Highlighter is on. Drag to highlight text. Click a highlight to remove it.
ALL / Rheumatology
Gout: management
Gout: management
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)Acute management
- NSAIDs or colchicine are first-line
- the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled
- gastroprotection (e.g. a proton pump inhibitor) may also be indicated
- colchicine
- inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
- has a slower onset of action
- may be used with caution in renal impairment: the BNF advises to reduce the dose if eGFR is 10-50 ml/min and to avoid if eGFR < 10 ml/min BNF
- the main side-effect is diarrhoea
- oral steroids may be considered if NSAIDs and colchicine are contraindicated.
- a dose of prednisolone 15mg/day is usually used
- another option is intra-articular steroid injection
- if the patient is already taking allopurinol it should be continued
Indications for urate-lowering therapy (ULT)
- the British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout
- ULT is particularly recommended if:
- >= 2 attacks in 12 months
- tophi
- renal disease
- uric acid renal stones
- prophylaxis if on cytotoxics or diuretics
Urate-lowering therapy
- it has traditionally been taught that urate-lowering therapy should not be started until 2 weeks after an acute attack, as starting too early may precipitate a further attack. The evidence base to support this however looks weak
- in 2017 the BSR updated their guidelines. They still support a delay in starting urate-lowering therapy because it is better for a patient to make long-term drug decisions whilst not in pain
- the key passage is: 'Commencement of ULT is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain'
- allopurinol is first-line
- initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 360 µmol/l #link31
- a lower target uric acid level below 300 µmol/L may be considered for patients who have tophi, chronic gouty arthritis or continue to have ongoing frequent flares despite having a uric acid below 360 µmol/L
- a lower initial dose of allopurinol should be given if the patient has a reduced eGFR
- colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated. The BSR guidelines suggest this may need to be continued for 6 months
- the second-line agent when allopurinol is not tolerated or ineffective is febuxostat (also a xanthine oxidase inhibitor)
- in refractory cases other agents may be tried:
- uricase (urate oxidase) is an enzyme that catalyzes the conversion of urate to the degradation product allantoin. It is present in certain mammals but not humans
- in patients who have persistent symptomatic and severe gout despite the adequate use of urate-lowering therapy, pegloticase (polyethylene glycol modified mammalian uricase) can achieve rapid control of hyperuricemia. It is given as an infusion once every two weeks
Lifestyle modifications
- reduce alcohol intake and avoid during an acute attack
- lose weight if obese
- avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
Other points
- consideration should be given to stopping precipitating drugs (such as thiazides)
- losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
- increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
+PassMedicine Notes
Gout is a form of microcrystal synovitis caused by the deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 450 µmol/l)
Acute management- NSAIDs or colchicine are first-line
- the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled
- gastroprotection (e.g. a proton pump inhibitor) may also be indicated
- colchicine
- inhibits microtubule polymerization by binding to tubulin, interfering with mitosis. Also inhibits neutrophil motility and activity
- has a slower onset of action
- may be used with caution in renal impairment: the BNF advises to reduce the dose if eGFR is 10-50 ml/min and to avoid if eGFR < 10 ml/min BNF
- the main side-effect is diarrhoea
- oral steroids may be considered if NSAIDs and colchicine are contraindicated.
- a dose of prednisolone 15mg/day is usually used
- another option is intra-articular steroid injection
- if the patient is already taking allopurinol it should be continued
- the British Society of Rheumatology Guidelines now advocate offering urate-lowering therapy to all patients after their first attack of gout
- ULT is particularly recommended if:
- >= 2 attacks in 12 months
- tophi
- renal disease
- uric acid renal stones
- prophylaxis if on cytotoxics or diuretics
- it has traditionally been taught that urate-lowering therapy should not be started until 2 weeks after an acute attack, as starting too early may precipitate a further attack. The evidence base to support this however looks weak
- in 2017 the BSR updated their guidelines. They still support a delay in starting urate-lowering therapy because it is better for a patient to make long-term drug decisions whilst not in pain
- the key passage is: 'Commencement of ULT is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain'
- allopurinol is first-line
- initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 360 µmol/l #link31
- a lower target uric acid level below 300 µmol/L may be considered for patients who have tophi, chronic gouty arthritis or continue to have ongoing frequent flares despite having a uric acid below 360 µmol/L
- a lower initial dose of allopurinol should be given if the patient has a reduced eGFR
- colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated. The BSR guidelines suggest this may need to be continued for 6 months
- the second-line agent when allopurinol is not tolerated or ineffective is febuxostat (also a xanthine oxidase inhibitor)
- in refractory cases other agents may be tried:
- uricase (urate oxidase) is an enzyme that catalyzes the conversion of urate to the degradation product allantoin. It is present in certain mammals but not humans
- in patients who have persistent symptomatic and severe gout despite the adequate use of urate-lowering therapy, pegloticase (polyethylene glycol modified mammalian uricase) can achieve rapid control of hyperuricemia. It is given as an infusion once every two weeks
- reduce alcohol intake and avoid during an acute attack
- lose weight if obese
- avoid food high in purines e.g. Liver, kidneys, seafood, oily fish (mackerel, sardines) and yeast products
- consideration should be given to stopping precipitating drugs (such as thiazides)
- losartan has a specific uricosuric action and may be particularly suitable for the many patients who have coexistent hypertension
- increased vitamin C intake (either supplements or through normal diet) may also decrease serum uric acid levels
