Gout — treating it properly, not just managing the flares

In brief

• Gout is a chronic crystal arthritis, driven mainly by genetics and how the kidneys handle urate, with food and alcohol as triggers.
• Treat a flare early with an NSAID, low-dose colchicine or a steroid; a first flare settles in 7 to 14 days, but untreated gout progresses.
• Two or more flares a year, tophi, kidney stones or kidney disease call for long-term urate-lowering treatment, usually to a urate below 0.36 mmol/L.
• Before allopurinol we discuss HLA-B*5801 testing, as carriers (more common in East and Southeast Asians) have a much higher risk of a severe skin reaction.
• On allopurinol, stop and get same-day care for a widespread rash, mouth or eye sores, fever, or facial swelling.
• A hot, swollen joint with fever or feeling unwell may be septic arthritis and needs urgent assessment.

We diagnose gout and manage urate-lowering treatment at our Punggol clinic. See our chronic disease care.

What gout actually is

Gout is a crystal arthritis. Monosodium urate (MSU) crystals deposit in joints and soft tissues and trigger intense inflammation. The underlying driver is hyperuricaemia, a blood urate level above saturation, over months to years.

• Most hyperuricaemia is a kidney-handling problem, not an overeating problem. About 90% of people with gout under-excrete urate through the kidneys rather than over-produce it, largely for genetic reasons. Food and alcohol are triggers, but rarely the root cause.
• Gout is common in Singapore. In the Singapore Chinese Health Study, about 4 in 100 middle-aged and older Chinese adults reported a doctor’s diagnosis of gout. Worldwide, it is commoner in men.
• Gout travels with other conditions: hypertension, type 2 diabetes, chronic kidney disease, cardiovascular disease, obesity and metabolic-associated fatty liver disease. Treating it well is part of the broader cardiovascular-kidney-metabolic (CKM) picture.
• Untreated, gout progresses. Attacks become more frequent, joints develop chronic changes and tophi (urate deposits) form; some patients develop joint destruction and disability. This is entirely preventable with properly used treatment.

How it shows up

The acute flare

The classic first attack is in the big-toe joint (metatarsophalangeal joint, “podagra”): swollen, hot, red and intensely painful, often at night. Within hours, even a bedsheet’s weight is unbearable. A low-grade fever and feeling unwell are common.

Other common sites are the ankle, midfoot, knee, wrist, elbow (especially as gout progresses) and small hand joints.

A first attack usually settles over 7 to 14 days even without treatment, so patients may assume the problem is over. It rarely is.

Chronic tophaceous gout

In long-standing, poorly controlled disease:

• Tophi: firm, usually painless lumps of urate, classically on the ears, fingers, elbows, top of the foot and Achilles tendon. They can ulcerate and discharge chalky white material.
• Chronic arthropathy: stiff, swollen, deformed joints from repeated inflammation.
• Uric acid kidney stones.
• Chronic urate nephropathy.

Visible tophi on your fingers or ears mean the disease has been uncontrolled for a long time, and urate-lowering treatment is overdue.

Common triggers

A flare usually needs a high urate level plus a trigger, such as:

• Dietary excess: particularly organ meats, certain seafoods (see the diet section) and a heavy high-purine meal.
• Alcohol, especially beer, then spirits; wine is less of a trigger.
• Sugar-sweetened drinks, particularly with high-fructose corn syrup or other fructose-based sweeteners.
• Dehydration: hot weather, strenuous exercise without enough fluid, after surgery.
• Sudden weight loss or fasting, which can release stored urate.
• Medicines: thiazide and loop diuretics (a very common culprit in older patients), low-dose aspirin, some chemotherapy drugs, ciclosporin, tacrolimus.
• Acute illness or surgery, as the stress response shifts urate.
• Injury to a joint.
• Starting urate-lowering treatment too abruptly (see flare prophylaxis below).
• Stopping urate-lowering treatment, even briefly.

If flares keep coming for no obvious reason, we review all your medicines and supplements.

How we diagnose gout

The gold standard

Joint aspiration with polarised-light microscopy is the definitive test: needle-shaped, negatively birefringent urate crystals confirm gout. It is done when the diagnosis is genuinely uncertain, or septic arthritis is possible (see below).

In practice — clinical diagnosis

For a classic presentation in someone with a compatible profile (middle-aged or older, known high urate, typical joints, rapid onset, response to treatment), a clinical diagnosis is usually enough. We don’t always need to aspirate.

Serum urate — timing matters

• During a flare, serum urate is often normal or even low, because inflammation uses up circulating urate. A normal result then does not rule out gout.
• Check serum urate 2–4 weeks after the flare settles to get a true baseline.
• Targets are judged from this baseline and later monitoring, not during flares.

Other tests

• Inflammatory markers (CRP, ESR, white cell count): raised in gout, but also in infection and other inflammatory arthritis.
• Kidney function and lipids, as gout often travels with metabolic disease.
• Ultrasound: can show the “double contour sign” (urate crystals on the cartilage surface) and identify tophi.
• Dual-energy CT: images urate deposits directly; useful in tricky cases, through rheumatology.

What we must not miss — septic arthritis

A hot, swollen, painful joint is septic arthritis until proven otherwise if:

• you have a fever or are generally unwell
• the picture is unusual for gout
• there is no history of gout and no classic risk factors
• there has been a recent bacterial infection, immunosuppression or joint surgery
• it is a prosthetic joint

These usually need joint aspiration before we accept a gout diagnosis. Septic arthritis destroys a joint in days if missed.

Managing the acute flare

Three options work; the choice depends on your other medical conditions. Start early: treatment within the first 24 hours works markedly better than starting on day three.

NSAIDs

First-line if there are no contraindications:

• Naproxen 500 mg twice daily, or
• Indomethacin 50 mg three times daily, or
• Etoricoxib 120 mg once daily, or
• Diclofenac 50 mg three times daily

Use for 5–7 days, then stop. Add a proton pump inhibitor to protect the stomach if there is any risk (previous ulcer, age, steroids, antiplatelet medicines).

NSAIDs are generally avoided with:

• significant kidney disease (eGFR < 60, and especially < 30)
• heart failure
• an active peptic ulcer or recent gut bleeding
• poorly controlled high blood pressure
• anticoagulant or antiplatelet treatment with a higher bleeding risk

Colchicine

Use colchicine when NSAIDs are unsuitable, or as an alternative first-line option. Current evidence supports a low-dose regimen, which is gentler on the gut and equally effective:

• 1.0–1.2 mg at the start of symptoms, then
• 0.5–0.6 mg 1 hour later, then
• 0.5–0.6 mg once or twice daily for the remaining 5–7 days

The old high-dose regimens (1 mg every 2 hours until symptoms resolved or diarrhoea started) are obsolete. They caused substantial gut toxicity and worked no better.

• Reduce the dose in kidney impairment and in older adults.
• Colchicine interacts with clarithromycin, erythromycin, some antifungals and some statins. Check with us before combining.
• Stop immediately if severe diarrhoea develops, a sign of toxicity.

Corticosteroids

If NSAIDs and colchicine are both unsuitable, or for severe flares in several joints:

• Oral prednisolone 30–40 mg daily for 5 days (tapering is not always needed for such short courses)
• Intra-articular steroid injection, an excellent option for a single large joint

Starting urate-lowering therapy during a flare — updated practice

Starting urate-lowering therapy during a flare was once thought to worsen or prolong it. Recent evidence, including a randomised trial by Hill et al. (2015), shows it doesn’t. The 2020 ACR gout guideline supports starting it either during the flare or after it settles, alongside flare treatment and prophylaxis.

Patients are often most motivated during a painful flare, and the decision can get lost if deferred. So if urate-lowering therapy is indicated anyway, we discuss it then.

If you already take urate-lowering treatment when a flare hits, don’t stop it. Continuing improves outcomes and avoids mobilisation flares on restarting.

What we focus on during the flare

The flare is also the time to talk about triggers, alcohol and the bigger plan, while the experience is still vivid.

The bigger decision — do you need urate-lowering therapy?

Too often a flare is treated and long-term control is never discussed, while the crystal load silently grows.

Urate-lowering therapy (ULT) is recommended if you have any of:

• two or more flares a year
• any tophi on examination or imaging
• chronic gouty arthropathy (changes on examination or X-ray)
• chronic kidney disease, stage 3 or worse
• a history of uric acid kidney stones
• persistently very high serum urate (typically >0.54 mmol/L / >9 mg/dL)

The case is stronger if you also have hypertension, diabetes, cardiovascular disease or a strong family history of gout.

Targets:

• Serum urate below 0.36 mmol/L (6 mg/dL) for most patients
• Below 0.30 mmol/L (5 mg/dL) with visible tophi, to help existing crystal deposits dissolve faster

For most patients, ULT is lifelong once started. Stopping after urate normalises often brings flares back within months. It is chronic treatment for a chronic condition, like blood pressure medication.

The medications we use

Allopurinol is first-line for most patients:

• It inhibits xanthine oxidase, reducing urate production.
• Start at 50–100 mg daily and increase every 2–5 weeks towards target, typically to 200–400 mg daily. The maximum is 900 mg if needed, under specialist guidance.
• The dose is adjusted in significant kidney impairment, but the old blanket caps have been relaxed; modern evidence supports careful up-titration with monitoring.
• It is inexpensive and widely available.
• Before starting, we discuss HLA-B*5801 genetic testing. Singapore guidance does not require it for everyone, but it may be considered if you are at higher risk of a severe reaction (see next section).

Febuxostat (Feburic) is an alternative:

• It is also a xanthine oxidase inhibitor, but structurally different.
• Start at 40 mg daily, increasing to 80 mg if the target is not met.
• It needs no HLA-B5801 test, and is useful when allopurinol is contraindicated, poorly tolerated, or unsuitable after a positive HLA-B5801 result.
• The CARES trial raised concerns about slightly higher cardiovascular mortality than allopurinol in people with established cardiovascular disease. A later trial (FAST) did not replicate this, but it needs careful discussion if you have coronary disease or heart failure.

Uricosurics (probenecid, benzbromarone) increase urate excretion in the urine. They suit people who under-excrete urate, with normal kidney function and no history of urate stones. We use them less often first-line, and benzbromarone is not routinely available in Singapore.

Pegloticase and other specialist options are reserved for severe, refractory disease under rheumatology.

Flare prophylaxis during ULT initiation

Starting ULT can trigger flares in the first few months as deposited crystals mobilise. So we routinely prescribe flare prophylaxis for 3–6 months at the start:

• colchicine 0.5 mg once or twice daily (adjusted for kidney function), or
• a low-dose NSAID if colchicine is not suitable

This greatly reduces the “I started the medicine and got a worse flare” experience that makes many patients give up.

Follow-up and monitoring

• Serum urate every 2–4 weeks while adjusting the dose, then every 3–6 months at target.
• Kidney function at baseline, at dose changes and periodically.
• Liver enzymes occasionally.
• Symptoms: flare frequency, and tophi shrinking over months to years.
• Adherence: the commonest reason for failure, usually improved by conversation rather than more medication.

HLA-B*5801 testing before starting allopurinol

Allopurinol is usually well tolerated. Rarely, it causes a severe cutaneous adverse reaction (SCAR): Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reaction with eosinophilia and systemic symptoms (DRESS). These usually occur in the first 2–3 months, carry a meaningful risk of death, and can leave lasting damage to the skin, eyes and mucous membranes.

The overall risk is low, but substantially higher in carriers of the HLA-B*5801 gene variant. The variant is more common in East and Southeast Asian populations, including Han Chinese, Thai and Korean people, and is also found in Malay and Indian populations. It is much less common in Japanese and European people. Carrying it raises the odds of allopurinol SCAR roughly 80-fold in most studies.

How we approach it at KTMC — a shared decision

HLA-B*5801 testing is a conversation rather than an automatic order. Guidance from Singapore’s Ministry of Health, HSA and ACE does not require routine testing before allopurinol. The test’s positive predictive value is low: only about 2 in 100 carriers who start allopurinol develop SCAR. Testing may be considered for people already at higher risk of SCAR, such as those with kidney impairment or of older age. In practice:

• Starting allopurinol for the first time: we discuss testing with everyone, and recommend it if you have kidney impairment or are older.
• Taken allopurinol long-term without any hypersensitivity reaction: testing is not needed. SCAR is then unlikely, and restarting is usually fine.
• No added risk factors: starting without a test is reasonable. You accept careful monitoring over the first 2–3 months, and agree to stop immediately and come in if warning features develop (see below).

Whether or not you are tested, we start allopurinol at a low dose and increase it slowly. A negative test lowers the risk but does not remove it.

If the test is negative, we start allopurinol as usual, with slow titration and flare prophylaxis. If it is positive, we avoid allopurinol and use an alternative, typically febuxostat.

Stop allopurinol immediately and seek same-day care if you develop:

• a widespread rash, particularly with peeling skin
• sores or ulcers in the mouth, eyes or genital area
• fever or feeling generally unwell, with or without a rash
• swelling of the face or lips

These typically appear within the first 2–3 months. After that, the risk of SCAR falls substantially.

Why we still use allopurinol first where safe

Febuxostat is more expensive and has its own considerations (CARES / FAST, above), particularly with existing cardiovascular disease. Allopurinol is globally the best-studied urate-lowering drug, with decades of experience. It remains guideline first-line where safe and is substantially cheaper long term. Used carefully, with or without testing first, it is the workhorse for most patients on ULT.

Cost and subsidy of HLA-B*5801 testing

MediSave coverage for genetic tests such as HLA-B*5801 varies and changes over time. We will tell you the current cost and coverage at your visit, so there are no surprises later.

If you’ve been on allopurinol for years without problems

If you have tolerated allopurinol well for a year or longer, you are past the main risk window. Testing now is not usually necessary, and you can continue.

Common misconceptions that derail long-term control

• “I can control gout with diet alone.” Usually wrong. A strict low-purine diet lowers serum urate by perhaps 0.06–0.09 mmol/L (1–1.5 mg/dL) at best, not enough for most patients who need ULT.
• “Urate-lowering medication is only for severe gout.” Two flares a year is already enough to make the case.
• “I’ll stop the medicine once my urate is normal.” Urate stays low because the medicine works. Stop it, and urate rises, flares return and deposits grow.
• “I got a flare after starting allopurinol, so it doesn’t work.” This is almost always a mobilisation flare as crystals dissolve, which is a good sign. Don’t stop the ULT.
• “Painkillers are enough.” They treat the flare, not the crystal load, so tophaceous gout can still develop.
• “If I just stop eating seafood, I’ll be fine.” Seafood’s contribution is usually modest. Plant purines (legumes, some vegetables) do not meaningfully raise serum urate on current evidence.
• “Colchicine is only for acute flares.” It is also the workhorse of prophylaxis when starting ULT.

Comorbidities and medications worth reviewing

We also review:

• Blood pressure, diabetes, lipids, kidney function and weight, the full CKM cluster.
• Diuretics. If you take a thiazide (e.g. hydrochlorothiazide, indapamide) or loop diuretic (furosemide) for high blood pressure or heart failure, we consider alternatives. Losartan (an ARB) mildly increases urate excretion and can be a good substitute for thiazides where appropriate.
• Low-dose aspirin. It raises urate, but rarely enough to stop aspirin for; we discuss it rather than change it by default.
• Hydration. Aim for 2–3 litres of water a day, unless your doctor has asked you to restrict fluids for heart or kidney reasons.

When we’d refer to rheumatology

• Diagnostic uncertainty: an unusual joint pattern, atypical presentation, or possible overlap with other inflammatory arthritis.
• Chronic tophaceous gout.
• Refractory disease: flares despite properly used ULT, or urate above target on maximum tolerated doses.
• Significant kidney disease limiting ULT choices.
• A positive HLA-B*5801 result with additional complexities.
• Pegloticase or other specialist-only treatment being considered.
• Suspected septic arthritis, usually to the emergency department rather than rheumatology in the first instance.

A low-purine diet — adapted for local eating

Purine intake has a modest but real effect on serum urate; diet supports treatment but doesn’t replace it. Old diet sheets restricted anything with a whisper of purine, without evidence, including foods now known to be fine (most vegetables, most legumes, soy).

Foods to minimise or avoid

These raise serum urate the most.

Organ meats and offal: liver, kidney, heart, tripe, brain, sweetbreads. Local examples include pig’s liver or kidney porridge, fried liver, kambing soup (often with innards), bak kut teh broth with organ meats, and hot-pot innards platters.

Meat-based concentrates and stocks (purines are water-soluble and concentrate in the broth):

• beef or pork bone soup simmered for many hours
• thick meat gravies, Bovril, Oxo, Marmite, Vegemite
• hot-pot or steamboat broth after long boiling of meat and bones
• commercial “essence of chicken” and similar concentrates
• lor mee, mee sua and pork rib soup, where the broth rather than the noodles is the concern

Specific seafood: anchovies (ikan bilis, including as a base in many local dishes), sardines, mackerel, herring, roe and fish eggs, mussels and scallops.

Alcohol: beer is the worst (yeast-derived purines plus ethanol), then spirits. Wine has less effect, and moderate intake may be acceptable.

Foods to have in moderation

These raise urate modestly at higher intakes but needn’t be cut out:

• Red meat (beef, pork, lamb, including mutton curry and rendang): smaller portions rather than big steaks.
• Poultry (chicken, duck): a reasonable portion at a meal is fine; avoid frequent large portions.
• Most fish: the oily fish above are higher; lean white fish is usually fine in moderate portions.
• Shellfish (prawns, crab, lobster, squid): in moderation, not avoided entirely.

Foods that are fine or actively helpful

• Vegetables, including those on old restrictive lists (spinach, asparagus, cauliflower, mushrooms).
• Legumes and pulses: beans, lentils, chickpeas, dhal, tofu, tempeh, soy milk, soya bean curd (tau huay / tau suan). Fine, with some evidence of a protective effect.
• Whole grains: brown rice, oats, barley, wholegrain bread.
• Fruit: most is fine, including cherries (possibly a modest benefit). Limit very high-fructose options such as large amounts of durian and sugared dried fruit.
• Low-fat dairy (milk, yogurt, Greek yogurt), which is linked with lower gout risk.
• Eggs in moderation, nuts and seeds, and plenty of water (see hydration above).
• Coffee (regular or decaf), linked with lower gout risk; tea is neutral.

Singapore-specific practical tips

• Hawker and coffee-shop choices. Lean towards steamed fish (not oily kinds), cai png (mixed rice) with vegetables, tofu and less protein, Indian vegetarian thali, or Malay fish and vegetables. Cut down on organ-meat dishes, bone broths and kambing soup.
• Bak kut teh. The broth is the issue more than the meat. Occasionally is reasonable; weekly probably isn’t.
• Buffets and steamboat often combine organ meats, concentrated broth and beer; use smaller plates, more vegetables and less broth.
• Chinese New Year is purine-heavy and alcohol-heavy, and many patients have their first flare after it. If you are on ULT and tend to flare then, ask us about prophylactic colchicine for a week or two around CNY.
• Soups. Choose clear, tomato-based or vegetable-based soups over long-simmered bone and meat broths.
• Chinese herbal tonic soups often contain shark’s fin, abalone or concentrated meat bases, so ask before ordering.
• Muslim patients avoid alcohol, which helps; watch mutton and lamb intake, which tends to be high in traditional dishes.
• Vegetarian patients: plant purines are not a concern, and in Taiwanese cohort studies a vegetarian diet was linked with a lower risk of gout. If gout develops, the cause is usually genetic or kidney-related.
• Indian patients: dhal, sambar, tofu and paneer are fine; limit mutton biryani portions and heavy ghee-based cooking.

A realistic summary

• Weight loss and metabolic gains come mostly from your overall eating pattern (more vegetables, moderate portions, less alcohol, fewer sugary drinks), not a long avoid-list.
• For most patients here, cutting down beer and spirits helps most, followed by cutting out organ meats and heavy concentrated broths.
• Diet supports ULT, but ULT does the heavy lifting for urate reduction in patients who need it.

The Singapore context — access and subsidy

• Gout is on MOH’s Chronic Disease Management Programme list, so chronic-disease schemes apply to it.
• Healthier SG Chronic Tier: CHAS, Pioneer Generation and Merdeka Generation cardholders enrolled with a Healthier SG clinic can get selected gout medicines (allopurinol, colchicine, selected NSAIDs, losartan) at prices similar to polyclinic rates. Febuxostat is not on the list.
• CHAS: means-tested chronic-condition subsidy at participating GP clinics.
• MediSave: usable for gout consultations, tests such as serum urate, and medicines under the Chronic Disease Management Programme; coverage for HLA-B*5801 testing varies, so confirm it at the visit.
• Specialist referral: we work with local rheumatology teams for patients who need them.

Get in touch

Punggol — 658 Punggol East, #01-04, Singapore 820658 · Tel 6312 4589

Joo Chiat — 172 Joo Chiat Road, #01-01, Singapore 427443 · Tel 6920 1952

Email — admin@ktmc.sg

References

Guidelines

• Agency for Care Effectiveness (ACE). Gout — achieving the management goal. ACE Clinical Guidance, Ministry of Health, Singapore. December 2023.
• FitzGerald JD, Dalbeth N, Mikuls T, et al. 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care Res. 2020;72(6):744–760.
• Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout. Ann Rheum Dis. 2017;76:29–42.

HLA-B*5801 and allopurinol safety

• Hung SI, Chung WH, Liou LB, et al. HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. Proc Natl Acad Sci USA. 2005;102:4134–4139.
• Ko TM, Tsai CY, Chen SY, et al. Use of HLA-B*58:01 genotyping to prevent allopurinol-induced severe cutaneous adverse reactions in Taiwan: national prospective cohort study. BMJ. 2015;351:h4848.
• Health Sciences Authority (HSA), Singapore. Advisory on HLA-B*5801 testing before initiation of allopurinol.
• Health Sciences Authority (HSA), Singapore. Allopurinol-induced severe cutaneous adverse reactions and the role of HLA-B*5801 genotyping – a reminder. Safety alert, 21 December 2021. hsa.gov.sg
• Kang HR, Jee YK, Kim YS, et al. Positive and negative associations of HLA class I alleles with allopurinol-induced SCARs in Koreans. Pharmacogenet Genomics. 2011;21:303–307.
• Pham HT, Tran MH, Mai Hoang TV, et al. HLA-B*58:01 genotyping prevalence and the association with allopurinol-induced severe cutaneous adverse reactions: a living systematic review and meta-analysis. Sci Rep. 2025;15:30742.

Acute flare treatment and ULT timing

• Terkeltaub RA, Furst DE, Bennett K, et al. High versus low dosing of oral colchicine for early acute gout flare: Twenty-four-hour outcome of the first multicenter, randomized, double-blind, placebo-controlled, parallel-group, dose-comparison colchicine study. Arthritis Rheum. 2010;62(4):1060–1068. (AGREE trial)
• Hill EM, Sky K, Sit M, Collamer A, Higgs J. Does starting allopurinol prolong acute treated gout? A randomized clinical trial. J Clin Rheumatol. 2015;21(3):120–125.
• Taylor TH, Mecchella JN, Larson RJ, Kerin KD, MacKenzie TA. Initiation of allopurinol at first medical contact for acute attacks of gout: a randomized clinical trial. Am J Med. 2012;125(11):1126–1134.

Febuxostat cardiovascular safety

• White WB, Saag KG, Becker MA, et al. (CARES Investigators). Cardiovascular Safety of Febuxostat or Allopurinol in Patients with Gout. N Engl J Med. 2018;378:1200–1210.
• Mackenzie IS, Ford I, Nuki G, et al. (FAST Investigators). Long-term cardiovascular safety of febuxostat compared with allopurinol in patients with gout (FAST): a multicentre, prospective, randomised, open-label, non-inferiority trial. Lancet. 2020;396:1745–1757.

Diet and gout

• Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350:1093–1103.
• Zhang Y, Chen C, Choi H, et al. Purine-rich foods intake and recurrent gout attacks. Ann Rheum Dis. 2012;71:1448–1453.
• Chiu THT, Liu CH, Chang CC, Lin MN, Lin CL. Vegetarian diet and risk of gout in two separate prospective cohort studies. Clin Nutr. 2020;39(3):837–844.

Epidemiology

• Teng GG, Ang LW, Saag KG, Yu MC, Yuan JM, Koh WP. Mortality due to coronary heart disease and kidney disease among middle-aged and elderly men and women with gout in the Singapore Chinese Health Study. Ann Rheum Dis. 2012;71:924–928.
• Dehlin M, Jacobsson L, Roddy E. Global epidemiology of gout: prevalence, incidence, treatment patterns and risk factors. Nat Rev Rheumatol. 2020;16:380–390.

Singapore schemes

• Ministry of Health, Singapore. Chronic Disease Management Programme (CDMP) — list of covered conditions. 2026. moh.gov.sg
• Ministry of Health, Singapore. Chronic Disease Management Programme: handbook for healthcare professionals (gout: claimable items). 2024, updated June 2025.
• Healthier SG. Healthier SG Chronic Tier. healthiersg.gov.sg
• Ministry of Health, Singapore. Healthier SG whitelisted drugs. Dataset, 2026. data.gov.sg

This information is for general education only and is not a substitute for medical advice. Gout management should be individualised to your specific urate level, comorbidities, medications, genetic status, and preferences — please speak with our team. v1.1 · October 2026 (v1.0 April 2026) · Review due April 2028.