Quality of Care Indicators for Gout Management

Special Report


Theodore R. Fields, MD, FACP

Attending Physician, Hospital for Special Surgery
Professor of Clinical Medicine, Weill Cornell Medical College

In view of the lack of clear-cut guidelines on gout management, a multi-institutional group has developed ten indicators for quality of care in the management of gout. The group's literature review supported their sense that gout is an under-studied condition.

In view of the common observation of variability in the management of gout, these indicators remain quite timely. The authors note that certain factors make the need for these indicators more acute, such as the common use of indomethacin to treat gout, a medication which should be used with great caution in the elderly. The literature has also described significant errors in the use of intravenous colchicine and in the use of allopurinol.

A 10-member gout treatment expert panel reviewed proposed indicators. An indicator was considered valid if the median rating of the panel was = 7 on a 1-9 scale of validity. The panel ultimately agreed on 120 articles for the final reference database, 23 of which were randomized clinical trials.

The quality indicators used included 3 categories: 1) use of urate-lowering therapy, 2) behavioral modifications and 3) use of anti-inflammatory medications. They are reviewed in detail in Table 1. In the article[1], supporting references for each recommended indicator were provided.

Table 1: Quality Indicators for Gout Management Rated Valid by Panel
Use of uric acid-lowering therapy
1 If a patient has renal insufficiency (creatinine = to 2.0 or creatinine clearance = to 50ml/min), the patient should be started on < 300mg/d of allopurinol, because of increased allopurinol toxicity with renal insufficiency.
2 If a patient receiving azathioprine or 6-MP is to receive allopurinol, then the dose of azathioprine or 6-MP must be reduced by a minimum of 50%, to avoid potentially toxic increases in azathioprine or 6-MP level.
3 If a patient with tophaceous gout is to be started on allopurinol, and the patient has neither renal insufficiency (as defined in #1 above) nor peptic ulcer disease, then she should receive colchicine or NSAID prophylaxis in view of the frequently increased gout attacks which occur early in allopurinol therapy.
4 Asymptomatic hyperuricemia should not be treated. Asymptomatic = no gout, tophi, kidney stone, hyperuricosuria or ongoing treatment of malignancy.
5 Patients with renal insufficiency (as defined in #1 above) or history of kidney stone should be treated with allopurinol rather than a uricosuric agent.
6 Indications for the use of a urate-lowering agent include: 1) tophi, 2) erosive changes on x-ray due to gout, 3) gout attacks = 2 per year.
7 If a patient is given allopurinol, serum urate should be checked at least once during the first 6 months, to consider dose adjustment.
8 If a patient with gout is obese (BMI = 28) or uses alcohol = 1 drink a day, they should be advised that weight loss and/or decreased alcohol use may be beneficial in therapy of gout.
9 If a patient with acute gouty arthritis has neither renal insufficiency (as defined in #1 above) nor peptic ulcer disease, then the patient should be treated with NSAID, ACTH or glucocorticoid (systemic or intra-articular) or colchicine.
10 If a gout patient is treated with colchicine at a minimum of 0.5mg daily for 6 months or longer, and has renal insufficiency (as defined in #1 above), then CBC and CPK should be checked at least once q6 months.

Now, 5 ½ years after these indicators have been published, they still contain many valuable suggestions. Some updates that may be considered are:

  1. These quality indicators do not specifically mention the goal uric level as being < 6.0. This goal is supported by the pathophysiology of uric acid crystals, which reach their saturation point at core body temperature (37.0 degrees C) at a level of 6.8 mg/dL, and lower at cooler locations such as the big toe. It is also supported by numerous clinical studies demonstrating a better outcome in terms of gout episodes, tophi, and joint damage by keeping the urate level < 6.0.
  2. The guidelines do not mention the clinical benefit of waiting 2-3 weeks after an acute attack to start a urate-lowering therapy. It is well-documented that urate-lowering therapy leads to increased gout attacks in the short term, and is likely to worsen a flare if given while the flare is active.
  3. Studies with the agent febuxostat, approved by the FDA in 2/09, show that two weeks after beginning the agent is the ideal time to check uric acid levels and determine if the goal level has been reached. This time-frame would be suitable for a guideline point.
  4. Febuxostat has 3% renal excretion versus 90% renal excretion for both allopurinol and its active metabolite, oxypurinol, and febuxostat has been studied in patients with mild to moderate renal insufficiency (eGFR 30-90 ml/min). A reasonable addition to the guidelines might state that in patients with renal insufficiency and gout that this agent may be considered (or this point could be added to guideline point #1, which addresses allopurinol dosing in renal insufficiency. Febuxostat should also be added as an option in guideline point #5, regarding using allopurinol rather than probenecid in patients with renal insufficiency. It should be added that if the eGFR is between 30 and 90, febuxostat is an option.
  5. Colchicine has been demonstrated, for an acute gout attack, to be equally effective if given at 1.2mg followed in an hour by 0.6mg, and no further doses, as compared with the standard regimen of 0.6mg every hour until improvement or diarrhea. Diarrhea was dramatically lower in the lower regimen, which was approved by the FDA in 4/09. This new dosage regimen could be an addition to the guidelines.
  6. Guideline point #2, regarding azathioprine and 6-MP, might be amended to note that combining these agents with allopurinol should be avoided if at all possible (e.g. by using mycophenolate mofetil rather than azathioprine in transplant patients). Also, it should be added that the same concerns with allopurinol apply to the newer agent febuxostat, which is likewise a xanthine oxidase inhibitor.
  7. In guideline point #3, regarding using prophylaxis against gout attacks when starting allopurinol, it should be added that these same precautions are appropriate when starting febuxostat or probenecid.
  8. In guideline point #7, regarding checking follow-up uric acid levels, both febuxostat and probenecid should be added to allopurinol as agents mandating uric acid follow-up. 

It is important to increase consistency in physician practice patterns where the medical literature is clear and consistent, and this is applicable to many of the recommendations in Table 1, and to the updated suggestions above. Where the published literature cannot provide definitive recommendations for specific areas of gout management, the availability of expert consensus opinion is valuable to clinicians.


[1] Mikuls TR, MacLean CH, Olivieri J, Patino F, Allison JJ, Farrar JT, Bilker WB, Saag KG: Quality of Care Indicators for Gout Management. Arthritis Rheum, 50:3, 937-943, 2004.
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