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Can Fam Physician. 2009 December; 55(12): 1209–1212.
PMCID: PMC2793228

Taking the stress out of managing gout

Tessa Laubscher, MB ChB CCFP FCFP
Assistant Professor of Academic Family Medicine at the University of Saskatchewan in Saskatoon
Zack Dumont
Pharmacist for the RxFiles Academic Detailing Program
Loren Regier
Program Coordinator of the RxFiles Academic Detailing Program for Saskatoon Health Region

Case 1

Mr J.P., a 43-year-old chemical engineer, is a relatively new patient in your practice. He is concerned about increasingly frequent episodes of “gout” over the past 6 months. He describes acute onset of red, swollen, painful joints in his big toes, ankles, and rarely his knees. He reports that he was diagnosed with gout 3 years ago, but cannot recall specific laboratory tests; he takes 50 mg of indomethacin 3 times daily, which is effective for each acute episode. He is now wondering about dietary and medical management to prevent gout, as the acute arthritis is interfering with his work (which involves frequent overseas travel) and his exercise (long-distance running). Mr J.P. has no other medical history of note; takes no other medications or supplements; and is a nonsmoker and has an alcohol intake of 1 to 2 glasses of wine per week. Results of his physical examination are unremarkable, with a body mass index of 25.9 kg/m2, blood pressure of 126/80 mm Hg, no acute arthritis, and no tophi. You provide Mr J.P. with a handout on a low-purine diet for gout and a requisition for laboratory tests.

Bringing evidence to practice

  • Consider nonsteroidal anti-inflammatory drugs (NSAIDs) other than indomethacin. Traditionally, indomethacin has been the NSAID of choice for acute attacks of gout; however, other NSAIDs have been shown to be effective in gout,18 and indomethacin has never been proven to be any more efficacious.9 Additionally, indomethacin might be associated with more adverse effects, including central nervous system disturbances in the elderly (eg, headaches, confusion).3,8 Suitable alternatives would include naproxen, ibuprofen, or celecoxib, depending on cardiovascular risk, gastrointestinal risk, or desire for availability without prescription.
  • Table 1 1016 provides an overview of the management of acute gouty arthritis; the full version of the RxFiles gout treatment chart is available on-line from CFPlus.*
    Table 1
    Managing acute gouty arthritis: The full version of the RxFiles gout treatment chart10 is available on-line from CFPlus.
  • Compliance with low-purine diets can be challenging and acceptance rates might be low. A low-calorie diet (1600 kcal/d) was shown to decrease serum uric acid (SUA) levels by almost 100 μmol/L in obese men.17 As many of the risk factors for gout (eg, hypertension, dyslipidemia, diabetes mellitus) are also risk factors for cardiovascular disease,18 the additional benefits of weight loss and healthy eating should not be overlooked.1927

The recurrent attacks over the past 6 months suggest this patient might have progressed to intercritical gout (ie, symptomatic gout with increasingly frequent attacks of acute gouty arthritis).2835 Checking SUA levels would assist in deciding whether to begin preventive treatment.31,32 If SUA levels are elevated, the patient could either overproduce or underexcrete uric acid; SUA-lowering therapy with allopurinol might be beneficial in either situation.31,32

Mr J.P. returns 3 weeks later. His SUA level is elevated at 614 μmol/L (normal 150 to 480 μmol/L), despite his following a low-purine diet. Other test results were normal—serum creatinine was 74 μmol/L; fasting glucose was 5.4 mmol/L. Given that weight loss is not likely to provide the same benefits for this patient as would be seen in an obese individual, the final-year medical student working with you today suggests starting treatment with allopurinol. He is uncertain how to do this, as he recalls that the drug might precipitate an acute attack of gout.

Bringing evidence to practice

  • Allopurinol, a xanthine-oxidase inhibitor, impedes the production of uric acid and can be used to prevent further attacks of acute gouty arthritis.3639 As any sudden change in SUA levels can precipitate an attack, preventive therapy with low-dose colchicine or NSAIDs during titration of allopurinol is recommended.18,31,32,40
  • Table 2 14,31,32,40 provides an overview of the considerations for when and how to initiate allopurinol; the full version of the RxFiles gout chart is available from cFPlus.*
    Table 2
    Starting preventive therapy for gout with allopurinol: When and how.

Mr J.P. was started on 100 mg of allopurinol and 0.6 mg of colchicine daily. He had no acute attacks and no medication side effects. After 4 weeks of therapy his SUA level was 443 μmol/L, so the dose of allopurinol was titrated to ideally achieve an SUA level below 360 μmol/L. After 6 months of taking 300 mg of allopurinol daily, the patient had no further episodes of arthritis and was back running in half marathons; his SUA was 335 μmol/L. Colchicine prophylaxis had been stopped after 3 months.

Case 2

Mr V.S., aged 76, is in your clinic complaining of 2 days of a red, swollen, and very painful right wrist and third proximal interphalangeal joint. He denies any trauma and states that this is similar to previous gout attacks. He was diagnosed with gouty arthritis about 10 years ago and has not had an attack for 3 years. He went to a medical clinic yesterday and was prescribed colchicine, 0.6 mg 3 times daily. Today he has severe nausea, mild diarrhea, and his hand does not feel much better. Examination confirms severe acute inflammatory arthritis.

Mr V.S. has long-standing hypertension, chronic atrial fibrillation, chronic kidney disease (estimated glomerular filtration rate of 35 mL/min), and obesity (body mass index of 32 kg/m2). Current medications include amlodipine 10 mg daily, perindopril 4 mg daily, hydrochlorothiazide 25 mg daily (dose increased from 12.5 mg daily about 6 months ago), metoprolol 25 mg twice daily, and warfarin 5 mg daily. He is an ex-smoker and abstains from alcohol. What are your therapeutic options for this acute episode of gouty arthritis?

Bringing evidence to practice

  • Colchicine or NSAIDs would be initial options for management of the acute attack.18,31,32 However, in a patient with contraindications or intolerance to these agents, a short course of corticosteroids might be a reasonable option.13,18,31,32,41
  • Systemic steroids, oral or intramuscular, are suit able for polyarticular attacks.13,18,41 When attacks are monoarticular, intra-articular injections of corticosteroids provide comparable pain relief16,31; this treatment is generally reserved for use by physicians with experience in this technique.
  • Diuretics have been associated with precipitating acute attacks of gout. However, a retrospective review showed that hydrochlorothiazide (12.5 mg daily) was not associated with an increased incidence of gout attacks.42 Hydrochlorothiazide, a first-line option for the treatment of hypertension,43 is an effective, low-cost medication, and in appropriate doses it can be used safely in many patients with gout.

In a patient like Mr V.S., who has a history of hypertension and chronic kidney disease, NSAIDs are best avoided.44 Furthermore, he has had an adverse reaction to low-dose colchicine (gastrointestinal upset), which also did not provide adequate pain relief. Because the attack appears to be polyarticular, a short course of oral prednisone is reasonable41 (See Table 11016 for dosage suggestions). It is possible that the recent attacks are drug-induced; therefore, consider stopping the hydrochlorothiazide and restarting the patient at 12.5 mg daily after the attack has resolved.

Mr V.S. returns to you 8 months later, having had 3 more episodes of acute arthritis involving his foot and hand, including 2 attacks after he self-terminated his hydrochlorothiazide therapy. He wants preventive therapy. His SUA level is 418 μmol/L, and his renal function remains stable.

Bringing evidence to practice

  • The risk of allopurinol rash, hypersensitivity syndrome, and Stevens-Johnson syndrome is increased in patients with chronic kidney disease.4547 Cautious initiation and dosage adjustments can reduce the risk47 (Table 214,31,32,40).
  • Adverse effects of colchicine appear to be dose-and can be minimized with lower-dosage regimens that are often effective11 (Table 11016). Additionally, to prevent attacks during initiation of SUA-altering therapy, a reduced dose of colchicine can be used safely in most patients with chronic kidney disease.


RxFiles is an academic detailing program providing objective comparative drug information. RxFiles incorporates information from family physicians, other specialists, and pharmacists with an extensive review of the literature to produce newsletters, question-and-answer summaries, trial summaries, and drug comparison charts. The RxFiles Drug Comparison Charts book and website have become practical tools for evidence-based and clinically relevant drug use information throughout Canada. For more information, go to


Competing interests

RxFiles and contributing authors do not have any commercial competing interests. RxFiles Academic Detailing Program is funded through a grant from Saskatchewan Health to Saskatoon Health Region; additional “not for profit; not for loss” revenue is obtained from sale of books and on-line subscriptions.

CFPlus Go

* The full version of the RxFiles gout treatment chart and gout newsletter are available at Go to the full text of the article on-line, then click on CFPlus in the menu at the top right of the page.


1. 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):1854–60. [PubMed]
2. Alloway JA, Moriarty MJ, Hoogland YT, Nashel DJ. Comparison of triamcinolone acetonide with indomethacin in the treatment of acute gouty arthritis. J Rheumatol. 1993;20(1):111–3. [PubMed]
3. Man CY, Cheung IT, Cameron PA, Rainer TH. Comparison of oral prednisolone/paracetamol and oral indomethacin/paracetamol combination therapy in the treatment of acute goutlike arthritis: a double-blind, randomized, controlled trial. Ann Emerg Med. 2007;49(5):670–7. [PubMed]
4. Shrestha M, Morgan DL, Moreden JM, Singh R, Nelson M, Hayes JE. Randomized double-blind comparison of the analgesic efficacy of intramuscular ketorolac and oral indomethacin in the treatment of acute gouty arthritis. Ann Emerg Med. 1995;26(6):682–6. [PubMed]
5. Cheng TT, Lai HM, Chiu CK, Chem YC. A single-blind, randomized, controlled trial to assess the efficacy and tolerability of rofecoxib, diclofenac sodium, and meloxicam in patients with acute gouty arthritis. Clin Ther. 2004;26(3):399–406. [PubMed]
6. Altman RD, Honig S, Levin JM, Lightfoot RW. Ketoprofen versus indomethacin in patients with acute gouty arthritis: a multicenter, double blind comparative study. J Rheumatol. 1988;15(9):1422–6. [PubMed]
7. Rubin BR, Burton R, Navarra S, Antigua J, Londoño J, Pryhuber KG, et al. Efficacy and safety profile of treatment with etoricoxib 120 mg once daily compared with indomethacin 50 mg three times daily in acute gout: a randomized controlled trial. Arthritis Rheum. 2004;50(2):598–606. [PubMed]
8. Willburger RE, Mysler E, Derbot J, Jung T, Thurston H, Kreiss A, et al. Lumiracoxib 400 mg once daily is comparable to indomethacin 50 mg three times daily for the treatment of acute flares of gout. Rheumatology (Oxford) 2007;46(7):1126–32. Epub 2007 May 3. [PubMed]
9. Bandolier. Indomethacin and other NSAIDs for gout [webpage] Oxford, UK: Bandolier; 2007. [Accessed 2009 Oct 12]. Available from:
10. Dumont Z, Jensen B, Regier L. RxFiles drug comparison charts. 7th ed. Saskatoon, SK: Saskatoon Health Region; 2008. [Accessed 2009 Oct 14]. The gout—Q&A and treatment options; p. 58. Available from:
11. US Food and Drug Administration. Information for health-care professionals: new safety information for colchicine (marketed as Colcrys) [FDA Alert] Silver Spring, MD: US Food and Drug Administration; 2009. [Accessed 2009 Oct 12]. Available from:
12. Ahern MJ, Reid C, Gordon TP, McCredie M, Brooks PM, Jones M, et al. Does colchicine work? The results of the first controlled study in acute gout. Aust N Z J Med. 1987;17(3):301–4. [PubMed]
13. McGettigan P, Henry D. Cardiovascular risk and inhibition of cyclooxygenase: a systematic review of the observational studies of selective and non-selective inhibitors of cyclooxygenase 2. JAMA. 2006;296(13):1633–44. [PubMed]
14. Kearney PM, Baigent C, Godwin J, Halls H, Emberson JR, Patrono C. Do selective cyclo-oxygenase-2 inhibitors and traditional non-steroidal anti-inflammatory drugs increase the risk of atherothrombosis? Meta-analysis of randomised trials. BMJ. 2006;332(7553):1302–8. [PMC free article] [PubMed]
15. Catella-Lawson F, Reilly MP, Kapoor SC, Cucchiara AJ, DeMarco S, Tournier B, et al. Cyclooxygenase inhibitors and the antiplatelet effects of aspirin. N Engl J Med. 2001;345(25):1809–17. [PubMed]
16. Fernández C, Noguera R, González JA, Pascual E. Treatment of acute attacks of gout with a small dose of intraarticular triamcinolone acetonide. J Rheumatol. 1999;26(10):2285–6. [PubMed]
17. Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000;59(7):539–43. [PMC free article] [PubMed]
18. Richette P, Bardin T. Gout. Lancet. 2009 Aug 17; [Epub ahead of print]
19. Choi HK, Curhan G. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study. BMJ. 2008;336(7639):309–12. Epub 2008 Jan 31. [PMC free article] [PubMed]
20. 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):1277–81. [PubMed]
21. Choi HK, Curhan G. Coffee, tea, and caffeine consumption and serum uric acid level: the third national health and nutrition examination survey. Arthritis Rheum. 2007;57(5):816–21. [PubMed]
22. Choi HK, Gao X, Curhan G. Vitamin C intake and the risk of gout in men: a prospective study. Arch Intern Med. 2009;169(5):502–7. [PMC free article] [PubMed]
23. Underwood M. Sugary drinks, fruit, and increased risk of gout. BMJ. 2008;336(7639):285–6. [PMC free article] [PubMed]
24. Krishnan E, Svendsen K, Neaton JD, Grandits G, Kuller LH. MRFIT Research Group. Long-term cardiovascular mortality among middle-aged men with gout. Arch Intern Med. 2008;168(10):1104–10. [PubMed]
25. Wheeler JG, Juzwishin KD, Eiriksdottir G, Gudnason V, Danesh J. Serum uric acid and coronary heart disease in 9,458 incident cases and 155,084 controls: prospective study and meta-analysis. PLoS Med. 2005;2(3):e76. Epub 2005 Mar 29. [PMC free article] [PubMed]
26. Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk. N Engl J Med. 2008;359(17):1811–21. [PMC free article] [PubMed]
27. Strasak A, Ruttmann E, Brant L, Kelleher C, Klenk J, Concin H, et al. Serum uric acid and risk of cardiovascular mortality: a prospective long-term study of 83 683 Austrian men. Clin Chem . 2008;54(2):273–84. Epub 2007 Nov 26. [PubMed]
28. Choi HK, Mount DB, Reginato AM. American College of Physicians; American Physiological Society. Pathogenesis of gout. Ann Intern Med. 2005;143(7):499–516. [PubMed]
29. Teng GG, Nair R, Saag KG. Pathophysiology, clinical presentation and treatment of gout. Drugs. 2006;66(12):1547–63. [PubMed]
30. Zhang W, Doherty M, Pascual E, Bardin T, Barskova V, Conaghan P, et al. EULAR evidence based recommendations for gout. Part I: diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT) Ann Rheum Dis . 2006;65(10):1301–11. Epub 2006 May 17. [PMC free article] [PubMed]
31. Zhang W, Doherty M, Bardin T, Pascual E, Barskova V, Conaghan P, 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):1312–24. Epub 2006 May 17. [PMC free article] [PubMed]
32. Jordan KM, Cameron JS, Snaith M, Zhang W, Doherty M, Seckl J, et al. British Society for Rheumatology and British Health Professionals in Rheumatology Standards guideline for the management of gout. Rheumatology (Oxford) 2007;46(8):1372–4. Epub 2007 May 23. [PubMed]
33. Underwood M. Diagnosis and management of gout. BMJ. 2006;332(7553):1315–9. [PMC free article] [PubMed]
34. Eggebeen AT. Gout: an update. Am Fam Physician . 2007;76(6):801–8. summary for patients 811–2. [PubMed]
35. Fox R. Management of recurrent gout. BMJ. 2008;336(7639):329. [PMC free article] [PubMed]
36. Peterson GM, Sugden JE. Educational program to improve the dosage prescribing of allopurinol. Med J Aust. 1995;162(2):74–7. [PubMed]
37. Lee MH, Graham GG, Williams KM, Day RO. A benefit-risk assessment of benzbromarone in the treatment of gout. Was its withdrawal from the market in the best interest of patients? Drug Saf. 2008;31(8):643–65. [PubMed]
38. Reinders MK, van Roon EN, Jansen TL, Delsing J, Griep EN, Hoekstra M, et al. Efficacy and tolerability of urate lowering drugs in gout: a randomised controlled trial of benzbromarone versus probenecid after failure of allopurinol. Ann Rheum Dis . 2009;68(1):51–6. Epub 2008 Feb 4. [PubMed]
39. Reinders MK, Haagsma C, Jansen TL, van Roon EN, Delsing J, van de Laar MA, 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):892–7. Epub 2008 Jul 16. [PubMed]
40. Borstad GC, Bryant LR, Abel MP, Scroggie DA, Harris MD, Alloway JA. Colchicine for prophylaxis of acute flares when initiating allopurinol for chronic gouty arthritis. J Rheumatol. 2004;31(12):2429–32. [PubMed]
41. 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. [PubMed]
42. Gurwitz JH, Kalish SC, Bohn RL, Glynn RJ, Monane M, Mogun H, et al. Thiazide diuretics and the initiation of anti-gout therapy. J Clin Epidemiol. 1997;50(8):953–9. [PubMed]
43. Tobe S, Lebel M. Recommendations for the management of hypertension. Canadian Hypertension Education Program; 2009. [Accessed 2009 Oct 21]. Available from:
44. Gooch K, Culleton BF, Manns BJ, Zhang J, Alfonso H, Tonelli M, et al. NSAID use and progression of chronic kidney disease. Am J Med. 2007;120(3):280.e1–7. [PubMed]
45. Halevy S, Ghislain PD, Mockenhaupt M, Fagot JP, Bouwes Bavinck JN, Sidoroff A, et al. Allopurinol is the most common cause of Stevens-Johnson syndrome and toxic epidermal necrolysis in Europe and Israel. J Am Acad Dermatol . 2008;58(1):25–32. Epub 2007 Oct 24. [PubMed]
46. Fam AG, Dunne SM, Iazzetta J, Paton TW. Efficacy and safety of desensitization to allopurinol following cutaneous reactions. Arthritis Rheum. 2001;44(1):231–8. [PubMed]
47. Hande KR, Noone RM, Stone WJ. Severe allopurinol toxicity. Description and guidelines for prevention in patients with renal insufficiency. Am J Med. 1984;76(1):47–56. [PubMed]

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