Gout — treating it properly, not just managing the flares

About this guide

Gout has a reputation problem. It has been called “the disease of kings,” blamed on feasting, and framed as a lifestyle failure. This framing has aged badly. Modern understanding is that gout is a chronic metabolic disease largely driven by genetics and kidney handling of urate — food and alcohol are triggers, but rarely the root cause. “Just eat better” is almost never a complete answer.

The other problem with gout is that the acute flare dominates the conversation — understandably, because it hurts — while the real long-term work is controlling serum urate so that flares stop happening and joints don’t get permanently damaged. A patient who is treated only during flares usually has progressive disease.

This guide covers:

• What gout actually is, and why diet alone usually isn’t enough
• How we diagnose it — and what we do instead of always sticking a needle in the joint
• Managing the acute flare
• The bigger decision: do you need urate-lowering therapy?
• HLA-B*5801 genetic testing before starting allopurinol — essential in our population
• Target urate levels, monitoring, and how long to stay on treatment
• Common misconceptions that trip up long-term control
• A practical low-purine diet adapted to local Singaporean eating

What gout actually is

Gout is a form of crystal arthritis — deposition of monosodium urate (MSU) crystals in joints and soft tissues, which triggers intense inflammation and acute attacks. The underlying driver is hyperuricaemia — a blood urate level above saturation — over months to years.

A few points worth knowing:

• 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-producing it. This is largely genetic.
• Singapore has a higher background prevalence of gout than Western countries, particularly in older men. It is rising across all ethnic groups locally, tracking obesity and metabolic syndrome.
• Gout travels with other conditions — hypertension, type 2 diabetes, chronic kidney disease, cardiovascular disease, obesity, and metabolic-associated fatty liver disease. Treating gout well is part of the broader cardiovascular-kidney-metabolic (CKM) picture.
• Untreated, gout progresses. Intermittent attacks become more frequent; joints develop chronic changes; tophi (firm urate deposits) appear under skin around ears, fingers, elbows, Achilles tendons; and in some patients there is joint destruction and disability. This is entirely preventable with properly-used treatment.

How it shows up

The acute flare

The classic first gout attack is a big-toe metatarsophalangeal joint (podagra) — swollen, hot, red, intensely painful, often waking the patient at night. Over a few hours the joint becomes so sensitive that even the weight of a bedsheet is unbearable. A low-grade fever and general malaise are common.

Other common sites:

• Ankle
• Midfoot
• Knee
• Wrist
• Elbow (especially when it progresses)
• Small hand joints

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

Chronic tophaceous gout

In long-standing, poorly-controlled disease:

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

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

Common triggers

A flare usually needs a pre-existing high urate level plus a trigger. Common triggers:

• Dietary excess — particularly organ meats, certain seafoods (see diet section below), and heavy intake of high-purine foods at a single meal
• Alcohol — beer is the worst (the yeast adds purines); spirits next; wine is less of a trigger
• Sugar-sweetened drinks — particularly those with high-fructose corn syrup or large amounts of fructose-based sweeteners
• Dehydration — hot weather, strenuous exercise without replacement, post-operative
• Sudden weight loss or fasting — can release stored urate
• Medications — thiazide and loop diuretics (very common culprit in older patients), low-dose aspirin, some chemotherapy agents, ciclosporin, tacrolimus
• Acute illness or surgery — the stress response shifts urate
• Trauma to a joint
• Starting urate-lowering treatment too abruptly — mobilisation flares (a reason why we titrate slowly and add prophylaxis)
• Stopping urate-lowering treatment — even for a short period

If you keep getting flares and we can’t obviously explain why, a review of all current medications (including OTC and supplements) is part of the conversation.

How we diagnose gout

The gold standard

Joint aspiration with polarised-light microscopy is the definitive test — the characteristic needle-shaped, negatively-birefringent monosodium urate crystals confirm the diagnosis unequivocally. This is done when the diagnosis is genuinely uncertain or when septic arthritis is on the differential (see below).

In practice — clinical diagnosis

For a classical presentation in a patient with a compatible profile (middle-aged or older, history of hyperuricaemia, typical joint distribution, rapid onset, response to appropriate treatment), a clinical diagnosis is usually sufficient. We don’t always need to aspirate every joint.

Serum urate — timing matters

A serum urate is useful, but with an important caveat:

• During an acute flare, serum urate is often normal or even low. The inflammatory response consumes circulating urate. A normal result during a flare does not rule out gout.
• Check serum urate 2–4 weeks after the flare settles to establish a true baseline.
• Target urate levels (see treatment section) are judged off this baseline and during ongoing monitoring, not during flares.

Other tests

• Inflammatory markers (CRP, ESR, white cell count) — elevated in acute gout, but also in infection and other inflammatory arthritides; not diagnostic on their own
• Kidney function and lipid profile — background work-up, since gout often travels with metabolic disease
• Ultrasound — can show a characteristic “double contour sign” (urate crystals on the cartilage surface) and identify tophi
• Dual-energy CT — specifically images urate deposits; useful in tricky cases, done through rheumatology

What we must not miss — septic arthritis

A hot, swollen, painful joint is septic arthritis until proven otherwise if any of the following apply:

• The patient is febrile or systemically unwell
• The clinical picture is unusual for gout
• There is no history of gout and no classical risk factors
• There has been a recent bacterial infection, immunosuppression, or joint surgery
• The joint is a prosthetic joint

These scenarios typically 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 other medical conditions. Earlier is better — effective treatment within the first 24 hours is markedly more effective 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 for gastric protection if there’s any risk (prior ulcer, age, concurrent steroids, antiplatelet).

NSAIDs are generally avoided in:

• Significant kidney disease (eGFR < 60, and especially < 30)
• Heart failure
• Active peptic ulcer or recent GI bleeding
• Poorly-controlled hypertension
• Concurrent anticoagulant or antiplatelet therapy at higher bleeding risk

Colchicine

Useful when NSAIDs are contraindicated or as an alternative first-line. The modern evidence supports a low-dose regimen — gentler on the gut and equally effective:

• 1.0–1.2 mg at onset 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 resolve or diarrhoea) are now considered obsolete — the GI toxicity was substantial and the efficacy no greater.

Important points:

• Dose-reduce in renal impairment and in older adults
• Interacts with clarithromycin, erythromycin, some antifungals, some statins — check with us before combining
• Stop immediately if severe diarrhoea develops — a signal of toxicity

Corticosteroids

For patients in whom NSAIDs and colchicine are both unsuitable, or for severe polyarticular flares:

• Oral prednisolone 30–40 mg daily for 5 days (tapering not always necessary for such short courses)
• Intra-articular corticosteroid injection — excellent option for a single large joint

Starting urate-lowering therapy during a flare — updated practice

An older teaching was to wait until the flare had fully resolved before starting urate-lowering therapy, on the theory that initiating treatment during a flare would worsen or prolong it. More recent evidence — including a randomised trial by Hill et al. (2015) — has shown this isn’t true. The 2020 ACR gout guideline now supports starting urate-lowering therapy either during the flare or after it settles, alongside appropriate flare treatment and prophylaxis.

This matters practically. Many patients are most motivated to start long-term treatment when they’re in the middle of a painful flare; deferring the conversation to a later visit often means the decision gets lost. We now discuss urate-lowering therapy in that window if it would have been indicated anyway.

If you’re already on urate-lowering treatment and a flare hits, don’t stop it — continuing improves outcomes and avoids mobilisation flares from restarting later.

What we keep focused during the flare

• The lifestyle conversation is worth having now — triggers, alcohol, the bigger plan — while the experience is vivid rather than next month when the pain has faded

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

This is where gout care often goes wrong. A flare gets treated with NSAIDs, the patient feels better, and the conversation about long-term control never happens. Six months later, another flare. The cycle repeats while the underlying crystal load silently grows.

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

• Two or more flares per year
• Any tophi visible on examination or imaging
• Chronic gouty arthropathy (changes on examination or X-ray)
• Chronic kidney disease, stage 3 or worse
• History of uric acid kidney stones
• Very high serum urate (typically >0.54 mmol/L / >9 mg/dL) persistently

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

The target we aim for:

• Serum urate below 0.36 mmol/L (6 mg/dL) for most patients
• Below 0.30 mmol/L (5 mg/dL) if you have visible tophi — a lower target helps existing crystal deposits dissolve faster

ULT is lifelong once started for most patients. Stopping after urate has normalised often leads to flares within months. This is a chronic condition and this is chronic treatment — the same framing as blood pressure or cholesterol medication.

The medications we use

Allopurinol is the first-line agent for most patients:

• Inhibits xanthine oxidase, reducing urate production
• Starting dose 50–100 mg daily, titrated every 2–5 weeks toward target urate, typically to 200–400 mg daily; maximum 900 mg if needed under specialist guidance
• Dose adjustment in significant renal impairment — but the old blanket caps have been relaxed; modern evidence supports up-titration with careful monitoring
• Generally inexpensive and widely available
• Requires HLA-B*5801 genetic testing before initiation in our population — see next section

Febuxostat (Feburic) is an alternative:

• Also a xanthine oxidase inhibitor but structurally different from allopurinol
• Starting dose 40 mg daily, increased to 80 mg if target not met
• Does not require HLA-B*5801 testing
• Useful when allopurinol is contraindicated, poorly tolerated, or not suitable after a positive HLA-B*5801 result
• The CARES trial raised concerns about slightly higher cardiovascular mortality compared with allopurinol in patients with established cardiovascular disease; subsequent trials (FAST) did not replicate this signal, but it is worth a careful discussion in patients with existing coronary disease or heart failure

Uricosurics (probenecid, benzbromarone) — increase urinary urate excretion:

• Useful in patients who under-excrete urate and have normal kidney function and no history of urate stones
• Less commonly used as first-line in our practice
• Benzbromarone not routinely available in Singapore

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

Flare prophylaxis during ULT initiation

Counter-intuitively, starting urate-lowering therapy can trigger flares in the first few months, as deposited crystals mobilise. We routinely prescribe flare prophylaxis for 3–6 months at the start of ULT:

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

This approach substantially reduces the “I started the medication and then got a worse flare” experience that often makes patients stop ULT and give up on it.

Follow-up and monitoring

• Serum urate every 2–4 weeks during titration, then every 3–6 months once target is reached
• Kidney function at baseline, at dose changes, and periodically
• Liver enzymes occasionally
• Symptom review — frequency of flares, tophi shrinking over months to years
• Adherence — the commonest reason for failure, and usually improvable with conversation rather than more medication

HLA-B*5801 testing before starting allopurinol

Allopurinol is usually well-tolerated. Rarely — but seriously — it can cause a severe cutaneous adverse reaction (SCAR): Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis (TEN), or drug reaction with eosinophilia and systemic symptoms (DRESS). These reactions typically occur in the first 2–3 months of treatment, carry meaningful mortality, and can leave lasting damage to skin, eyes, and mucosal surfaces.

The overall risk is low. But it is substantially higher in people who carry the HLA-B*5801 gene variant, and that variant is more common in East and Southeast Asian populations — roughly 9% of Han Chinese, 8% of Thais, and smaller but significant proportions of Korean, Japanese, Malay, and Indian populations. Carrying the variant increases the odds of allopurinol-SCAR by 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. We discuss it before starting allopurinol in any patient who hasn’t been on the medication before, and we recommend testing for most first-time patients — particularly those of higher-risk ancestry. There are, however, a few situations where testing is reasonably skipped after discussion:

• You’ve taken allopurinol before without any hypersensitivity reaction. Successful previous exposure is strong evidence that SCAR is unlikely, and restarting the same medication is usually fine.
• You’re not from a high-risk ethnic background. The risk is not zero in any group, but is considerably lower in European-ancestry and some other populations.
• You’ve heard the risks and prefer to proceed without testing, accepting careful monitoring over the first 2–3 months and agreeing to stop the medication immediately and come in if any warning features develop (see below). This is a valid choice for some patients — particularly where cost of the test is a factor — provided the risks are clearly understood.

If the test is done and is negative: standard allopurinol initiation is appropriate, with the usual slow titration and flare prophylaxis.

If positive: we avoid allopurinol and use an alternative (typically febuxostat).

Warning features that mean stop immediately and seek same-day care:

• 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 of starting allopurinol. Beyond this window the risk of SCAR falls substantially.

Why we still use allopurinol first where safe

Febuxostat is a reasonable alternative, but:

• It is more expensive
• It carries its own considerations (the CARES / FAST discussion above, particularly in patients with existing cardiovascular disease)
• Allopurinol is globally the best-studied urate-lowering drug with decades of experience, remains guideline first-line where safe, and is substantially cheaper on long-term therapy

Used carefully — with or without pre-treatment testing — allopurinol remains the workhorse for most patients who need urate-lowering therapy.

Cost and subsidy of HLA-B*5801 testing

MediSave coverage for genetic tests like HLA-B*5801 can vary and changes over time. We’ll be direct about the current cost and coverage at your visit so you can make an informed decision rather than be surprised later.

If you’ve been on allopurinol for years without problems

The risk window for SCAR is primarily the first 2–3 months. If you’ve tolerated allopurinol well for a year or longer, retrospective testing is not usually necessary — continuation is appropriate.

Common misconceptions that derail long-term control

A few patterns we see regularly, worth addressing directly:

• “I can control gout with diet alone.” Usually wrong. A strict low-purine diet reduces serum urate by perhaps 0.06–0.09 mmol/L (1–1.5 mg/dL) at best — not enough in most patients who need ULT. Diet supports treatment; it doesn’t replace it.
• “Urate-lowering medication is only for severe gout.” The indications are broader than patients often realise. Two flares a year is already enough to make the case.
• “I’ll stop the medication once my urate is normal.” The urate stays low because the medication is working. Stop it and urate rises again, flares return, crystal deposits grow.
• “I got a flare after starting allopurinol, so it doesn’t work for me.” This is almost always a mobilisation flare during crystal dissolution — a good sign, not a failure. Flare prophylaxis at initiation prevents most of these. Don’t stop the ULT.
• “Painkillers are enough.” Painkillers treat the flare but not the underlying crystal load. Chronic tophaceous gout can develop even in patients who “manage the flares well.”
• “If I just stop eating seafood, I’ll be fine.” Seafood is one class of purine source, and its contribution is usually modest compared to the overall pattern. And plant-derived purines (legumes, some vegetables) — which diet sheets of the past used to restrict — are not meaningful contributors to serum urate in current evidence.
• “Colchicine is only for acute flares.” It’s also the workhorse of prophylaxis during ULT initiation.

Comorbidities and medications worth reviewing

Gout rarely travels alone. We review:

• Blood pressure, diabetes, lipids, kidney function, weight — the full CKM cluster
• Diuretics — if you’re on a thiazide (e.g. hydrochlorothiazide, indapamide) or a loop diuretic (furosemide) for hypertension or heart failure, consider whether an alternative is possible. Losartan (an ARB) has a mild uricosuric effect and can be a good substitute for thiazides where appropriate.
• Low-dose aspirin — raises urate, but rarely enough to stop aspirin for. A conversation, not a default change.
• Hydration — aim for 2–3 litres of water per day unless your doctor has asked you to restrict fluids for heart or kidney reasons

When we’d refer to rheumatology

• Diagnostic uncertainty — unusual joint distribution, atypical presentation, or suspected overlap with other inflammatory arthritides
• Chronic tophaceous gout
• Refractory disease — flares continuing despite properly-used ULT, or urate not reaching target on maximum tolerated doses
• Significant kidney disease limiting ULT choices
• HLA-B*5801 positive with additional complexities
• Consideration of pegloticase or other specialist-only therapies
• Suspected septic arthritis — usually 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. It supports treatment but doesn’t replace it. The old restrictive diet sheets covering everything with even a whisper of purine were never evidence-based — much of that list included foods now known to be fine (most vegetables, most legumes, soy). This version reflects current evidence and local food choices.

Foods to minimise or avoid

These contribute the most to serum urate:

Organ meats and offal

• Liver, kidney, heart, tripe, brain, sweetbreads
• Common local dishes: pig’s liver / kidney porridge, fried liver, kambing soup (often contains innards), bak kut teh broth with organ meats, hot-pot innards platters

Meat-based concentrates and stocks

• Beef/pork-bone soup that has simmered for many hours — purines are water-soluble and concentrate in the broth
• Thick meat gravies, Bovril, Oxo, Marmite, Vegemite
• Hot-pot / steamboat broth after extended boiling of meats and bones
• Commercial “essence of chicken” products and similar concentrates
• Lor mee, mee sua, pork rib soup — the broth rather than the noodles is the concern

Specific seafood

• Anchovies (ikan bilis) — including those used as a base ingredient in many local dishes
• Sardines, mackerel, herring
• Roe and fish eggs
• Mussels, scallops

Alcohol

• Beer is the worst (yeast-derived purines plus ethanol)
• Spirits next
• Wine has less effect; moderate intake may be acceptable

Foods to have in moderation

These raise urate modestly at higher intakes but don’t need to be eliminated:

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

Foods that are fine or actively helpful

Modern evidence supports these being OK or beneficial:

• Vegetables — including those on old restrictive lists (spinach, asparagus, cauliflower, mushrooms). Plant purines are not meaningful contributors to serum urate.
• Legumes and pulses — beans, lentils, chickpeas, dhal, tofu, tempeh, soy milk, soya bean curd (tau huay / tau suan) — fine; some evidence of protective effect
• Whole grains — brown rice, oats, barley, wholegrain bread
• Fruits — most fruits are fine, including cherries (possibly modest benefit); limit very-high-fructose options (durian in large quantities, sugared dried fruits)
• Low-fat dairy — milk, yogurt, Greek yogurt — associated with lower gout risk
• Eggs — moderate intake is fine
• Nuts and seeds — fine
• Coffee (regular or decaf) — associated with lower gout risk; tea is neutral
• Water — 2–3 litres per day unless your doctor has asked you to restrict fluids

Singapore-specific practical tips

• Hawker / coffee-shop choices. Lean toward steamed fish (limit oily varieties), cai png (mixed-rice) with vegetables and tofu and a smaller portion of protein, Indian vegetarian thali, Malay fish and vegetables. Reduce organ-meat dishes, bone broths, and kambing soup.
• Bak kut teh. The broth is the issue more than the meat. Having it occasionally is reasonable; weekly is probably not.
• Buffets and steamboat. High-risk settings — organ meats, concentrated broth, beer often combined. A conscious approach (smaller plates, more vegetables, watch the broth consumption) helps.
• Chinese New Year. Rich, purine-heavy, alcohol-heavy. Many patients see their first flare after the festive period. Prophylactic colchicine for a week or two around CNY is reasonable for some patients on ULT who tend to flare in this window — ask at your visit.
• Soups at restaurants and hawkers. Long-simmered bone and meat broths concentrate purines. Clear soups, tomato-based soups, and vegetable-based soups are better options.
• Chinese herbal tonic soups often contain shark’s fin, abalone, or concentrated meat bases — worth asking before ordering.
• Muslim patients — no alcohol (a benefit); watch for mutton/lamb intake, which tends to be high in traditional dishes.
• Hindu / vegetarian patients — generally lower background gout risk; purines from legumes and vegetables are not a meaningful concern. If gout still develops, the drivers are usually genetic / kidney-handling related rather than dietary.
• Indian patients — dhal, sambar, tofu, paneer are all fine; limit mutton biryani portions and heavy ghee-based cooking.

A realistic summary

• Most weight reduction and metabolic improvement comes from overall eating pattern — more vegetables, moderate portions, less alcohol, fewer sugary drinks — rather than from ticking off a long avoid-list
• The biggest single lever for most SG patients is reducing beer and spirits
• The second-biggest is cutting out organ meats and heavy concentrated broths
• Diet supports ULT; ULT does the heavy lifting for urate reduction in the patients who need it

The Singapore context — access and subsidy

• Healthier SG Chronic Tier — patients enrolled with us can access gout-related medications (allopurinol, colchicine, selected NSAIDs, losartan) at prices similar to polyclinic rates
• CHAS — means-tested subsidy at participating GP clinics
• MediSave — usable for chronic disease consultations and selected medications; coverage for HLA-B*5801 testing specifically varies and is worth confirming at the visit
• Specialist referral — we work with local rheumatology teams for the subset of patients who need them

Get in touch

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

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

Email — admin@ktmc.sg

References

Guidelines

• Agency for Care Effectiveness (ACE). Gout: diagnosis and management. 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.

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.

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. v1.0 · April 2026 · Review due April 2028.