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Case 3: Acute Gout—Risk Factors and Inappropriate Therapy
The American Journal of Medicine (2006) Vol 119 (11A), S9 –S12
Case 3: Acute Gout—Risk Factors and Inappropriate Therapy Arthur L. Weaver, MD Division of Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA
CASE Patient MA, a 56-year-old postmenopausal white woman with sudden onset of acute pain in the right great toe, was seen by her primary care physician the following day. She walked with support from her husband because she was unable to walk or bear weight without assistance. The patient—a homemaker—reported that she had had 2 previous episodes of similar pain in the great toe and ankle lasting 4 to 5 days that were treated by emergency room physicians with analgesics.
HISTORY AND PHYSICAL EXAMINATION The patient’s past history was unremarkable except for a recent weight loss of approximately 25 lb (11.25 kg) over 3 months related to the initiation of the Atkins diet and the prescribing of a thiazide diuretic for mild hypertension. Physical examination revealed a blood pressure reading of 138/86 mm Hg, a weight of 185 lb (83.25 kg), body mass index (BMI) of 31.8, and height of 5=4⬙ (162.56 cm). Patient MA presented with an acutely swollen, red, and tender right great toe. She was diagnosed with gout and placed on allopurinol 300 mg/day and celecoxib 200 mg twice daily. Two days later, the patient was called by the nurse and told that her serum uric acid level of 8.3 mg/dL (0.49 mmol/L) substantiated the diagnosis of gout. The patient complained of continuing pain in the toe. Ten days after this consultation, the patient called and complained of continued pain in the toe and a recent swelling with severe pain in the left knee. She was told to discontinue use of allopurinol and to seek an appointment with a rheumatologist. At 3 weeks after the onset of pain in her right toe and 5 days after the episode in her left knee, the patient was seen by a rheumatologist. Her right toe was slightly swollen and
Requests for reprints should be addressed to Arthur L. Weaver, MD, 9914 Weavers Point Road, Pequot Lakes, Minnesota 56472. E-mail address: [email protected].
0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2006.06.026
tender, but her left knee was swollen and she was limping significantly. Her left knee was aspirated and injected, and the synovial fluid showed a cell count of 15,000 (15.0 ⫻ 109/L) and the presence of urate crystals. A repeat measurement revealed a uric acid level of 7.6 mg/dL (0.45 mmol/L). The patient was advised to switch the thiazide diuretic to a -blocker; she was also instructed to discontinue the Atkins diet but to monitor her caloric intake. She was started on colchicine 0.6 mg twice daily; allopurinol therapy was reinitiated 4 weeks later at a starting dose of 100 mg/day. Although the patient said that allopurinol worsened her symptoms, she was advised that acute attacks should be expected during the 6 months after the institution of therapy and that allopurinol preceded by colchicine should work effectively. Over the next 3 months the patient had 1 mild attack in her right great toe while taking allopurinol 300 mg/day and colchicine 0.6 mg twice daily. Laboratory results showed that her uric acid level was reduced to 6.3 mg/dL (0.38 mmol/L). She was advised to continue on treatment and to have her primary care physician check her uric acid level and liver function in 3 months. She experienced no further attacks; at the follow-up visit her liver enzymes were normal and her uric acid level had decreased to 5.8 mg/dL (0.35 mmol/L).
DISCUSSION The case of Patient MA illustrates that urate-lowering therapy should not be initiated during an acute attack, because it will prolong the attack or “make the whole thing worse,” as Patient MA stated so succinctly. It is also important to wait 4 to 6 weeks after an acute gout attack before instituting urate-lowering therapy. (However, should an attack occur while the patient is taking allopurinol, treatment must continue.) The case also underscores some of the lifestyle- and medication-related risk factors that can predispose patients to gout. In some cases, serum uric acid levels can be low-
S10
The American Journal of Medicine, Vol 119 (11A), November 2006
Figure 1 Cumulative incidence of gouty arthritis by prior urate levels. Solid curve ⫽ actual findings; dotted curve ⫽ probability. To achieve serum uric acid conversions in millimoles per liter, multiply by 0.0595. (Reprinted with permission from Am J Med.2)
ered sufficiently by appropriate dietary and medication changes to avoid the need for uric acid–lowering therapies; however, the majority of patients will require treatment. Risk factors for gout may be divided into those that are not modifiable and those that are modifiable through changes in diet, lifestyle, or medication.
NONMODIFIABLE RISK FACTORS FOR GOUT Age is the primary nonmodifiable risk factor for gout. The increasing longevity of populations in the United States may contribute to an increased prevalence of gout through an association with age-related diseases and treatments for age-related diseases. Moreover, the clinical manifestations of gout are more likely to present in patients with longstanding hyperuricemia. In this case, Patient MA is 56 years old and, therefore, at substantially higher risk for gout than a younger patient. Sex is the second primary nonmodifiable risk factor for gout.1 Among patients aged ⬍65 years, gout is 4 times more common among men than women. However, gout in the elderly has a more equal sex distribution, probably reflecting the loss of the uricosuric effect of estrogen after menopause. In patients aged ⬎65 years, the gender gap narrows to 1 woman for every 3 men with gout and/or hyperuricemia. With declining use of estrogen replacement therapy, the number of elderly female patients with gout may increase.
articular deposition of monosodium urate monohydrate crystals; hyperuricemia, defined as a serum uric acid level ⬎6.8 mg/dL (⬎0.41 mmol/L), is the primary risk factor for crystal deposition and symptomatic gout.2 The annual incidence of gout is 4.9% among patients with baseline serum urate levels of ⱖ9 mg/dL (ⱖ0.54 mmol/L); in these patients, the cumulative 5-year incidence is 22%. The annual incidence of gouty arthritis is 0.5% among those with urate levels of 7.0 to 8.9 mg/dL (0.42 to 0.53 mmol/L) and 0.1% among those with urate levels ⬍7.0 mg/dL (⬍0.42 mmol/L) (Figure 1).2
Diet and Alcohol Intake
Modifiable risk factors for gout include serum urate levels, diet, alcohol intake, use of certain medications, hypertension, renal disease, transplantation, obesity, and the metabolic syndrome.
Patient MA was on the Atkins diet—a low-carbohydrate, high-protein diet. Although she was successful in losing weight while on the diet, it also may have played a role in the development of hyperuricemia and gout (Table 1).3 The relation between gout and purine-rich foods, high protein intake, and dairy intake was examined in a study by Choi and colleagues,4 conducted in 47,120 men who had no history of gout at baseline. Increased meat and seafood intake was associated with a 1.41-fold increased risk for gout for the highest quintile of intake and a 1.51-fold increased risk for the lowest quintile of intake. The risk for gout was not influenced by purine-rich vegetable consumption or total protein intake. Interestingly, high dairy intake reduced the risk for gout by 50%. Consumption of purine-rich alcoholic beverages (e.g., beer and spirits) is also linked with gout. In 1 study, conducted using data from 14,809 subjects, beer and spirit intake was associated positively with increased serum uric acid levels (P ⬍0.001 for trend). In contrast, wine intake was significantly associated with reduced serum uric acid levels before, but not after, adjusting for other risk factors.5
Serum Urate Levels
Medications
The relation between serum uric acid levels and gout is well established. Gouty arthritis is characterized by the intra-
At high dosages (⬎3 g daily), aspirin reduces uric acid levels; at lower dosages (1–2 g daily) aspirin causes uric
MODIFIABLE RISK FACTORS FOR GOUT
Weaver
Case 3: Acute Gout—Risk Factors and Inappropriate Therapy Table 1
S11
Purine content of select foods and beverages
● High-purine foods and beverages — Meats, including organ meats and meat extracts — Seafood — Yeast and yeast extracts — Vegetables: peas, beans, lentils, asparagus, spinach, and mushrooms — Beer and alcoholic drinks ● Low-purine foods and beverages — Dairy products: milk, cheese, butter, eggs — Grains/cereals and products: bread, pasta, cakes — Vegetables, fruits, nuts: other than peas, beans, lentils, asparagus, spinach, and mushrooms — Sugars, sweets, and gelatin — Water, juices, carbonated beverages, tea, coffee, and cocoa Reprinted with permission from J Rheumatol.3
acid retention.6 Currently, approximately 46% of women and 59% of men at high risk for cardiovascular events take aspirin; in addition, a large number of patients take prophylactic over-the-counter aspirin (e.g., an 81-mg tablet daily) to prevent cardiovascular events. In this case, Patient MA—who has clinically significant hypertension—was switched from a diuretic to a -blocker. Hypertension alone is linked with a 2.31-fold greater risk for gout; however, treatment with diuretics appears to be the primary cause of the increased risk for gout in patients with hypertension. In 1 study, patients who received diuretics were at almost 2-fold greater risk for gout than were those who received other antihypertensive medications.7 The results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and subsequent changes in guideline recommendations suggest that a greater number of patients with hypertension are likely to be prescribed first-line diuretics. The incidence of gout related to diuretic use is therefore likely to grow. It should also be noted that diuretics have been shown to exacerbate the effect of aspirin on uric acid levels.8
ing glucose)—may increase the risk for hyperuricemia and gout.11 Each of the components of the metabolic syndrome appears to increase risk for hyperuricemia; however, adiposity, insulin levels, and—in men— elevated triglycerides increase the risk significantly.12
ADDITIONAL CONSIDERATIONS Patient MA should be advised to further reduce her weight and to limit her intake of alcoholic beverages. A low-purine, protein-restricted diet is advisable; however, most patients find such a diet unpalatable. Moreover, purine-restricted diets, when followed closely, result in only small (1 to 2 mg/dL [0.6 to 0.12 mmol/L]) decreases in serum urate levels.3 Because dietary control is impractical in many patients, many will benefit from treatment with a urate-lowering drug.
TEACHING POINTS ●
Obesity and the Metabolic Syndrome High BMI increases the risk for gout. Compared with individuals with a BMI of 21 to 22.9, the relative risk for gout increases to 1.40 for a BMI of 23 to 24.9, 2.35 for a BMI of 25 to 29.9, 3.26 for a BMI of 30 to 34.9, and 4.41 for a BMI ⱖ35.7 Weight gain is positively associated with serum uric acid levels.9 Conversely, weight reduction has been shown in prospective studies to be associated with declines in uric acid levels.10 In this case, Patient MA had lost substantial weight in the recent past, which may have reduced her serum uric acid levels; however, the diet she used to achieve weight loss may have, at least in part, counteracted this reduction in uric acid levels. The metabolic syndrome—a complex cluster of cardiovascular risk factors in which the patient presents with any 3 of 5 features (hypertriglyceridemia, low high-density lipoprotein cholesterol, elevated blood pressure, central obesity [measured by waist circumference], and elevated fast-
●
●
●
●
Urate-lowering therapy should not commence during an acute gout attack — Wait 4 to 6 weeks — Should an attack occur while on allopurinol, continue therapy Colchicine and nonsteroidal anti-inflammatory drugs are not urate-lowering agents; reserve them for suppression of recurrent attacks Risk factors for gout include: — Serum urate levels ⬎6.8 mg/dL (⬎0.41 mmol/L) — Hypertension — Medications (low-dose aspirin, diuretics, certain immunosuppressive agents) — Obesity — Metabolic syndrome — Intake of high-purine foods and beverages Reduced-purine diets may be impractical because they are unpalatable and result in only small serum uric acid reductions Most patients with hyperuricemia benefit from urate-lowering therapies
S12
The American Journal of Medicine, Vol 119 (11A), November 2006
References 1. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol. 2004;31:1582– 1587. 2. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia: risks and consequences in the Normative Aging Study. Am J Med. 1987;82:421– 426. 3. Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheumatol. 2002;29:1350 –1355. 4. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093–1103. 5. Choi HK, Curhan G. Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2004;51:1023–1029. 6. Yu TF, Gutman AB. Study of the paradoxical effects of salicylate in low, intermediate and high dosage on the renal mechanisms of excretion of urate in man. J Clin Invest. 1959;38:1298 –1313. 7. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the
8.
9. 10.
11.
12.
health professionals follow-up study. Arch Intern Med. 2005;165: 742–748. Caspi D, Lubart E, Graff E, Habot B, Yaron M, Segal R. The effect of mini-dose aspirin on renal function and uric acid handling in elderly patients. Arthritis Rheum. 2000;43:103–108. Glynn RJ, Campion EW, Silbert JE. Trends in serum uric acid levels 1961–1980. Arthritis Rheum. 1983;26:87–93. Yamashita S, Matsuzawa Y, Tokunaga K, Fujioka S, Tarui S. Studies on the impaired metabolism of uric acid in obese subjects: marked reduction of renal urate excretion and its improvement by a low-calorie diet. Int J Obes. 1986;10:255–264. Grundy SM, Cleeman JI, Daniels SR, et al, for the American Heart Association and the National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005;112:2735–2752. Rathmann W, Funkhouser E, Dyar AR, Roseman JM. Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA [Coronary Artery Risk Development in Young Adults] study. Ann Epidemiol. 1998;8:250 –261.
Case 3: Acute Gout—Risk Factors and Inappropriate Therapy Arthur L. Weaver, MD Division of Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA
CASE Patient MA, a 56-year-old postmenopausal white woman with sudden onset of acute pain in the right great toe, was seen by her primary care physician the following day. She walked with support from her husband because she was unable to walk or bear weight without assistance. The patient—a homemaker—reported that she had had 2 previous episodes of similar pain in the great toe and ankle lasting 4 to 5 days that were treated by emergency room physicians with analgesics.
HISTORY AND PHYSICAL EXAMINATION The patient’s past history was unremarkable except for a recent weight loss of approximately 25 lb (11.25 kg) over 3 months related to the initiation of the Atkins diet and the prescribing of a thiazide diuretic for mild hypertension. Physical examination revealed a blood pressure reading of 138/86 mm Hg, a weight of 185 lb (83.25 kg), body mass index (BMI) of 31.8, and height of 5=4⬙ (162.56 cm). Patient MA presented with an acutely swollen, red, and tender right great toe. She was diagnosed with gout and placed on allopurinol 300 mg/day and celecoxib 200 mg twice daily. Two days later, the patient was called by the nurse and told that her serum uric acid level of 8.3 mg/dL (0.49 mmol/L) substantiated the diagnosis of gout. The patient complained of continuing pain in the toe. Ten days after this consultation, the patient called and complained of continued pain in the toe and a recent swelling with severe pain in the left knee. She was told to discontinue use of allopurinol and to seek an appointment with a rheumatologist. At 3 weeks after the onset of pain in her right toe and 5 days after the episode in her left knee, the patient was seen by a rheumatologist. Her right toe was slightly swollen and
Requests for reprints should be addressed to Arthur L. Weaver, MD, 9914 Weavers Point Road, Pequot Lakes, Minnesota 56472. E-mail address: [email protected].
0002-9343/$ -see front matter © 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.amjmed.2006.06.026
tender, but her left knee was swollen and she was limping significantly. Her left knee was aspirated and injected, and the synovial fluid showed a cell count of 15,000 (15.0 ⫻ 109/L) and the presence of urate crystals. A repeat measurement revealed a uric acid level of 7.6 mg/dL (0.45 mmol/L). The patient was advised to switch the thiazide diuretic to a -blocker; she was also instructed to discontinue the Atkins diet but to monitor her caloric intake. She was started on colchicine 0.6 mg twice daily; allopurinol therapy was reinitiated 4 weeks later at a starting dose of 100 mg/day. Although the patient said that allopurinol worsened her symptoms, she was advised that acute attacks should be expected during the 6 months after the institution of therapy and that allopurinol preceded by colchicine should work effectively. Over the next 3 months the patient had 1 mild attack in her right great toe while taking allopurinol 300 mg/day and colchicine 0.6 mg twice daily. Laboratory results showed that her uric acid level was reduced to 6.3 mg/dL (0.38 mmol/L). She was advised to continue on treatment and to have her primary care physician check her uric acid level and liver function in 3 months. She experienced no further attacks; at the follow-up visit her liver enzymes were normal and her uric acid level had decreased to 5.8 mg/dL (0.35 mmol/L).
DISCUSSION The case of Patient MA illustrates that urate-lowering therapy should not be initiated during an acute attack, because it will prolong the attack or “make the whole thing worse,” as Patient MA stated so succinctly. It is also important to wait 4 to 6 weeks after an acute gout attack before instituting urate-lowering therapy. (However, should an attack occur while the patient is taking allopurinol, treatment must continue.) The case also underscores some of the lifestyle- and medication-related risk factors that can predispose patients to gout. In some cases, serum uric acid levels can be low-
S10
The American Journal of Medicine, Vol 119 (11A), November 2006
Figure 1 Cumulative incidence of gouty arthritis by prior urate levels. Solid curve ⫽ actual findings; dotted curve ⫽ probability. To achieve serum uric acid conversions in millimoles per liter, multiply by 0.0595. (Reprinted with permission from Am J Med.2)
ered sufficiently by appropriate dietary and medication changes to avoid the need for uric acid–lowering therapies; however, the majority of patients will require treatment. Risk factors for gout may be divided into those that are not modifiable and those that are modifiable through changes in diet, lifestyle, or medication.
NONMODIFIABLE RISK FACTORS FOR GOUT Age is the primary nonmodifiable risk factor for gout. The increasing longevity of populations in the United States may contribute to an increased prevalence of gout through an association with age-related diseases and treatments for age-related diseases. Moreover, the clinical manifestations of gout are more likely to present in patients with longstanding hyperuricemia. In this case, Patient MA is 56 years old and, therefore, at substantially higher risk for gout than a younger patient. Sex is the second primary nonmodifiable risk factor for gout.1 Among patients aged ⬍65 years, gout is 4 times more common among men than women. However, gout in the elderly has a more equal sex distribution, probably reflecting the loss of the uricosuric effect of estrogen after menopause. In patients aged ⬎65 years, the gender gap narrows to 1 woman for every 3 men with gout and/or hyperuricemia. With declining use of estrogen replacement therapy, the number of elderly female patients with gout may increase.
articular deposition of monosodium urate monohydrate crystals; hyperuricemia, defined as a serum uric acid level ⬎6.8 mg/dL (⬎0.41 mmol/L), is the primary risk factor for crystal deposition and symptomatic gout.2 The annual incidence of gout is 4.9% among patients with baseline serum urate levels of ⱖ9 mg/dL (ⱖ0.54 mmol/L); in these patients, the cumulative 5-year incidence is 22%. The annual incidence of gouty arthritis is 0.5% among those with urate levels of 7.0 to 8.9 mg/dL (0.42 to 0.53 mmol/L) and 0.1% among those with urate levels ⬍7.0 mg/dL (⬍0.42 mmol/L) (Figure 1).2
Diet and Alcohol Intake
Modifiable risk factors for gout include serum urate levels, diet, alcohol intake, use of certain medications, hypertension, renal disease, transplantation, obesity, and the metabolic syndrome.
Patient MA was on the Atkins diet—a low-carbohydrate, high-protein diet. Although she was successful in losing weight while on the diet, it also may have played a role in the development of hyperuricemia and gout (Table 1).3 The relation between gout and purine-rich foods, high protein intake, and dairy intake was examined in a study by Choi and colleagues,4 conducted in 47,120 men who had no history of gout at baseline. Increased meat and seafood intake was associated with a 1.41-fold increased risk for gout for the highest quintile of intake and a 1.51-fold increased risk for the lowest quintile of intake. The risk for gout was not influenced by purine-rich vegetable consumption or total protein intake. Interestingly, high dairy intake reduced the risk for gout by 50%. Consumption of purine-rich alcoholic beverages (e.g., beer and spirits) is also linked with gout. In 1 study, conducted using data from 14,809 subjects, beer and spirit intake was associated positively with increased serum uric acid levels (P ⬍0.001 for trend). In contrast, wine intake was significantly associated with reduced serum uric acid levels before, but not after, adjusting for other risk factors.5
Serum Urate Levels
Medications
The relation between serum uric acid levels and gout is well established. Gouty arthritis is characterized by the intra-
At high dosages (⬎3 g daily), aspirin reduces uric acid levels; at lower dosages (1–2 g daily) aspirin causes uric
MODIFIABLE RISK FACTORS FOR GOUT
Weaver
Case 3: Acute Gout—Risk Factors and Inappropriate Therapy Table 1
S11
Purine content of select foods and beverages
● High-purine foods and beverages — Meats, including organ meats and meat extracts — Seafood — Yeast and yeast extracts — Vegetables: peas, beans, lentils, asparagus, spinach, and mushrooms — Beer and alcoholic drinks ● Low-purine foods and beverages — Dairy products: milk, cheese, butter, eggs — Grains/cereals and products: bread, pasta, cakes — Vegetables, fruits, nuts: other than peas, beans, lentils, asparagus, spinach, and mushrooms — Sugars, sweets, and gelatin — Water, juices, carbonated beverages, tea, coffee, and cocoa Reprinted with permission from J Rheumatol.3
acid retention.6 Currently, approximately 46% of women and 59% of men at high risk for cardiovascular events take aspirin; in addition, a large number of patients take prophylactic over-the-counter aspirin (e.g., an 81-mg tablet daily) to prevent cardiovascular events. In this case, Patient MA—who has clinically significant hypertension—was switched from a diuretic to a -blocker. Hypertension alone is linked with a 2.31-fold greater risk for gout; however, treatment with diuretics appears to be the primary cause of the increased risk for gout in patients with hypertension. In 1 study, patients who received diuretics were at almost 2-fold greater risk for gout than were those who received other antihypertensive medications.7 The results of the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) and subsequent changes in guideline recommendations suggest that a greater number of patients with hypertension are likely to be prescribed first-line diuretics. The incidence of gout related to diuretic use is therefore likely to grow. It should also be noted that diuretics have been shown to exacerbate the effect of aspirin on uric acid levels.8
ing glucose)—may increase the risk for hyperuricemia and gout.11 Each of the components of the metabolic syndrome appears to increase risk for hyperuricemia; however, adiposity, insulin levels, and—in men— elevated triglycerides increase the risk significantly.12
ADDITIONAL CONSIDERATIONS Patient MA should be advised to further reduce her weight and to limit her intake of alcoholic beverages. A low-purine, protein-restricted diet is advisable; however, most patients find such a diet unpalatable. Moreover, purine-restricted diets, when followed closely, result in only small (1 to 2 mg/dL [0.6 to 0.12 mmol/L]) decreases in serum urate levels.3 Because dietary control is impractical in many patients, many will benefit from treatment with a urate-lowering drug.
TEACHING POINTS ●
Obesity and the Metabolic Syndrome High BMI increases the risk for gout. Compared with individuals with a BMI of 21 to 22.9, the relative risk for gout increases to 1.40 for a BMI of 23 to 24.9, 2.35 for a BMI of 25 to 29.9, 3.26 for a BMI of 30 to 34.9, and 4.41 for a BMI ⱖ35.7 Weight gain is positively associated with serum uric acid levels.9 Conversely, weight reduction has been shown in prospective studies to be associated with declines in uric acid levels.10 In this case, Patient MA had lost substantial weight in the recent past, which may have reduced her serum uric acid levels; however, the diet she used to achieve weight loss may have, at least in part, counteracted this reduction in uric acid levels. The metabolic syndrome—a complex cluster of cardiovascular risk factors in which the patient presents with any 3 of 5 features (hypertriglyceridemia, low high-density lipoprotein cholesterol, elevated blood pressure, central obesity [measured by waist circumference], and elevated fast-
●
●
●
●
Urate-lowering therapy should not commence during an acute gout attack — Wait 4 to 6 weeks — Should an attack occur while on allopurinol, continue therapy Colchicine and nonsteroidal anti-inflammatory drugs are not urate-lowering agents; reserve them for suppression of recurrent attacks Risk factors for gout include: — Serum urate levels ⬎6.8 mg/dL (⬎0.41 mmol/L) — Hypertension — Medications (low-dose aspirin, diuretics, certain immunosuppressive agents) — Obesity — Metabolic syndrome — Intake of high-purine foods and beverages Reduced-purine diets may be impractical because they are unpalatable and result in only small serum uric acid reductions Most patients with hyperuricemia benefit from urate-lowering therapies
S12
The American Journal of Medicine, Vol 119 (11A), November 2006
References 1. Wallace KL, Riedel AA, Joseph-Ridge N, Wortmann R. Increasing prevalence of gout and hyperuricemia over 10 years among older adults in a managed care population. J Rheumatol. 2004;31:1582– 1587. 2. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia: risks and consequences in the Normative Aging Study. Am J Med. 1987;82:421– 426. 3. Fam AG. Gout, diet, and the insulin resistance syndrome. J Rheumatol. 2002;29:1350 –1355. 4. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093–1103. 5. Choi HK, Curhan G. Beer, liquor, and wine consumption and serum uric acid level: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2004;51:1023–1029. 6. Yu TF, Gutman AB. Study of the paradoxical effects of salicylate in low, intermediate and high dosage on the renal mechanisms of excretion of urate in man. J Clin Invest. 1959;38:1298 –1313. 7. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the
8.
9. 10.
11.
12.
health professionals follow-up study. Arch Intern Med. 2005;165: 742–748. Caspi D, Lubart E, Graff E, Habot B, Yaron M, Segal R. The effect of mini-dose aspirin on renal function and uric acid handling in elderly patients. Arthritis Rheum. 2000;43:103–108. Glynn RJ, Campion EW, Silbert JE. Trends in serum uric acid levels 1961–1980. Arthritis Rheum. 1983;26:87–93. Yamashita S, Matsuzawa Y, Tokunaga K, Fujioka S, Tarui S. Studies on the impaired metabolism of uric acid in obese subjects: marked reduction of renal urate excretion and its improvement by a low-calorie diet. Int J Obes. 1986;10:255–264. Grundy SM, Cleeman JI, Daniels SR, et al, for the American Heart Association and the National Heart, Lung, and Blood Institute. Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation. 2005;112:2735–2752. Rathmann W, Funkhouser E, Dyar AR, Roseman JM. Relations of hyperuricemia with the various components of the insulin resistance syndrome in young black and white adults: the CARDIA [Coronary Artery Risk Development in Young Adults] study. Ann Epidemiol. 1998;8:250 –261.