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Clinical Review Hyperuricemia and Gout

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Clinical Review Hyperuricemia and Gout Clinical Review Hyperuricemia and Gout Richard W. Sloan, MD Hershey, Pennsylvania Although chronic tophaceous gout has become increasingly uncommon, hyperuricemia and acute gout are still common clinical entities. Most patients with hyperuricemia are under- excreters, and many of these cases are drug induced. Since longstanding asymptomatic hyperuricemia does not appear to cause progressive renal insufficiency, and uric acid renal stones are uncommon in underexcreters, these patients gen­ erally require no treatment. The minority of patients who overproduce uric acid are at increased risk for urolithiasis, and therapy should be decided on an individual basis. Acute gout is best treated with colchicine or indomethacin. The newer non­ steroidal anti-inflammatory drugs (ie, ibuprofen, sulindac) may prove to be equally effective and are associated with fewer gastrointestinal side effects. Prophylaxis should be undertaken in patients with recurrent gout or documented uric acid urolith­ iasis. Although uricosuric drugs appear to be less toxic than allopurinol, they should not be used in patients who overpro­ duce uric acid or in patients who have a history of urolithiasis or renal insufficiency. The allopurinol hypersensitivity syn­ drome is being reported with increased frequency and may be fatal. Uric Acid Metabolism sources: dietary purines, and purines resulting Uric acid is the end product of purine metabo­ from the normal metabolic turnover of cells. The total amount of urate in the body may vary widely lism. Purines are derived from two general among individuals. In an adult man on a purine- free diet, the average total body urate is 1200 mg. In women, the total urate pool may be only 50 From the Department of Family and Community Medicine, The Milton S. Hershey Medical Center, The Pennsylvania percent of this value. In patients with chronic State University, Hershey, Pennsylvania. Requests for re­ tophaceous gout, the total urate pool can exceed prints should be addressed to Dr. Richard W. Sloan, The Pennsylvania State University, 500 University Drive, Her­ 25 gm. Since approximately 50 percent of the urate shey, PA 17033. pool is turned over each day, an average man 0094-3509/82/050923-07$01.75 5 1982 Appleton-Century-Crofts THE JOURNAL OF FAMILY PRACTICE, VOL. 14, NO. 5: 923-934, 1982 923 HYPERURICEMIA AND GOUT Etiology Although hyperuricemia may be primary with no identifiable cause, secondary causes should be Glomerulus sought and excluded. There are a number of drugs that may compete with uric acid for renal secre­ tory sites and subsequently cause hyperuricemia (Table 1). Diuretics and aspirin are the most com­ mon drugs that cause a secondary hyperuricemia. All diuretics in common use have been associated Renal Tubule with hyperuricemia except for spironolactone (Al- dactone). Low-dose aspirin therapy (less than 2 g/d) is another common cause of secondary hyper­ uricemia. Ethyl alcohol, when used in excess, is also commonly associated with hyperuricemia and is thought to be caused by the lactic acidosis in­ duced by alcohol; lactic acid competes with uric acid for renal secretory sites. Some alcoholic bev­ erages also have a high purine content. Hyperuricemia is common in a number of neo­ = 6- 12% plastic disorders, including polycythemia vera, Figure 1. Uric acid excretion and mechanism of myeloid metaplasia, acute leukemia, and multiple drug interactions myeloma. In these disorders, hyperuricemia is secondary to an increased production of uric acid secondary to the rapid turnover of neoplastic cells. would excrete 600 mg of uric acid per day: two Serum uric acid levels may increase rapidly when thirds of this amount is excreted in the urine, and chemotherapy is instituted and cause the precipi­ one third is excreted in the feces.1 tation of uric acid crystals in the renal tubules, The renal handling of uric acid is rather com­ with subsequent acute renal failure. This compli­ plex, and some details are still controversial (Fig­ cation may be prevented by treating these patients ure 1). Approximately 100 percent of the uric acid with allopurinol (Zyloprim). Other disease states is filtered by the glomerulus, most of which is re­ associated with rapid turnover of cells, such as sorbed in the proximal tubule. Approximately 50 psoriasis and exfoliative dermatitis, can also cause percent of the uric acid is then actively secreted hyperuricemia. back into the proximal tubule. Postsecretory re­ Heavy metals, such as lead, interfere with the sorption also occurs to a varying degree. The net ability of the proximal tubule to secrete uric acid, amount of uric acid excreted in the urine depends causing hyperuricemia as well as progressive renal on the balance between secretory and resorptive insufficiency. A recent study of 44 patients with processes and averages 6 to 12 percent of the fil­ gout demonstrated that those patients with renal tered load.2 insufficiency had significantly elevated urinary lead concentrations after calcium disodium ede- tate (EDTA) mobilization.4 Genetically linked enzyme defects are an un­ common cause of hyperuricemia but have Asymptomatic Hyperuricemia increased our understanding of primary hyperuri­ Although hyperuricemia is usually diagnosed cemia. These metabolic defects result in the over­ after several serum uric acid measurements are production of uric acid, associated with an greater than 8.0 mg/100 mL in men or greater than increased rate of de novo purine biosynthesis. One 7.0 mg/100 mL in women, the normal values may such defect is hypoxanthine-guanine phosphori- vary among laboratories, according to methodol­ bosyl transferase (HPRT) deficiency, which oc­ ogy, and among study populations.3 curs in the Lesch-Nyhan syndrome. In addition to 924 THE JOURNAL OF FAMILY PRACTICE, VOL. 14, NO. 5, 1982 HYPERURICEMIA AND GOUT Table 1. Drugs That Interfere With during the urine collection. The results of the 24- Uric Acid Excretion hour urine test will divide hyperuricemic patients into two general categories: overproducers Decrease Increase Uric Acid Excretion Uric Acid Excretion (greater than 600 mg/d of uric acid), and under- excreters (less than 600 mg/d of uric acid). An out­ Alcohol Aspirin (high dose) patient on an ordinary diet with a 24-hour urine Diuretics Probenecid uric acid reading of greater than 1,000 mg/d is Nicotinic acid Sulfinpyrazone considered to be an overproducer. L-dopa Phenylbutazone Of all patients with hyperuricemia, approxi­ (high dose) mately 25 percent are overproducers and 75 per­ Ethambutol cent are underexcreters. Overproducers are at in­ Aspirin (low dose) creased risk for urolithiasis. Another indicator of Phenylbutazone the risk of urolithiasis is the urine uric acid to cre­ (low dose) atinine ratio. If this ratio is greater than 1 to 1, the patient may be at increased risk for urolithiasis. Additional factors that increase the risk of uric acid urolithiasis are urine concentration and pH, hyperuricemia, this syndrome is characterized by since uric acid is more likely to crystallize in a mental and growth retardation, choreoathetosis, highly concentrated acid urine.5 spasticity, and self-mutilating behavior. A second enzyme defect resulting in primary hyperuricemia Treatment is increased activity of phosphoribosylpyrophos- The question of when to treat an asymptomatic phate (PRPP) synthetase. hyperuricemic patient has been debated through Hypertension, obesity, hyperlipidemia, and di­ the years. A decision to treat commits the patient abetes mellitus are commonly associated with to lifelong therapy. An acute attack of gouty ar­ primary hyperuricemia and gout. Often these pa­ thritis, although painful, is readily treatable and tients have a positive family history, and although tends to resolve completely. In the past the major the exact biochemical defect has not been eluci­ reason given for treating asymptomatic hyperuri­ dated, it is likely that these disorders are also cemia was to prevent uric acid-induced renal dis­ under genetic control. ease. Hyperuricemia was thought to cause three general types of renal disease: gouty nephropathy, Diagnostic Evaluation intratubular crystallization of uric acid, and uro­ In evaluating a patient with hyperuricemia, a lithiasis. Recent studies have cast considerable useful diagnostic study is the 24-hour urine test for doubt on the existehce of gouty nephropathy.6-8 uric acid. Before performing this test, a thorough Patients with longstanding hyperuricemia do not drug history should be taken. Many drugs will appear to have any greater incidence of progres­ alter the total amount of uric acid excreted in the sive renal failure than would a closely matched urine per day (Table 1). Low-dose aspirin therapy control group. Intratubular crystal deposition may cause hyperuricemia and low 24-hour urine continues to be a well-recognized complication of uric acid levels (less than 450 mg). A hyperuri- chemotherapy in patients with certain neoplastic cemic patient on diuretic therapy may also be ex­ disorders and can lead to acute renal failure. This pected to have low 24-hour urine uric acid levels, complication can be prevented with allopurinol and the 24-hour urine collection may not be helpful. therapy. Urolithiasis also continues to be a well- In general, the 24-hour urine for uric acid test recognized complication of hyperuricemia and is allows the physician to determine the most appro­ most common in overproducers and in patients priate therapy and to assess the risk of urolithiasis. with a highly concentrated acid urine. If untreated, Ideally, the test should be performed when the the resulting obstruction and infection from recur­ patient is on a purine-free diet. Foods high in rent urolithiasis can cause significant irreversible purines include liver, sweetbreads, kidney, tripe, renal damage. and other visceral meats. The patient should ab­ In the family practice setting, a significant num­ stain from alcohol for 24 hours prior to the test and ber of patients with asymptomatic hyperuricemia the JOURNAL OF FAMILY PRACTICE, VOL. 14, NO. 5, 1982 925 HYPERURICEMIA AND GOUT receive thiazide diuretics for the treatment of volved, a few patients may experience an acute hypertension.
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