• Confirm gout and exclude alternative diagnoses.
• Assess the severity of the attack, and identify risk factors and any associated conditions.
• Manage an acute attack of gout by prescribing a nonsteroidal anti-inflammatory drug (NSAID) (e.g. diclofenac, indometacin, naproxen) as soon as possible, with or without gastroprotection. If NSAIDs are contraindicated or not tolerated, consider oral colchicine. Advise the person to rest, elevate the affected limb, and avoid trauma to the affected joint. If the diagnosis is confirmed and there is no improvement in symptoms within 2–3 days, either try an alternative drug, consider combining treatment, or seek specialist advice.
• Follow up the person 4–6 weeks after an acute attack of gout has resolved, and check the serum uric acid (SUA) level then.
• Manage recurrent attacks of gout by starting allopurinol after two or more attacks within a year. Start allopurinol 1–2 weeks after the inflammation has settled and titrate the dose every few weeks until the SUA level is below 300 micromol/L. Use a low dose of an NSAID or low-dose colchicine to prevent acute attacks when starting urate-lowering therapy.
• When starting allopurinol, check the SUA level and renal function every 3 months in the first year, then annually, and aim for a SUA below 300 micromol/L.
• Consider starting febuxostat (an alterative second-line urate-lowering therapy) if allopurinol is not tolerated due to adverse effects or is contraindicated. If the SUA level is above 360 micromol/L after 2–4 weeks of initial treatment, a higher dose may be used.
• Provide lifestyle advice on losing weight, modifying diet, reducing alcohol intake, increasing exercise, and stopping smoking.

• Confirm gout and exclude alternative diagnoses, especially septic arthritis.
• Assess the severity of the attack (number of joints affected, the person's ability to mobilize, impact on work and functioning).
• Ask about previous attacks and which drugs (if any) the person is taking or has tried (nonsteroidal anti-inflammatory drug [NSAID] or urate-lowering drugs).
• Assess risk factors such as medication (e.g. diuretics), alcohol, diet, and obesity.
• Identify any associated conditions (e.g. hypertension, diabetes, cardiovascular disease), and arrange follow up to manage these as appropriate.
• Measure the person's serum uric acid level 4–6 weeks after the acute attack.

• The diagnosis of gout is based on clinical history and examination. The serum uric acid (SUA) level can be normal during an acute attack, especially if the person is taking urate-lowering drugs, high-dose aspirin, or corticosteroids, or drinks excessive amounts of alcohol. See Diagnosing gout for more information.
• If septic arthritis is suspected, then either refer urgently or aspirate the joint and arrange urgent microscopy and culture. See Differential diagnosis.
• Assess a person's cardiovascular risk (usually after the attack has settled). Provide lifestyle advice and manage any associated conditions. See Follow up for more information.

These recommendations are based on published expert opinion, pragmatic advice and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007].

• Prescribe a nonsteroidal anti-inflammatory drug (NSAID) such as diclofenac, indometacin, or naproxen as soon as possible, and continue the treatment until 48 hours after the attack has resolved.
• Co-prescribe a proton pump inhibitor (PPI) or misoprostol for gastric protection in people at risk of peptic ulcers, gastric bleeds, or perforations. For more information, see Preventing GI adverse effects in the CKS topic on NSAIDs - prescribing issues.
• If NSAIDs are contraindicated, not tolerated, or have been ineffective in previous attacks, prescribe oral colchicine 500 micrograms, two to four times a day, until relief of pain is achieved, or diarrhoea or vomiting occurs.
• If NSAIDs and colchicine are contraindicated, consider systemic corticosteroids.
• Use paracetamol, with or without codeine, in addition to other drug treatment, or alone, if NSAIDs, colchicine, and corticosteroids are all contraindicated.
• In people who are already established on allopurinol or febuxostat urate-lowering therapy, do not stop this during an acute attack of gout.

• Tailor the drug regimen to the individual. For some people with a high risk of adverse effects and mild symptoms, consider only self-care rather than any specific drug therapy.
• Diclofenac, indometacin, and naproxen are all fast acting nonsteroidal anti-inflammatory drugs (NSAIDs) with short half-lives, so clinical benefit will often be seen within a couple of days.
• See Management with no alarm features, taking NSAID in the CKS topic on Dyspepsia - unidentified cause for more information on whether or not to give gastroprotective medication in this scenario.
• Oral colchicine: lower doses are preferred to reduce the risk of adverse effects such as diarrhoea and vomiting.
• Corticosteroids can be given orally, intramuscularly, intravenously, or intra-articularly [Jordan et al, 2007]:
• Intra-articular corticosteroids are an option if the diagnosis is certain and only one or two (particularly large) joints are affected, and they are suitable for injecting, and the expertise to inject the joint is available. For more information, see the section on intra-articular corticosteroids.
• Ask the person to return if symptoms get worse, or if there is no improvement after 3–4 days. See Treatment failure for more information.

These recommendations are based on a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. There is little good quality evidence on the treatment of acute gout. Treatment needs to be based on patient preference and a balance of risk and benefits.

• Nonsteroidal anti-inflammatory drugs (NSAIDs): the evidence comes mainly from non-randomized controlled trials (non-RCTs) using indometacin. All NSAIDs appear equally effective. There is normally symptomatic relief within 24 hours, but CKS could find no head-to-head comparisons with colchicine [Underwood, 2006b].
• Of the cyclo-oxygenase-2 selective NSAIDs, only etoricoxib is licensed for the treatment of gout and there are trial data to support its effect [Schumacher et al, 2002; Rubin et al, 2004], but it may have a small increased risk of cardiovascular thrombotic events associated with its use [Aldington et al, 2005]. As people with gout may be at higher risk of cardiovascular disease, etoricoxib is best avoided.
• Diclofenac and naproxen are widely considered to have acceptable adverse effect profiles [CSM, 2002]. Indometacin has been studied more in gout than any other NSAID, and its safety profile is classed as intermediate risk of causing serious gastrointestinal (GI) adverse effects, although it is associated with more GI adverse events than naproxen or diclofenac.
• Ketoprofen, piroxicam, and sulindac are other standard NSAIDs that are licensed for the treatment of gout, but they are less frequently used and their adverse effect profiles are probably less favourable than diclofenac or naproxen.
• Ibuprofen and other standard NSAIDs not listed here are not licensed for the treatment of acute gout.
• Modified-release NSAIDs offer no additional benefit in terms of efficacy compared with standard preparations.
• Colchicine: the evidence comes from one small RCT (n = 43) showing the drug to be more effective than placebo, and more effective if taken in the first 24 hours. However, most people suffered adverse effects (diarrhoea and/or vomiting) with the higher dose of colchicine [Schlesinger et al, 2006a; Underwood, 2006b]. The BSR recommend lower doses of colchicine than that advised in the British National Formulary, to minimize the risk of adverse effects [Jordan et al, 2007].
• Systemic corticosteroids: the evidence from one small RCT (n = 90) shows that oral prednisolone (30 mg for 5 days) may be equally as effective as indometacin with fewer adverse effects [Man et al, 2007]. CKS could find no studies on the optimum dose and duration of corticosteroids but a short course of prednisolone 40 mg or less is relatively safe. Most people in case series reports respond in 24 hours with no adverse effects or rebound symptoms after stopping corticosteroids. In people with a monoarthritis, an intra-articular corticosteroid injection is highly effective in terminating an attack [Jordan et al, 2007].
• Analgesia: there is no trial evidence supporting the role of paracetamol or codeine in acute gout, but expert opinion and best practice suggests a role when symptoms are inadequately controlled using conventional measures.

• Advise the person to rest, elevate the limb, and avoid trauma to the affected joint.
• Keep the joint in a cool environment by avoiding clothing and using an ice pack.
• Discuss lifestyle issues such as weight loss, exercise, diet, alcohol consumption, and fluid intake. See Lifestyle advice for more information.

• Advise the person not to cover the joint with a sock, shoe, or bed clothing, to help cooling.
• Consider using a pack of frozen peas as an ice pack, as it moulds to fit the affected part. The pack should be wrapped in a towel to avoid ice-burn and applied for about 20 minutes. Repeat as often as required, making sure the temperature of the affected part has returned to normal before repeating the application.

• These recommendations are based on expert opinion, pragmatic advice, and the guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007].
• CKS could only find one small randomized controlled trial (n = 19) and a survey looking at the role of ice and cooling of the affected joint in acute gout.
• Ice: pain was reduced in 48% (95% CI 8 to 67) of people who used an ice pack (NNT was 3, 95% CI 2 to 13) [Schlesinger et al, 2002].
• Cooling: people with gout prefer cooling the affected joint compared with heat, and this can help to distinguish gout from other forms of inflammatory arthritis [Schlesinger, 2006].

• If there is no improvement in symptoms after 2–3 days:
• Review the diagnosis, check compliance with medication, and encourage self-care strategies.
• Increase the dose of medication to maximum and add paracetamol, with or without codeine.
• If there is still no improvement in symptoms in a confirmed case of gout, either:
• Try an alternative drug or consider combining treatment, or
• Seek specialist advice, especially if the person may be at risk of adverse effects.

• Most people with gout will respond within 2–3 days to a nonsteroidal anti-inflammatory drug (NSAID), colchicine, or oral prednisolone. If there is no improvement after this time, reviewing the diagnosis is necessary to exclude any other underlying pathology. See Differential diagnosis for more information.
• People should ideally be started on the maximum dose of medication, but if colchicine has been prescribed at a lower dose (to avoid adverse effects), consider increasing to the maximum tolerated dose.
• Always seek specialist advice if unsure about the next step if someone fails to respond to standard treatment. Switching to an alternative NSAID or colchicine may be worth trying, provided there are no contraindications.

These recommendations are based on published expert opinion, pragmatic advice and the guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007].

• There is no evidence regarding switching medication or combining treatment when first-line drugs fail in acute gout. Nevertheless, if there are no contraindications, this may be an option. A survey of American Rheumatologists found that combining medication is common practice [Schlesinger et al, 2006b].
• People with gout are more likely to be elderly and have comorbidities, so are generally more vulnerable to drug adverse effects. If considering combining treatment, make a decision based on the risks and benefits.

• Follow up the person 4–6 weeks after an acute attack of gout has resolved, and:
• Check the serum uric acid level.
• Measure their blood pressure and take blood for fasting glucose, renal function, and lipid profile.
• Identify underlying conditions such as hypertension, diabetes, or renal impairment, and assess the person's overall cardiovascular risk.
• Assess and provide advice on risk factors such as obesity, diet, excessive alcohol consumption, and exercise.
• Consider the need to start prophylactic medication if the person is having two or more attacks of gout in a year. See the section on Recurrent attacks of gout for more information.
• Consider providing an advance prescription of effective treatment to facilitate swift relief of future attacks of gout.

• Measuring the baseline serum uric acid (SUA) level at 4–6 weeks will help confirm the diagnosis of gout. If the person has no further symptoms, then urate-lowering therapy is not recommended, even if the SUA level is above the target value of 360 micromol/L. However, certain people who are at a higher risk of subsequent attacks (e.g. people with a SUA level of 600 micromol/L or more, or who have other risk factors), or those developing end-organ damage (affecting joints and kidneys) should be considered for prophylactic treatment earlier, such as after the first attack of gout. See Recurrent attacks of gout for more information.

These recommendations are based on published expert opinion, pragmatic advice and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007].

• An overall cardiovascular risk assessment should be made and lifestyle advice should be given [Saag and Choi, 2006; Underwood, 2006a; Stamp et al, 2007]. For more information, see the CKS topic on CVD risk assessment and management.

• Start allopurinol after two or more attacks of gout within a year or after the first attack in people who are at higher risk with one or more tophi, X-ray features of gouty arthritis, renal impairment, uric acid stones, or on long-term diuretic medication:
• Start allopurinol 1–2 weeks after the inflammation has settled and titrate the dose every few weeks until the serum uric acid (SUA) level is below 300 micromol/L.
• Co-prescribe a low dose of nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose colchicine for a minimum of 6 weeks, to prevent acute attacks of gout when starting allopurinol. Consider the need for gastroprotective medication when prescribing an NSAID.
• If NSAIDs and colchicine are contraindicated or not tolerated, low-dose oral prednisolone once a day for 4 to 12 weeks is recommended.
• Consider febuxostat as second-line therapy if allopurinol is not tolerated or contraindicated. The dose may be increased after 2–4 weeks if the SUA level remains above 360 micromol/L.
• Co-prescribe a low dose of nonsteroidal anti-inflammatory drugs (NSAIDs) or low-dose colchicine for at least 6 months, to prevent acute attacks of gout when starting febuxostat. Consider the need for gastroprotective medication when prescribing an NSAID.
• If NSAIDs and colchicine are contraindicated or not tolerated, low-dose oral prednisolone once a day for 4 to 12 weeks is recommended.

• It is important to explain that urate-lowering medication is normally lifelong and regular monitoring is needed.
• Advise the person that allopurinol or febuxostat 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 to stop their allopurinol or febuxostat during acute attacks.

The recommendations regarding allopurinol are based on published expert opinion, pragmatic advice and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. The quality of the evidence on allopurinol is poor and CKS could not find any prospective randomized controlled trials (RCTs) comparing different agents.

The recommendations regarding febuxostat are based on a NICE technology appraisal Febuxostat for the management of hyperuricaemia in people with gout [NICE, 2008], and the Summary of Product Characteristics [ABPI Medicines Compendium, 2010].

• In the UK, allopurinol is the first-line urate-lowering drug recommended. Probenecid, sulfinpyrazone, or benzbromarone are not commonly used and have limitations to their use.
• Starting a urate-lowering drug is usually recommended after a second attack of gout in a year, as 40% of people will not experience another attack within the first year and lifestyle modifications can be effective. People with very high serum uric acid levels, renal impairment, previous uric acid stones, visible tophi, or on diuretic medication may be vulnerable to repeated attacks of gout and end organ damage (kidneys and joints), so treatment may be advisable after the first attack [Jordan et al, 2007].
• Urate-lowering drugs: the evidence suggests that use of a urate-lowering drug is effective at reducing recurrent acute attacks of gout. Clinical observation suggests that starting prophylactic treatment too early after an attack (before 1–2 weeks after the inflammation has settled) can lead to a prolonged flare up of gout.
• Evidence for using nonsteroidal anti-inflammatory drugs (NSAIDs) or colchicine: there is no evidence base for prophylactic low-dose NSAIDs, although these are routinely used in practice. One small RCT (n = 43) showed that colchicine (0.6 mg) twice daily for 6 months reduced the number of flares when starting allopurinol, compared with placebo (at least one flare occurred in 33% of the colchicine group compared with 77% of the placebo group, NNT = 3) [Borstad et al, 2004].
• Evidence for duration of NSAIDs or colchicine: it is recommended to co-prescribe a low-dose NSAID or colchicine for a minimum of 6 weeks when starting allopurinol, although this may be necessary for up to 6 months. The British National Formulary recommends gout flare prophylaxis for 3 months [BNF 53, 2007]. The Summary of Product Characteristics for febuxostat recommends gout flare prophylaxis for at least 6 months [ABPI Medicines Compendium, 2010].
• Oral prednisolone: if the use of NSAIDs and colchicine are contraindicated, the recommendation to use oral prednisolone for up to 3 months is based on the professional opinion of expert reviewers.

• Once allopurinol or febuxostat is started, treatment is usually lifelong, especially in people at higher risk:
• Who have renal impairment, gouty tophi, uric acid stones, or those taking long-term diuretics.
• Who have recurrent attacks of gout when trying to stop urate-lowering treatment.
• Consider stopping allopurinol or febuxostat in people who have had a normal serum uric acid level for many years with no acute attacks of gout.

• If considering discontinuing urate-lowering medication, explain that there is no certainty that a further episode of gout will not recur.
• Make sure they have a supply of home medication to use in an acute attack, but advise them not to start allopurinol or febuxostat immediately if an acute attack develops, and to seek medical advice.
• Stress the importance of a healthy lifestyle and avoidance of trigger factors.
• Provide early and close follow up as needed.
• It is likely that gout attacks will not recur until urate load has become excessive again, so after a long period with a low serum uric acid level, it may be several years till they need to restart.
• Allopurinol or febuxostat may be stopped if a person is unable to tolerate adverse effects.

These recommendations are based on published expert opinion, pragmatic advice and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. The evidence in this area is limited and comes from small observational studies.

• The evidence from one study shows that people with milder gout may be able to stop treatment without any attacks of gout for over 3 years.
• Another observational study (n = 109) suggested that the lower the serum uric acid level prior to stopping urate-lowering therapy, the longer the person will remain free of gout [Perez-Ruiz et al, 2006].
• Discontinuing allopurinol or febuxostat is not common practice but a trial free period may be a pragmatic approach in an elderly person who has remained symptom-free from gout for years, but who takes multiple medications for comorbidities.

• If the person is taking allopurinol, check the serum uric acid (SUA) level and renal function every 3 months in the first year, then annually, and aim for a SUA level below 300 micromol/L.
• If the person is taking febuxostat, use clinical judgement to decide if liver function tests need to be retested periodically after starting treatment.
• If the person is still having frequent attacks of gout despite achieving the target SUA level:
• Assess compliance with prophylactic medication and increase the dose appropriately.
• Review any trigger factors such as medication (e.g. diuretics), trauma, diet, weight gain, and excess alcohol consumption.
• Provide a home supply of medication to use during an acute attack to minimize the impact on the person's functioning.
• Review cardiovascular risk factors and provide ongoing lifestyle advice. For more information, see the CKS topic on CVD risk assessment and management.
• In a person with hypertension, stop diuretics during an acute attack and change to an alternative antihypertensive. For more information, see the CKS topic on Hypertension - not diabetic.
• In a person with heart failure, continue diuretics during an acute attack. If using a nonsteroidal anti-inflammatory drug (NSAID) for pain relief, monitor renal function closely. For more information, see the CKS topic on Heart failure - chronic.
• Consider referral to secondary care, if the person is still having attacks despite all these measures.

The recommendations regarding allopurinol recommendations are based on the best available evidence and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. The recommendations regarding febuxostat are based on the Summary of Product Characteristics [ABPI Medicines Compendium, 2010].

• If a person is still symptomatic despite optimum management in primary care, refer for specialist advice as other urate-lowering agents (sulfinpyrazone, benzbromarone, or probenecid) may be tried or combined by a specialist.

• People with gout should be advised to:
• Aim for an ideal body weight — but avoid crash dieting and high protein/low carbohydrate diets.
• Eat sensibly — by restricting the amount of red meat and avoiding a high protein intake. Avoid foods rich in purines such as liver, kidneys, and seafood.
• Drink alcohol sensibly — by avoiding binge drinking and restricting alcohol consumption to 21 units per week for men and 14 units per week for women.
• Avoid dehydration by drinking water (up to 2 litres/day unless there is a medical contraindication).
• Take regular exercise — but avoid intense muscular exercise and trauma to joints.
• Stop smoking — refer for smoking cessation advice if the person is motivated to quit.
• Provide written information and patient support via the UK Gout Society. For more information, see www.ukgoutsociety.org.

These recommendations are based on published expert opinion, pragmatic advice, and the guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. There are no controlled trials (mainly observational studies and case studies) of the effect on lifestyle changes on the incidence of gout, but expert opinion is that lifestyle changes can be beneficial [Sutaria et al, 2006].

• Weight: there is evidence suggesting obesity is linked with gout. Gradual weight loss may improve uric acid levels and reduce the frequency of gout attacks, but weight loss should not involve diets that increase urate levels, such as high-protein diets or starvation regimens [Saag and Choi, 2006].
• Exercise: swimming and walking should be encouraged, but strenuous exercise or trauma to joints may precipitate attacks of gout.
• Diet: there is evidence that restricting dietary purines can improve serum uric acid levels. A low-purine diet may have some clinical benefit in reducing attacks of gout, and this is especially important in people with renal impairment [Choi, 2005].
• The diet should be nutritionally balanced, but purine intake limited. Foods which are very rich in purines such as liver, kidneys, red meat, yeast extracts, seafood (herring, sardines, and shellfish), and certain vegetables (asparagus, beans, cauliflower, lentils, mushrooms, oatmeal, and spinach), should be avoided. 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. However, if the person is keen to measure quantities of food, they should aim for a maximum total daily purine intake of around 200 mg. People with diabetes should continue with their diabetic diet as this will help with lowering urate levels.
• Alcohol: the evidence suggests that drinking alcohol above the recommended limit (especially beer, stout, port, and fortified wines) is associated with a higher incidence of gout. Moderate consumption of wine (two glasses per day) was not associated with a significant increased risk [Choi, 2005].
• The aim of lifestyle advice is not only to reduce episodes of gout but to reduce overall cardiovascular risk, which is higher in people with gout. For more information, see the CKS topic on CVD risk assessment and management.

• Check serum uric acid (SUA) level 4–6 weeks after an acute attack of gout.
• For people on urate lowering therapy, see Follow up for information about monitoring SUA levels.

• There is no indication for screening for hyperuricaemia in people without symptoms of gout. Asymptomatic people with a raised SUA level do not usually need to be treated with a urate-lowering drug, as gout is not an inevitable consequence of hyperuricaemia. There may be indications for starting a urate-lowering drug in asymptomatic people with malignancy or a very high SUA level (> 800 micromol/L), but this is beyond the scope of this CKS topic [Underwood, 2006a].

These recommendations are based on published expert opinion, pragmatic advice, and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007].

• Checking the serum uric acid (SUA) level after the first acute attack of gout will help to confirm the diagnosis and may influence the decision to start prophylactic treatment earlier. If a person has a very high level of SUA (e.g. 600 micromol/L or more) they may be more likely to have further attacks.
• A SUA level below 300 micromol/L will not allow urate to crystallize and existing deposits should mobilize. However, even if this target is not reached, any reduction in SUA concentration should reduce the incidence of recurrence [Underwood, 2006a].
• Cohort studies have demonstrated a reduced frequency of subsequent gout attacks in people who achieve a target level of SUA below 360 micromol/L [DynaMed, 2007]. However, some people with even lower SUA levels still have attacks, and attacks may even remit without a reduction in SUA.

• Admit the person if septic arthritis is suspected.
• Seek specialist advice when:
• The diagnosis is uncertain.
• There is a suspicion of an underlying systemic illness (e.g. rheumatoid arthritis or connective tissue disorder).
• Gout occurs during pregnancy or in a young person (under 25 years of age).
• Allopurinol or febuxostat is at maximum dose but a person is still having recurrent attacks of gout.
• A person has persistent symptoms during an acute attack despite maximum doses of anti-inflammatory medication (alone or in combination).
• An intra-articular steroid injection is indicated but the facilities or expertise are not available.
• Complications are present, including urate kidney stones, urate nephropathy, or troublesome tophi.

These recommendations are based on published expert opinion, pragmatic advice and a guideline produced by expert representatives of the British Society for Rheumatology (BSR). The evidence supporting the BSR recommendations is based on a systematic review of literature [Jordan et al, 2007]. The recommendation regarding febuxostat is based on the Summary of Product Characteristics [ABPI Medicines Compendium, 2010].

• Many people with gout have comorbidities, so close monitoring for adverse effects and deteriorating renal function is needed. A referral to secondary care or further specialist advice may be advisable if the person is inadequately controlled on routine medication or there are contraindications to starting treatment.

• Acute attacks of gout are relatively rare in people with renal impairment, due to the anti-inflammatory effects of uraemia. However, following a kidney transplant, people are vulnerable to gout (which has an atypical upper limb and polyarticular presentation due to the effects of immunosuppressant drug regimens).
• Allopurinol is effective in people with renal impairment and it can be used after transplantation, but interactions with cytotoxic medication (e.g. azathioprine) need to be considered, and colchicine and nonsteroidal anti-inflammatory drugs (NSAIDs) are best avoided in these people.
• Since allopurinol is excreted by the kidney, impaired renal function may lead to retention of allopurinol and/or its metabolites, with consequent prolongation of plasma half-life, therefore the dose should be modified based on the person's creatinine clearance or glomerular filtration rate (GFR) as outlined in Table 1.
• Once allopurinol has been started, it is best to check urate levels and renal function every 2–4 weeks for the first 3 months.
• See the section on allopurinol for more prescribing information.

• It is not necessary to adjust the dose of febuxostat in people with mild or moderate renal impairment. However, as with allopurinol, it may increase azathoprine and mercaptopurine levels. The efficacy and safety of using febuxostat in people with severe renal impairment (creatinine clearance <30 ml/min) has not been fully evaluated [ABPI Medicines Compendium, 2010].

• The principles of management of people with tophi (and other complications of gout) are similar to those for managing people with frequent recurrences of gout.
• The natural history of tophi may vary from individual to individual. Tophi can remain static, enlarge, or dissolve with urate-lowering therapy. As tophi dissolve they may ulcerate through the skin. This can be misinterpreted as evidence of local infection. Reassure the person that the ulcer should heal as the tophaceous material completely resolves or discharges [Gibson, 2005].
• Rarely, tophi may be so large or painful that referral is indicated. Occasionally surgical excision may be considered.
• A case report describes successful surgical removal of a large painful tophaceous nodule on the plantar aspect of the first metatarsophalangeal joint. Surgery relieved the pain and restored the ability to wear shoes and walk without discomfort [Naas and Sanders, 1998].