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Gout - clinical essentials and MCQ

04 March 2025 - Quality Use of Medicines Alliance

In Australia, gout is one of the most common forms of inflammatory arthritis that affects adults, with self-reported prevalence rates of up to 6.8%. It is a lifelong condition that primarily causes acute monoarthritis. It is associated with an increased risk of joint damage and deformity, kidney and heart disease. Aetiology includes genetic factors, chronic kidney disease and obesity.

Essential resources for gout management

Diagnosing gout

Differential diagnosis for gout includes septic arthritis and pseudogout. All of these conditions can have a similar clinical presentation.

  • Joint aspiration: only way to achieve a definitive diagnosis. Request cell count, microbiology (MCS), and crystal analysis.

  • Dual Energy CT: visualises uric acid and calcium deposits. It is not considered a tool for routine diagnosis, especially in early disease state.

  • X-Ray: useful to identify joint damage but not monosodium urate crystals.

  • Serum urate: levels may be falsely low during an acute flare so should not be solely relied on to make a diagnosis of gout.

Managing an acute flare

For detailed guidance, refer to the Gout Treatment Algorithm.

First-line treatment:
  • NSAIDs: consider contraindications and precautions - generally preferred in younger patients. 

OR

  • Prednisolone/prednisone: 15-30 mg orally daily for 3-5 days or intra-articular methylprednisolone if ≤2 joints are affected and reduced systemic absorption desired.

Second-line treatment:
  • Colchicine: single course — 1 mg orally initially, then 500 micrograms 1 hour later, as a single one day course (total 1.5 mg). Do not repeat the course within 3 days. Avoid if on colchicine for flare prophylaxis.

Urate lowering therapy (ULT)

  • Treat-to-target: aim for <0.36 mmol/L for non tophaceous gout, and <0.30 mmol/L if tophi, gouty arthritis or recurrent attacks are present.

  • Monitor serum urate concentration, renal, and liver function monthly until target levels are reached.

First-line: allopurinol
  • Safe to start and modify during a flare. Can be initiated immediately after a diagnosis of gout is confirmed.
  • Using a treat-to-target approach, start at a low dose and slowly up-titrate to reduce the risk of flares and likelihood of developing allopurinol hypersensitivity.
  • Doses above 300 mg are commonly needed to reach target and are safe in renal impairment.
  • Do not stop allopurinol during a flare, illness or perioperatively
Gout_treatment_algorithm-allopurinol.png
Special consideration:
  • Consider HLA-B*5801 screening in patients from certain Asian sub-populations (e.g. Han Chinese, Korean, Thai) and African Americans (higher risk of hypersensitivity to allopurinol). If positive, use second line agent febuxostat (with caution in cardiovascular, kidney, or liver impairment).

Flare prophylaxis

  • Recommended for all patients starting or changing the dose of ULT.
  • Colchicine prophylaxis: 500 micrograms daily for at least 6 months. Halve dose for kidney impairment and poor tolerability (e.g. diarrhoea)

Diet and gout

  • Main risk factors for gout are genetic predisposition, impaired kidney function and obesity.
    Diet and alcohol intake are no longer thought to play as big a role.

  • Diet: some foods and beverages may trigger flares but are not the cause of gout. Advise patients to reduce consumption rather than eliminate their intake of alcohol, animal based foods high in purine (i.e. shellfish, fish, red meat) and sugary drinks high in fructose. 

  • Eat a balanced diet and maintain adequate hydration.

 

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The Quality Use of Medicines Alliance a consortium of eight health and consumer organisations, will align their work across the two grants, awarded under the Australian Government’s Quality Use of Diagnostics, Therapeutics and Pathology (QUDTP) Program.  

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