A GP guide to managing gout
- Gout is one of the most common inflammatory joint diseases worldwide, affecting up to one in 15 Australians.1 Although known to be more prevalent in men, postmenopausal women and certain ethnic groups also experience a high burden of disease.
- Gout is often undertreated and can lead to irreversible joint damage, tophi formation, kidney stones and gouty nephropathy.
- Gout is linked to hypertension, chronic kidney disease, obesity and cardiovascular disease.2
- Patients are likely to experience recurrent flares following their first gout episode. Initiating urate-lowering therapy (ULT) early, combined with appropriate flare prophylaxis, is essential.
- Titration of ULT to achieve a target serum uric acid level of 0.36mmol/L, (0.30mmol/L for those with tophi or joint damage) is key to dissolving existing crystal deposition and
preventing new deposits. - There is currently no evidence to treat isolated asymptomatic hyperuricaemia (>0.42mmol/L of uric acid) to prevent the development of gout.
- Incorporating care plans, expectation setting and promoting shared
decision-making can improve adherence.
Gout is one of the most common inflammatory joint diseases and presents a significant burden for many people in Australia. There are several gaps between evidence and practice that need to be addressed to improve the management of these patients.3,4
These evidence–practice gaps stem from several factors, including updated management recommendations, limited time for clinicians to educate patients on medications, deprioritising gout compared with other coexisting conditions, and enduring myths that perpetuate the stigma surrounding gout (see figure 1).
Poor control is worsened when patients have negative views of urate-lowering therapy (ULT) following gout flares with treatment initiation. Early education and setting expectations about appropriate use of prophylaxis can effectively combat this.
| Resources: |
Medcast: • Gout treatment algorithm • My gout plan (shared decision-making tool for patients) • Deciding how to manage your gout (shared decision-making tool for patients) • Gout Treatment Decision Support Tool Arthritis Australia: • arthritisaustralia.com.au |
Fact versus fiction
Gout has always faced significant misconceptions and stigmatisations, which have in turn affected health professionals’ perceptions and management.
Table 1 shows how some of these myths link with gaps in evidence–practice.
| Table 1. Gout fiction vs fact | ||
| Gap | Fiction | Fact |
| Overemphasis on lifestyle and diet as the cause of disease | Gout is primarily caused by poor diet and lifestyle choices and can be managed through lifestyle changes alone | Gout is predominantly driven by genetic and metabolic factors; ULT is essential for effective management |
| Lack of ULT for flare prophylaxis | Flare-ups when starting or adjusting ULT indicate treatment is ineffective | Flare-ups during ULT initiation or dose adjustments are common but preventable with appropriate prophylaxis, such as colchicine or NSAIDs; failure to communicate the likelihood of flares on ULT initiation often puts patients offside and limits adherence |
| Not treating to target with ULT | Lower doses of ULT are adequate for managing gout | Suboptimal ULT dosing often fails to reach target serum uric acid levels, leading to persistent flares and disease progression; patients with normal renal function will often require doses of allopurinol >300mg to reach their target serum uric acid level; doses of allopurinol up to 900mg are sometimes required to achieve a patient’s target level |
| Not managing gout as a chronic condition | Gout is an acute condition that only needs treatment during flare-ups | Gout is a chronic condition requiring ongoing management and often lifelong ULT;2 focusing solely on acute flares without addressing the underlying hyperuricaemia risks long-term complications, such as irreversible joint damage, tophi and gouty nephropathy |
Diagnosis
Confirming a gout diagnosis is essential as ULT is typically lifelong. A definitive diagnosis requires aspiration of fluid from affected joints, bursae or tophi to detect monosodium urate crystals.2 In certain cases, synovial or bursal fluid analysis is also necessary to rule out the differential diagnosis, such as septic arthritis and calcium pyrophosphate deposition disease — both of which can present similarly to gout.
Investigations to support diagnosis
Serum uric acid
Hyperuricaemia (uric acid >0.45mmol/L in males or >0.40mmol/L in females) supports a diagnosis of gout, although it is insufficient on its own to confirm the condition is present.5
The risk of developing gout is three times greater if serum urate concentration consistently exceeds 0.42mmol/L compared with those with a serum urate in the normal range. Additionally, serum uric acid levels often appear normal during an acute flare, further complicating diagnosis.
Plain X-rays
X-rays play a limited role in the early diagnosis of gout but can be helpful in assessing chronic cases.2 They may reveal joint damage, tophi or other structural changes. However, early-stage gout often does not present visible changes on X-rays, so their utility is more significant in monitoring disease progression and assessing joint damage in chronic gout management.
Dual-energy cT
Dual-energy CT is a non-invasive imaging technique that is useful in complex or atypical gout cases, such as when joint aspiration is challenging, multiple joints are involved or disease burden needs monitoring. It is not recommended for routine diagnosis because of lower sensitivity in early-stage gout or cases without visible tophi. Additionally, its higher cost, limited availability and radiation exposure make it less practical for widespread use compared with joint aspiration.
Investigations to inform medication selection
Renal function
Renal impairment is both a risk factor and consequence of gout. Its presence influences dosing of ULT and the choice of agents used for management of acute flares, as well as flare prophylaxis when starting or increasing ULT.
Liver function
Hepatic impairment also influences the choice and dosing of ULT.
Ethnicity and HLA-B*5801 allele
Testing for the HLA-B*5801 allele is recommended in certain ethnic groups before starting allopurinol treatment because of the increased risk of severe hypersensitivity reactions.
This allele is more commonly found in some Asian subpopulations, including those of Korean, Han Chinese and Thai ancestry, as well as in African-Americans. Screening for HLA-B*5801 in these groups helps identify patients at risk for allopurinol-induced severe cutaneous adverse reactions. If HLA-B*5801 is present, allopurinol should not be used.2
This test is currently not MBS funded and has a cost to the patient of around $75.60.
Acute gout management
Effective management of acute gout focuses on reducing pain and inflammation using corticosteroids, NSAIDs or colchicine.2 The choice of treatment should be guided by patient-specific factors, including comorbidities and potential side effects. The gout treatment algorithm (see online resources) provides specific dose instructions.
Once treatment for acute flares has been prescribed, patients will often self-manage recurrent acute flares with these agents. With every prescription of acute flare medication, it is important to educate and explain to patients the importance of ULT to promote treatment of the underlying disease.
Corticosteroids
These are administered orally or via local intra-articular injection (up to two joints). Corticosteroids provide rapid symptom relief and are as effective as NSAIDs. They are particularly useful when colchicine or NSAIDs are contraindicated.
NSAIDs
These agents are a common first-line treatment for acute gout, offering effective symptom relief, and may be preferred in younger patients. Selective NSAIDs may have a lower risk of adverse effects and are preferred for some patients.
Colchicine
Low-dose colchicine is another effective option, particularly when treatment begins early in a flare and corticosteroids and NSAIDs are contraindicated. However, its use is limited by a narrow therapeutic index. It is generally not recommended for patients with renal impairment or patients using colchicine as flare prophylaxis.
When to start long-term urate-lowering therapy
Lifelong ULT is recommended for all patients with a confirmed diagnosis of gout, particularly those with recurrent flares (more than one a year), tophi, chronic gouty arthritis, X-ray evidence of erosions, impaired renal function or a history of urolithiasis.2
Patients are often reluctant to begin long-term ULT after their first 1-2 gout flares. It is important to identify patient concerns and discuss the risks and benefits of treatment options, including potential harms that can result from untreated gout.
These include irreversible joint damage, functional impairment and increased risk of hypertension, diabetes, ischaemic heart disease, chronic kidney disease and obesity.2 There is also emerging evidence linking gout flares to an increased risk of cardiovascular disease.7,8 Patients can be reassured that gout is one of the few diseases that can be completely controlled with medicines.
To assist in weighing up the pros and cons of treatment, consider using a gout treatment decision support tool (see online resources).
Uptitration and treating to target
ULT follows a treat-to-target approach. Although this is a well-established approach, up to 60% of Australian gout patients have not reached a target urate of <0.36mmol/L.3
Advise patients that it can take between 6-9 months to reach their target serum urate concentration (SUC). It is also important to explain that gout flares may still occur for 12-18 months after SUC is achieved, although will likely be reduced in frequency and severity.9
Reaching a patient’s target SUC is critical to dissolve existing crystals in joints, soft tissues and kidneys, and preventing new ones from forming. For patients without tophi or joint damage, the target serum uric acid level is 0.36mmol/L, while for those with tophi or joint damage, the recommended target is 0.30mmol/L.2
There is currently no evidence to treat isolated asymptomatic hyperuricaemia (>0.42mmol/L of uric acid) to prevent the development of gout.2
Conclusion
GPs play a pivotal role in closing the evidence–practice gaps associated with gout management. Early identification of gout, definitive diagnosis via joint aspiration where feasible and a proactive treat-to-target approach with ULT are essential for preventing irreversible joint damage and comorbidities.
Equally important is ensuring patients understand the chronic nature of gout and the need for lifelong management, which may include higher doses of ULT than those commonly prescribed.
By addressing patient concerns about therapy, providing appropriate flare prophylaxis and fostering shared decision-making, GPs can help optimise treatment adherence and improve long-term outcomes. With the availability of concise treatment algorithms, patient-friendly decision-support tools and timely access to specialist input when needed, effective gout care is both attainable and vital for reducing the significant burden of this disease in the Australian community.
Professor Catherine Hill is a clinical rheumatologist and epidemiologist. She is head of the department of rheumatology at the Queen Elizabeth Hospital, Adelaide, and clinical professor in the faculty of health and medical sciences, University of Adelaide, SA.
Jarrah Anderson is a clinical lead at Medcast, a pharmacist and an advocate for the quality use of medicines.
- References on request from Dr Kate Kelso.
