have a lot of purine and should be avoided. Finally, we say that every diet, how well it is made, can only download around 25% (approximately 1 mg%) of plasma levels of uric acid.