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Gout is a disorder of purine metabolism characterised by a raised uric acid level in the blood (hyperuricaemia) and the deposition of urate crystals in joints and other tissues.
Hyperuricaemia and joint pain do not always equate to a diagnosis of gout: Hyperuricaemia may occur without gout and acute gout attacks may present without hyperuricaemia.
For list of formulary choice drugs used in the treatment of gout see 10.1.4 Gout and cytotoxic-induced hyperuricaemia.
When considering specialist referral see: North Devon Referral Guideline: Gout (excluding septic arthritis)
Acute attacks should be treated as early as possible (as soon as an attack occurs).
Advise the person to:
Discuss lifestyle measures such as weight loss, exercise, diet, alcohol consumption, and fluid intake
Choice of first-line agent depends on patient preference, renal function and co-morbidities.
Consider paracetamol as an adjunct for pain relief.
Do not stop allopurinol or febuxostat during an acute attack of gout if the person is already established on these drugs.
Prescribe either of the following first-line agents, provided that there are no contraindications:
A short course of oral corticosteroids or a single intramuscular corticosteroid injection may be considered in people who cannot tolerate NSAIDs or colchicine, and if intra-articular injection is not possible (see below).
Guidance from the British Society of Rheumatology for the management of musculoskeletal and rheumatic conditions with corticosteroids during the Coronavirus (COVID-19) pandemic can be found here
Joint aspiration and intra-articular injection of corticosteroids (unlicensed use) are an option in people with acute monoarticular gout and co-morbidity provided the diagnosis is certain, the person (and joint) are suitable for injecting and the expertise to inject the joint is available.
Irrespective of the treatment used, advise the person to return if symptoms get worse, or if there is no improvement after 1-2 days.
If there is an inadequate response to treatment after 1-2 days:
After an acute attack of gout has resolved, follow up the person after 4–6 weeks, and:
Consider the underlying cause of hyperuricaemia.
Review all medication and consider any that may cause hyperuricaemia or gout such as diuretics, β-blockers and ACE inhibitors and non-losartan angiotensin II receptor blockers.
The British Society for Rheumatology Guideline for the Management of Gout (2017) states that
Losartan should not be used as primary ULT but where treatment for hypertension is required, it may be considered as possessing a weak uricosuric effect.
Discuss lifestyle measures such as weight loss, exercise, diet, alcohol consumption, smoking cessation and fluid intake:
Urate-lowering therapy (ULT) should be discussed and offered to all people with a diagnosis of gout.
Asymptomatic hyperuricaemia alone is not an indication to institute preventative therapy.
In particular, it is important to advise the use of ULT to people with:
Consider ULT initiation at acute attack follow-up (normally 4-6 weeks). Do not initiate ULT until at least 1-2 weeks after an acute attack has settled.
Can be used as an alternative first-line agent only for patients who are intolerant of allopurinol or for whom allopurinol is contraindicated (in line with NICE TA164).
Consider prescribing colchicine (500 micrograms once or twice daily) or a low-dose NSAID when initiating or increasing the dose of a ULT as prophylaxis against acute attacks secondary to ULT. For allopurinol this will be until at least one month after hyperuricaemia is corrected (normally 3 months) and for febuxostat continue for at least 6 months after initiation.
If taking urate-lowering therapy (allopurinol or febuxostat), check the SUA level and renal function every 4 weeks until SUA is in target range, then annually thereafter, and aim for a SUA level below 300 micromol/L.
After some years of treatment, once SUA target is reached and clinical 'cure' has been achieved (acute attacks have stopped and tophi have resolved), consider reducing the dose of ULT to maintain the SUA level between 300-360 micromol/L.