Gout is a condition which is characterised by an increased level of uric acid in the blood, storage of urate crystals in the joints or soft tissues, and the formation of uric acid calculi (urates) in the urinary ducts. Uric acid is a final product of purine base metabolism. It is eliminated from the body by the kidneys. Filtration of uric acid (approximately 95% of its total content in the plasma) takes place in the renal glomeruli; its virtually complete reabsorption is carried out in the proximal renal tubules. The second stage includes uric acid secretion in the proximal tubules and another round of active reabsorption (~80%).
Drugs that are used for the treatment of gout include preparations that lower uric acid levels in the blood and antiinflammatory agents. Reduction in uric acid content may be achieved by two methods:
• Increasing uric acid elimination from the body;
• Blocking uric acid synthesis.
Drugs that promote uric acid excretion are called uricosuric agents. Sulfinpyrazone, etebenecid, probenecid and benzbromarone (Fig. 25.1) belong to this group. They are used for the prevention of acute attacks of gout.
Sulfinpyrazone (anturan) is a derivative of pyrasolon (the chemical structure of sulfinpyrasone is similar to that of phenylbutazone). When used in large doses, it inhibits uric acid reabsorption in the proximal renal tubules thus enhancing its excretion from the body. Low doses of this preparation diminish uric acid secretion retaining it in the body. The drug also reduces excretion (secretion) of bensylpenicillin by the kidneys.
As discussed above, sulfinpyrason decreases platelet aggregation (see Chapter 19; 19.1). It is well absorbed from the gastrointestinal tract.