
Gout is the most common form of inflammatory arthritis, caused by a build-up of uric acid crystals in the joints. When uric acid levels in the blood remain elevated, crystals deposit in joints and surrounding tissues, triggering sudden and intensely painful flares. The big toe is most commonly affected, though gout can also affect the ankle, knee, wrist, and fingers.
Without treatment, flares can become more frequent and longer-lasting, and chronic gout can develop, causing permanent joint damage. With appropriate management, most people can significantly reduce or prevent future attacks.
How common is Gout?
Gout affects an estimated 4.8% of Australian adults — approximately 1.5 million people. It is three to four times more common in men than women, with women's risk increasing after menopause. People with kidney disease, cardiovascular disease, diabetes, or obesity are at significantly higher risk.
Gout typically presents as sudden, severe attacks of joint pain. Symptoms of an acute gout flare include:
Between flares, many people are completely symptom-free.
With repeated untreated flares or persistently high uric acid levels, gout can progress to:
Gout is caused by sustained hyperuricaemia – elevated levels of uric acid in the blood.
This occurs when the body either produces too much uric acid, or the kidneys excrete too little of it.
Risk factors include:
An acute gout attack can be triggered by sudden changes in uric acid levels, dehydration, injury, surgery, illness, or heavy alcohol consumption.
A diagnosis of gout is often made based on the clinical picture – sudden onset of severe pain, redness, and swelling in a single joint, particularly the big toe.
However, confirmation may involve:
Treatment for gout has two distinct phases: managing acute flares and long-term prevention through urate-lowering therapy.
Acute flare treatment
The goal is rapid reduction of inflammation and pain.
Options include:
Long-term urate-lowering therapy (ULT)
ULT is recommended for people who have frequent flares, tophi, joint damage, or ongoing hyperuricaemia. It is started between flares, not during an acute attack.
The goal is to lower uric acid levels to below 0.36 mmol/L (or below 0.30 mmol/L in those with tophi), causing crystals to dissolve and preventing new ones from forming.
Lifestyle
Dietary and lifestyle changes can support medical treatment: reducing purine-rich foods and alcohol, staying well hydrated, achieving and maintaining a healthy weight, and reviewing any medications that raise uric acid levels.
The following specialty medications may be available at Ace, a specialty pharmacy for Gout.
Note: Corticosteroids (prednisolone) and NSAIDs are used in acute gout treatment but are not specialty medications.
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