The Treatment of Gout

,

Medical Education Library

The Treatment of Gout

June 2012 · Vol. 61, No. 06 Suppl: S11-S15

By

Gary Ruoff, MD

References

1. Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011;63(10):3136-3141.

2. Weaver AL. Epidemiology of gout. Cleve Clin J Med. 2008;75(suppl 5):S9-S12.

3. Choi HK, Atkinson K, Karlson EW, Curhan G. Obesity, weight change, hypertension, diuretic use, and risk of gout in men: the health professionals follow-up study. Arch Intern Med. 2005;165(7):742-748.

4. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336(7639):309-312.

5. 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(11):1093-1103.

6. Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Alcohol intake and risk of incident gout in men: a prospective study. Lancet. 2004;363(9417):1277-1281.

7. Choi HK, Ford ES, Li C, Curhan G. Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 2007;57(1):109-115.

8. Perlstein TS, Gumieniak O, Williams GH, et al. Uric acid and the development of hypertension: the normative aging study. Hypertension. 2006;48(6):1031-1036.

9. Bos MJ, Koudstaal PJ, Hofman A, Witteman JC, Breteler MM. Uric acid is a risk factor for myocardial infarction and stroke: the Rotterdam study. Stroke. 2006;37(6):1503-1507.

10. Iseki K, Ikemiya Y, Inoue T, Iseki C, Kinjo K, Takishita S. Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis. 2004;44(4):642-650.

11. Tomita M, Mizuno S, Yamanaka H, et al. Does hyperuricemia affect mortality? A prospective cohort study of Japanese male workers. J Epidemiol. 2000;10(6):403-409.

12. Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82(3):421-426.

13. Mandell BF. Clinical manifestations of hyperuricemia and gout. Cleve Clin J Med. 2008;75(Suppl 5):S5-S8.

14. Hamburger M, Baraf HS, Adamson TC III, et al. 2011 Recommendations for the diagnosis and management of gout and hyperuricemia. Postgrad Med. 2011;123 (6 suppl 1):3-36.

15. Zhang W, Doherty M, Bardin T, et al. EULAR evidence based recommendations for gout. Part II: Management. Report of a task force of the EULAR Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65(10):1312-1324.

16. Schumacher HR Jr, Boice JA, Daikh DI, et al. Randomised double blind trial of etoricoxib and indometacin in treatment of acute gouty arthritis. BMJ. 2002;324(7352):1488-1492.

17. Jordan KM, Cameron JS, Snaith M, et al. British Society for Rheumatology and British Health Professionals in Rheumatology guideline for the management of gout. Rheumatology (Oxford). 2007;46(8):1372-1374.

18. Trelle S, Reichenbach S, Wandel S, et al. Cardiovascular safety of non-steroidal anti-inflammatory drugs: network meta-analysis. BMJ. 2011;342:c7086.-

19. Schmidt M, Christiansen CF, Mehnert F, Rothman KJ, Sorensen HT. Non-steroidal anti-inflammatory drug use and risk of atrial fibrillation or flutter: population based case-control study. BMJ. 2011;343:d3450.-

20. NSAIDS and chronic kidney disease. US Centers for Disease Control and Prevention. http://www.cdc.gov/diabetes/news/docs/nsaid_video.htm. Published 2012. Accessed April 22, 2012.

21. Gislason GH, Rasmussen JN, Abildstrom SZ, et al. Increased mortality and cardiovascular morbidity associated with use of nonsteroidal anti-inflammatory drugs in chronic heart failure. Arch Intern Med. 2009;169(2):141-149.

22. Janssens HJ, Lucassen PL, Van de Laar FA, Janssen M, Van de Lisdonk EH. Systemic corticosteroids for acute gout. Cochrane Database Syst Rev. 2008;(2):CD005521.-

23. Janssens HJ, Janssen M, van de Lisdonk EH, van Riel PL, van Weel C. Use of oral prednisolone or naproxen for the treatment of gout arthritis: a double-blind, randomised equivalence trial. Lancet. 2008;371(9627):1854-1860.

24. Schlesinger N, Schumacher R, Catton M, Maxwell L. Colchicine for acute gout. Cochrane Database Syst Rev. 2006;(4):CD006190.-

25. Terkeltaub RA, Furst DE, Bennett K, Kook KA, Crockett RS, Davis MW. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62(4):1060-1068.

26. Colcrys [package insert]. Philadelphia, PA: AR Scientific, Inc.; 2011.

27. Becker MA, Ruoff GE. What do I need to know about gout? J Fam Pract. 2010;59(6 suppl):S1-S8.

28. Wortmann RL, Macdonald PA, Hunt B, Jackson RL. Effect of prophylaxis on gout flares after the initiation of urate-lowering therapy: analysis of data from three phase III trials. Clin Ther. 2010;32(14):2386-2397.

29. Luk AJ, Levin GP, Moore EE, Zhou XH, Kestenbaum BR, Choi HK. Allopurinol and mortality in hyperuricaemic patients. Rheumatology (Oxford). 2009;48(7):804-806.

30. Goicoechea M, de Vinuesa SG, Verdalles U, et al. Effect of allopurinol in chronic kidney disease progression and cardiovascular risk. Clin J Am Soc Nephrol. 2010;5(8):1388-1393.

31. Reinders MK, Haagsma C, Jansen TL, et al. A randomised controlled trial on the efficacy and tolerability with dose escalation of allopurinol 300-600 mg/day versus benzbromarone 100-200 mg/day in patients with gout. Ann Rheum Dis. 2009;68(6):892-897.

32. Stamp LK, O’Donnell JL, Zhang M, et al. Using allopurinol above the dose based on creatinine clearance is effective and safe in patients with chronic gout, including those with renal impairment. Arthritis Rheum. 2011;63(2):412-421.

33. Zyloprim [package insert]. San Diego, CA: Prometheus Laboratories Inc.; 2003.

34. Becker MA, Schumacher HR Jr, Wortmann RL, et al. Febuxostat compared with allopurinol in patients with hyperuricemia and gout. N Engl J Med. 2005;353(23):2450-2461.

35. Becker MA, Schumacher HR, Espinoza LR, et al. The urate-lowering efficacy and safety of febuxostat in the treatment of the hyperuricemia of gout: the CONFIRMS trial. Arthritis Res Ther. 2010;12:doi:10.1186/ar2978.

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Table of Contents

Introduction

Managing the Multiple Symptoms of Benign Prostatic Hyperplasia — CME

The Treatment of Gout

Managing Type 2 Diabetes in Men

Meeting New Challenges with Antiplatelet Therapy in Primary Care

Coronary Heart Disease in Men

Addressing Key Questions with Statin Therapy — CME

DISCLOSURES

Dr. Ruoff has disclosed that he is on the speakers’ bureau for and has received research grants from Takeda Pharmaceuticals.

SUPPORT

This program is sponsored by the PCEC and is supported by funding from URL Pharma, Inc.

DB is a 50-year-old obese male visiting the clinic for symptoms suggestive of allergic rhinitis. The nurse has informed the family physician that DB was limping from the waiting room to the examination room. DB reports that he has been experiencing pain in his left big toe and ankle over the past few days. The last time this happened, the pain resolved within 7 to 10 days.

DB reports that he has experienced 4 or 5 similar episodes over the past 3 years. The first attacks affected his left big toe, but he now also experiences some pain in his left ankle. The pain is moderate, peaks in 1 to 2 days, and resolves within 7 to 10 days. Acetaminophen provided little pain relief so DB now takes ibuprofen 400 mg 3 times daily, as it “helps take the edge off.” Other medications include aspirin 81 mg per day and an oral antihistamine as needed for hay fever. DB reports that he eats seafood 2 to 3 times per week and red meat 1 to 2 times per week; he drinks 2 six-packs of beer per week.

Physical examination: weight, 186 lb (body mass index [BMI], 27 kg/m²); blood pressure, 126/76 mm Hg; and temperature, 98.8°F. His left big toe and ankle are red, slightly swollen, and warm with a small subcutaneous nodule noted on the first metatarsophalangeal joint. There is no sign of skin or joint infection.

The impression from his history and physical exam is that DB is suffering from an acute attack of gout, but the family physician also considers other diagnoses.

Background

Gout is a heterogeneous disorder that peaks in incidence in the fifth decade. Gout is caused by hyperuricemia, generally as a result of reduced excretion of uric acid by the kidneys; hyperuricemia may also result from overproduction of uric acid. Data from the National Health and Nutrition Examination Survey (NHANES) 2007-2008 indicate that the prevalence of gout continues to rise in the United States, likely related to the increasing frequency of adiposity and hypertension. Overall, about 75% of the 8.3 million people with gout are men.¹

Risk Factors

Clinically defined hyperuricemia—a serum urate (sUA) level greater than 6.8 mg/dL, the concentration at which urate exceeds its solubility in most biological fluids—is the major risk factor for gout. However, not all persons with hyperuricemia have gout. Data from NHANES 2007-2008, in which the definition of hyperuricemia was an sUA level greater than 7.0 mg/dL for men and greater than 5.7 mg/dL for women, showed the mean sUA level to be 6.1 mg/dL in men and 4.9 mg/dL in women, corresponding to hyperuricemia prevalences of 21.2% and 21.6%, respectively.¹

There are several other risk factors for gout, including hypertension, diabetes, hyperlipidemia, chronic kidney disease, cardiovascular disease (CVD), and metabolic syndrome.² For a man with hypertension, the relative risk (RR) of gout is 2.3 compared with a normotensive man.³ Furthermore, it is well established that the use of diuretics increases the risk of gout (RR, 1.8).³ Several other medications increase sUA level as well: aspirin (including low-dose), cyclosporine, pyrazinamide, ethambutol, and niacin.²

Lifestyle and diet also pose a risk for gout. The risk of gout increases with BMI such that, compared with a man with a BMI of 21 to 22.9 kg/m², the RR of gout is doubled for a man with a BMI of 25 to 29.9 kg/m²; for a man with a BMI of 35 kg/m² or more, the RR is tripled.³ Sugar-sweetened soft drinks (but not diet soft drinks) and fructose-rich fruits and fruit juices also increase the risk of gout, as do a high alcohol intake, particularly beer, and a diet rich in meat (especially organ meat, turkey, or wild game) or seafood.⁴ A moderate intake of purine-rich vegetables (eg, peas, beans, lentils, spinach, mushrooms, oatmeal, and cauliflower) or protein is not associated with an increased risk of gout, while a high consumption of dairy products is associated with a decreased risk.^5,6