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Breaking down the latest in gout care

14 February 2025 - Dr Alana Bruce

Gout is a chronic but treatable condition. One of the reasons why I love looking after patients with gout is because we can fix it. Treatment is simple, extremely effective and usually well tolerated. 

Therapeutic Guidelines have just updated their information about gout, and the new resource suite produced by Quality Use of Medicines Alliance and its partners found here, will help you implement these management updates. The updated Therapeutic Guidelines and the education tools address many widely held misconceptions and will in turn improve patient outcomes.

Initiate preventative gout treatment early and opportunistically - including during an acute gout flare

Patients with confirmed gout should be recommended urate-lowering therapy (ULT), usually allopurinol, especially for patients experiencing recurrent attacks (>1 attack per year), or who have tophi, evidence of erosions on X-ray, chronic gouty arthritis, renal impairment or urolithiasis.

Past practice was to commence allopurinol after the gout flare was resolved. However, current evidence supports early initiation, including during a flare. There are two advantages to this approach. Firstly, having the conversation about preventative ULT treatment during a flare enables the clinician to start the process early to reduce the risk of future flares and long-term complications. Secondly, patients may be more inclined to commence a preventative program when the pain and frustration of an acute gout flare is still fresh in their minds.

Why treat-to-target matters

The role of serum urate (also referred to as serum uric acid) concentration monitoring is to guide dosing decisions to support a treat-to-target strategy. This matters because about 60% of Australian patients are receiving inadequate doses of ULT. Many remain on a dose of allopurinol 100 mg or 300 mg daily because these are the available tablet preparations and historically doses of >300 mg of allopurinol were not used in patients with renal impairment. We now know that in up to 50% of patients with normal renal function, 300 mg allopurinol daily is ineffective in achieving a serum urate target of less than 0.36 mmol/L, which is required to dissolve gout crystals, which in turn, reduces gout flare frequency and severity long term. For patients with tophi, chronic gouty arthritis, or recurrent flares, the guidelines recommend a target of less than 0.30 mmol/L

A word of caution: Serum uric acid measurements can have limited diagnostic value. Additionally, during an acute gout flare serum uric acid measurements can be reduced and therefore do not reflect actual serum uric acid levels upon which we can determine if the patient has achieved the target. Serum urate pathology should instead be measured following flare resolution to ensure the target level is reached.

Dosing guidance

Start allopurinol at a dose of 50 mg or 100 mg daily, increasing monthly by 100 mg (or 50 mg if there is renal impairment). Doses up to 900 mg daily are safe and may be needed to reach target serum levels. The main concern for patients with renal impairment is the risk of a hypersensitivity reaction from too rapid or too large a dose incrementation, rather than the total final dose. 

The Gout Treatment Algorithm, developed by the Quality Use of Medicines Alliance provides straightforward information to guide treatment, including the initiation and “uptitration” of ULT, supporting clinicians and other primary health care staff to assist in this process. 

Patient resources are also available to help explain the process to patients and enable them to record their progress towards achieving a target serum urate concentration.

In patients at high risk of allopurinol hypersensitivity (eg patients of Han Chinese, Korean and Thai backgrounds), alternatives to allopurinol should be considered or consider testing for (HLA)-B*5801 allele before initiating treatment with allopurinol.

Once the patient has achieved their target serum urate level, the monosodium urate crystals (MSU) start to dissolve (sometimes this takes 2–3 years) and the gout attacks become less frequent and eventually do not recur. This is an important message to reiterate to patients, so that they have faith in the process, especially if flares occur during initiation or uptitration of ULT. 

Another word of caution: When determining the correct dosing of allopurinol, it is important to check that the patient does not have active gout at the time of collection. In light of this, it is useful to repeat serum urate 1 month after achieving the target urate to ensure that the dose of allopurinol has indeed achieved a target serum urate.

Flare prophylaxis – the key to success.

Discontinuation of allopurinol occurs frequently, both according to local and international data and one of the reasons for this is that changes in allopurinol dosing dissolves MSU crystals which can lead to gout flares. 

Using a second medication as ‘flare prophylaxis’ is a vital component of the urate-lowering strategy, both for control of disease and patient adherence. This is where colchicine comes in, yet currently less than 10% of Australian patients are co-prescribed colchicine when starting allopurinol8.

Several agents can be used for flare prophylaxis. Colchicine is recommended as the first line, in the absence of contraindications, to be taken as a daily dose of 500 mcg (it causes less diarrhoea at this dose) for at least 6 months. Other options may be required depending on an individual patient’s comorbidities, other prescribed medications and intolerances. These are listed in more detail in the Gout Treatment Algorithm and new Therapeutic Guidelines.

Is allopurinol for life?

Yes, unless the patient has a hypersensitivity reaction. 

Previous practice was to stop allopurinol during a gout flare. This is no longer recommended as sudden changes in serum urate concentration can exacerbate symptoms and unnecessarily interrupt incremental titration. Stopping allopurinol can take a patient several steps backwards on their journey towards a happy life, free of gout flares. 

Once a patient has reached target serum urate they should remain at that dose long term.

Set expectations and educate to improve adherence in gout management 

Medication adherence remains a major stumbling block to successful gout management. Patient education is a critical element in solving this issue.

Patients need to understand that gout is a genetic condition, not a moral failing, that needs medication, and that dietary modification alone is unlikely to control the disease.

Patients need to understand the consequences of untreated and undertreated gout, such as further flares, joint damage and potentially poorer cardiovascular outcomes. Evidence supports the use of pictorial resources and showing patients their own imaging to explain gout and the treatment process.

Managing expectations is also helpful and part of this is to describe the procedure for ULT and set realistic timeframes. In my practice, I explain it will take 6–9 months to obtain the target serum urate level and ensure the adequacy of ULT dosing, and that flares may continue for 2–3 years after starting ULT. 

Patient Resources have been created by Arthritis Australia with the Quality Use of Medicines Alliance and endorsed by the Australian Rheumatology Association. These support information delivered during consultations and address common patient concerns about gout and its treatment. 

In today’s climate, where clinicians in primary care are time-poor, it may be worthwhile providing opportunities for further discussion or offering follow-up counselling with a practice nurse. In the early phase of care, these opportunities can be part of the monthly contact that occurs with each blood test and allopurinol dose change. 

To support the implementation of the recommendations above, new clinician resources, including a Gout Management Algorithm have been designed to guide you in critical management decisions and are freely available.

 

  1. Gout [published 2024 December]. In: Therapeutic Guidelines. Melbourne: Therapeutic Guidelines Limited; . accessed 21 January 2025.https://www.tg.org.au

  2. Hill EM, Sky K, Sit M, Collamer A, Higgs J. Does starting allopurinol prolong acute treated gout? A randomized clinical trial. J Clin Rheumatol 2015;21(3):120–25.

  3. Taylor TH, Mecchella JN, Larson RJ, Kerin KD, Mackenzie TA. Initiation of allopurinol at first medical contact for acute attacks of gout: A randomized clinical trial. Am J Med 2012;125(11):1126–34 e7.

  4. Robinson PC, Taylor WJ, Dalbeth N. An Observational Study of Gout Prevalence and Quality of Care in a National Australian General Practice Population. J Rheumatol. 2015 Sep;42(9):1702–7. 

  5. Richette P, Dalbeth N, Treat-to-target or treat-to-dissolve strategy to improve gout treatment. Nat Rev Rheumatol. 2024 Jul;20(7): 393-394. 

  6. Stamp, L, Frampton C, et al. Association between serum urate and flares in people with gout and evidence for surrogate status: a secondary analysis of two randomised controlled trials. Lancet Rheumatol. 2022; 4(1): E53-60.

  7. Coleshill MJ, Day RO, Tam K, Kouhkamari M, Caillet V, Aung E, et al. Persistence with urate-lowering therapy in Australia: A longitudinal analysis of allopurinol prescriptions. Br J Clin Pharmacol. 2022;88(11):4894–901. 

 

Dr Alana Bruce
Dr Alana Bruce

Dr Alana Bruce is a rheumatologist currently working in private practice and at Austin Health. She has previous research interest in inflammatory arthritis, crystal arthritis and the interplay between rheumatic disease and cancer. She completed a Master of Research at Macquarie University in 2022, investigating rheumatic toxicities associated with cancer immunotherapy in patients with advanced melanoma.

Dr Bruce is currently serving on the Australian Rheumatology Association Clinical Resources Committee. She is a clinical educator for medical students affiliated with St Vincent’s clinical school and Melbourne University.

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