Gout Prophylaxis

See also our records on Gout and Management of Acute Gout.

Asymptomatic hyperuricaemia is NOT gout and does not warrant management with drugs. This is a topical issue as it is becoming increasingly recognised that nearly 25% of men with raised serum urate levels but no evidence of clinical gout, will go on and develop gout in the next 5-6 years.¹ Also, hyperuricaemia may be a marker for the risk of subsequent cardiovascular disease and in the future may require treatment. Despite these concerns a patient with asymptomatic hyperuricaemia should be given advice on lifestyle modification:²

• Drink alcohol sensibly - beer or spirits should be avoided (there is a particularly strong link with beer, stout and port wines), but wine in moderation is not associated with an increased risk.³
  • There is a good evidence base that reducing alcohol intake to moderate levels is helpful.⁴.
• Avoid dehydration.
• Dietary intervention - reduction of purine-based foods.
  • A large longitudinal study found that increased intake of meat or seafood significantly increased the incidence of gout.
  • Highest purine levels are found in heart, herring, sardines and mussels.⁵
  • Other foods which are very rich in purines include liver, kidneys, red meat, yeast extracts, seafood (herring, sardines, and shellfish) and asparagus, beans, cauliflower, lentils, mushrooms, oatmeal and spinach.
  • Soya foods are also high in purines but are less likely to lead to gout than meats and seafood.
  • It is the quantity of purine-rich food consumed that is more important than the absolute purine content in each food.
  • Soft drinks containing high levels of fructose can affect the levels of purines and should also be avoided.³
  • There is no evidence to support a reduction in purine-rich vegetables such as peas, beans, mushrooms or cauliflower, unless intake is extreme.⁶
• Weight reduction - there are no controlled trials available, but some evidence suggests a link between obesity and high uric acid levels.⁷
• Take regular exercise.
• Stop smoking.
• Recent evidence from a 20-year follow-up study, suggests that high vitamin C intake make prevent gout.⁸

Manage risk factors

These may include:

• Drugs causing hyperuricaemia:
  • Thiazides and loop diuretics
  • Low dose salicylates e.g. aspirin < 1 g/day, pyrazinamide, ethambutol, nicotinic acid, ciclosporin⁹
• Hypertension⁷
• Impaired renal function⁵
• Hyperlipidaemia, especially hypertriglyceridaemia¹⁰
• Vascular disease⁵
• Chemotherapy - consider starting prophylaxis before treatment begins
• Myeloproliferative disease¹¹

General principles

• It is important to explain that medication is normally lifelong and regular monitoring is needed.
• Advise the person that allopurinol may cause acute attacks of gout just after initiating treatment, and for some weeks afterwards.
• Explain that they should start their anti-inflammatory treatment as soon as possible and not stop their allopurinol during acute attacks.

Pharmacological management

• Allopurinol should never be started during an acute attack. Wait for 1-2 weeks after the attack resolves.
• Start with a low dose (50-100 mg) and increase in 50-100 mg increments every 2-4 weeks until serum uric acid (SUA) level is below 300 micromol/L.
• Maximum dose is 900 mg daily.
• The timescale for increasing in dose may need to be slower in some patients, with frequent checks of renal function, if renal function is known to be impaired.
• Co-prescribe colchicine or a low dose non-steroidal anti-inflammatory drug (NSAID) to prevent an attack of gout whilst initiating therapy, and continue until after hyperuricaemia has settled (usually a total of three months).
• If an acute attack develops during treatment, maintain the dose but add colchicine or NSAIDs.¹³
• If neither NSAIDs nor colchicine are tolerated, or both are contra-indicated, consider low dose oral prednisolone.⁵ However, it may be preferable to seek specialist advice.

Allopurinol

This drug is traditionally the first choice for long-term control of gout. ^12,13

• It is not indicated for asymptomatic hyperuricaemia.^13,14
• It is useful where renal function is impaired or renal stones are present.^5,13
• Densitisation therapy is sometimes used in cases where the only adverse effect is a mild rash.²
• Check the SUA level and renal function every 3 months in the first year, then annually, and aim for an SUA below 300 micromol/L.

Sulfinpyrazone¹⁵

This can be used as alternative to allopurinol if toxicity occurs, or as an adjunct in resistant cases.

• It can be difficult to obtain and is contra-indicated in renal failure and urolithiasis.
• Dose is 200-800 mg/day in patients with normal renal function.

Colchicine

• Although not a urate-lowering drug per se, colchicine is sometimes prescribed at low dose in early gout - to 'buy time' in patients undergoing lifestyle modification, before a commitment to urate-lowering drugs is made.

Other options

• Low dose corticosteroids and NSAIDs have also been used to buy time, in the same way as colchicine.¹⁴
• Probenecid is a less powerful uricosuric agent and is relatively contra-indicated in urolithiasis.
• Benzbromarone can also be used in patients with mild/moderate renal insufficiency at a dose of 50-200 mg/day. However, it carries a small risk of hepatotoxicity.²