Allopurinol is an enzyme blocker that lowers high levels of uric acid in your body by decreasing the amount produced. It is used to treat gout and certain types of kidney stones. This drug is also used to prevent high uric acid levels in patients who receive cancer chemotherapy. Cancer cells that are destroyed with therapy release large amounts of uric acid into the bloodstream. This medicine works by causing less uric acid to be produced by the body. Allopurinol will not relieve a gout attack that has already started. Also, it does not cure gout, but it will help prevent gout attacks. However, it works only after you have been taking it regularly for a few months. Allopurinol will help prevent gout attacks only as long as you continue to take it.
Allopurinol (Lopurin, Zurinol, Zyloprim) reduces the amount of uric acid in the blood and urine by slowing the rate of production of uric acid. It is the best medicine for people who have kidney problems or kidney stones caused by uric acid. Occasional side effects include skin rash and stomach upset. Infrequently, allopurinol can cause a allergic reaction - skin rash, hives, itching, fever, nausea, and muscle pain are typical symptoms.
Allopurinol inhibits xanthine oxidase, the enzyme that catalyzes the conversion of hypoxanthine to xanthine and of xanthine to uric acid. Oxypurinol, a metabolite of allopurinol, also inhibits xanthine oxidase. By inhibiting xanthine oxidase, allopurinol and its metabolite block conversion of the oxypurines (hypoxanthine and xanthine) to uric acid, thus decreasing serum and urine concentrations of uric acid. The drug differs, therefore, from uricosuric agents which lower serum urate concentrations by promoting urinary excretion of uric acid. Xanthine oxidase concentrations are not altered by long-term administration of the drug.
Accompanying the decrease in uric acid produced by allopurinol is an increase in serum and urine concentrations of hypoxanthine and xanthine. Plasma concentrations of these oxypurines do not, however, rise commensurately with the fall in serum urate concentrations and are often 20?0% less than would be expected in view of urate concentrations prior to allopurinol therapy. This discrepancy occurs because renal clearance of the oxypurines is at least 10 times greater than that of uric acid. In addition, normal urinary purine output is almost exclusively uric acid, but after treatment with allopurinol, it is composed of uric acid, xanthine, and hypoxanthine, each having independent solubility. Thus, the risk of crystalluria is reduced. Alkalinization of the urine increases the solubility of the purines, further minimizing the risk of crystalluria. Decreased tubular transport of uric acid also results in increased renal reabsorption of calcium and decreased calcium excretion.
Allopurinol is used to lower serum and urinary uric acid concentrations in the management of primary and secondary gout. The drug is indicated in patients with frequent disabling attacks of gout. Because therapy with allopurinol is not without risks, the drug is not recommended for the management of asymptomatic hyperuricemia. Some clinicians have suggested that therapy should be initiated when serum urate concentrations exceed 9 mg/dL because these concentrations are often associated with increased joint changes and renal complications.
Allopurinol is used for the management of gout when uricosurics cannot be used because of adverse effects, allergy, or inadequate response; when there are visible tophi or radiographic evidence of uric acid deposits and stones; or when serum urate concentrations are greater than 8.5? mg/dL and a family history of tophi and low urate excretion exists. Allopurinol is also used for the management of primary or secondary gouty nephropathy with or without secondary oliguria. The goal of therapy is to lower serum urate concentration to about 6 mg/dL. Allopurinol will often promote resolution of tophi and uric acid crystals by decreasing serum urate concentrations.