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Health condition · Clinically reviewed

Gout, crystal attacks, urate control and life beyond the big toe.

The commonest inflammatory arthritis in the UK, and one of the most treatable. Treat the attack, then lower the urate and keep it low.

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Why trust this guide

  • 01

    Clinically reviewed

    Written by our editorial team and reviewed by a registered UK clinician before publication.

  • 02

    Sourced from guidance

    Checked against NICE NG219, BSR and EULAR standards you can see at the end.

  • 03

    Current for 2026

    Reflects modern UK practice including early urate-lowering therapy after a first attack.

Key facts

Gout at a glance.

The essentials, in plain English, what it is, how it presents and how UK rheumatology treats it today.

  • What it is

    The most common inflammatory arthritis, driven by monosodium urate (MSU) crystal deposition and a brisk inflammatory response.

  • How common

    Affects up to 3% of UK adults, more often men. Prevalence is rising with obesity, alcohol and metabolic disease.

  • Classic attack

    Podagra, a red, hot, exquisitely painful first metatarsophalangeal (1st MTP) joint, often waking you at night.

  • Gold-standard test

    Joint aspiration and polarised light microscopy showing negatively birefringent needle-shaped urate crystals.

  • Acute treatment

    NSAIDs, colchicine 500 mcg two to three times daily, or corticosteroids, started at the first sign of an attack.

  • Long-term fix

    Urate-lowering therapy (usually allopurinol) titrated to serum urate below 360 micromol/L, with colchicine cover.

Why this guide matters

Two problems, one plan.

Gout is really two problems. There is the attack in front of you, and there is the crystal load underneath. Treating one without the other is why gout comes back.

  • Treat the attack quickly

    The sooner you start NSAIDs, colchicine or a steroid, the shorter the flare. Waiting to see if it settles is usually a mistake.

  • Lower urate to a real target

    Below 360 micromol/L, or below 300 in tophaceous disease. Anything higher is treatment in name only.

  • Stay on treatment between flares

    Attacks stop long before crystals dissolve. Stopping urate-lowering therapy when you feel well is the commonest cause of relapse.

How the diagnosis is made

From first flare to a settled plan.

The steps a UK GP or rheumatologist normally follows, in order, so you know what to expect and why.

  1. 01

    Assessing

    History and risk factors

    Alcohol pattern (beer more than spirits), fructose intake, red meat and seafood, diuretics, low-dose aspirin, ciclosporin or tacrolimus, family history and ethnicity.

  2. 02

    Assessing

    Joint examination

    Look for classic podagra, midfoot, ankle, knee, wrist, hand or olecranon involvement, plus tophi on the ear helix, olecranon or digits.

  3. 03

    Assessing

    Comorbidity check

    Hypertension, dyslipidaemia, type 2 diabetes, chronic kidney disease and cardiovascular risk all cluster with gout and steer treatment.

  4. 04

    Confirming

    Serum urate

    A level above 360 micromol/L supports the diagnosis, but can be normal during an acute flare. Repeat 4 to 6 weeks after the attack settles.

  5. 05

    Confirming

    Joint aspiration

    Polarised light microscopy of synovial fluid is the gold standard, showing negatively birefringent needle-shaped urate crystals. See our joint aspiration guide.

  6. 06

    Confirming

    Blood and imaging work-up

    FBC, U&Es, CRP, HbA1c, lipids and LFTs. X-ray for erosions and late tophaceous change, ultrasound for the double contour sign, dual-energy CT in selected specialist cases.

  7. 07

    Referring

    Rheumatology referral

    Diagnostic doubt, refractory attacks, tophaceous disease, chronic kidney disease or planned pegloticase all warrant specialist input.

Typical timeline: first attack to a settled plan in a few weeks, once urate is at target.

Symptoms

What gout actually looks like.

The classic acute flare, the quiet intercritical phase and the chronic tophaceous end of the spectrum, plus the features that mean it is time to escalate.

  • Podagra

    A hot, red, swollen and exquisitely tender first MTP joint is the textbook picture, often waking you from sleep.

  • Rapid-onset monoarthritis

    One joint, going from fine to unbearable inside a few hours, is very suggestive of a crystal attack.

  • Midfoot, ankle and knee flares

    Beyond the big toe, gout commonly hits the midfoot, ankle and knee, and can mimic septic arthritis.

  • Wrist, hand and elbow attacks

    Wrist, small hand joints and olecranon bursitis are all typical, particularly in longstanding disease.

  • Tophi

    Firm, chalky lumps on the ear helix, olecranon, fingers or Achilles tendon signal chronic tophaceous gout and joint damage.

  • Intercritical phase

    Between attacks most people feel entirely well, which can lull them into stopping treatment. Crystals are still there.

  • Kidney involvement

    Urate nephropathy and uric acid kidney stones are the quieter consequences of persistent hyperuricaemia.

  • Red flag, hot joint with fever

    Any hot swollen joint with fever needs urgent assessment to exclude septic arthritis, which can coexist with gout.

Treatment

How gout is treated in the UK.

Stop the attack, then quietly dissolve the crystals. NICE NG219, BSR and EULAR now favour offering urate-lowering therapy after a first attack in most people.

  • NSAIDs

    Ibuprofen or naproxen at full anti-inflammatory dose for a short course, with gastric and renal caution as usual.

  • Colchicine

    500 mcg two to three times daily, capped at 6 mg per course. Reduce in renal impairment and beware statin and macrolide interactions.

  • Corticosteroids

    Oral prednisolone, intramuscular or intra-articular steroid when NSAIDs and colchicine are unsuitable or when several joints are involved.

  • IL-1 inhibitors

    Canakinumab or anakinra for refractory or contraindicated cases, on a specialist commissioned pathway.

  • Allopurinol

    First-line urate-lowering therapy. Start at 100 mg, titrate to target, and screen HLA-B*5801 in East Asian patients to reduce SJS/TEN risk.

  • Febuxostat

    Xanthine oxidase inhibitor alternative to allopurinol, with cardiovascular caution informed by the FAST and CARES trials.

  • Uricosurics

    Probenecid, benzbromarone or lesinurad in selected under-excretors, usually specialist-initiated.

  • Pegloticase

    Pegylated recombinant uricase for severe refractory tophaceous gout, specialist commissioned. See our pegloticase clinic guide.

What this guide is based on

The sources behind every claim on this page.

UK national guidance and specialist society standards, current at the time of last review.

Key references

Guidelines and standards we relied on.

A quiet reminder

This guide is for information, not medical advice.

Your GP or rheumatologist knows your joints, kidneys and other medicines, and can tell you which parts apply to you. If in doubt, get seen.

  • NICE. Gout: diagnosis and management (NG219).

  • British Society for Rheumatology (BSR). Guideline for the management of gout.

  • EULAR. Recommendations for the management of gout.

  • MHRA. Allopurinol and HLA-B*5801 screening guidance.

Red flags

When gout needs urgent attention.

Most gout is manageable in primary care. These are the situations that are not, and where a specialist opinion is needed.

  • Hot swollen joint with fever

    Assume septic arthritis until proven otherwise. Same-day assessment, joint aspiration and blood cultures.

  • Rapidly destructive arthritis

    Erosive change on X-ray, deformity or loss of function needs prompt rheumatology and urate-lowering therapy.

  • Tophi

    Any tophus on ear, olecranon, fingers or Achilles signals crystal burden that will keep damaging joints without ULT.

  • Kidney stones or falling eGFR

    Recurrent urate stones or worsening renal function need joined-up urology, nephrology and rheumatology input.

  • Recurrent flares on treatment

    Attacks despite ULT usually mean urate is not yet at target. Recheck level and titrate, do not stop.

  • Suspected allopurinol reaction

    Rash, fever, eosinophilia or mucosal involvement can herald DRESS or SJS/TEN. Stop the drug and seek urgent review.

  • Cardiovascular clustering

    Gout sits alongside hypertension, dyslipidaemia and diabetes. Missing that context misses most of the risk.

  • Pregnancy or planned conception

    Colchicine and steroids are usually acceptable, but many ULT and NSAID choices are not. Plan ahead.

  • Diagnostic doubt

    Atypical joints, seronegative arthropathy or an unwell patient deserves aspiration and specialist review rather than empirical treatment.

Living with it

A treatable condition, with a clear ladder.

Four things that make the biggest difference day to day, gentle weight loss, sensible drinks, a fresh look at the drugs that raise urate, and staying on urate-lowering therapy.

A quiet reminder

Consistency beats intensity, every time.

Small, steady habits, kept up for months, do more than a heroic week that does not last.

  1. 01 Weight

    Gentle, sustained weight loss

    Even modest weight loss lowers urate and flare frequency. Crash diets can paradoxically trigger attacks, so keep it steady.

  2. 02 Drinks

    Rethink alcohol and fructose

    Beer is the biggest driver, spirits less so and wine in moderation is usually fine. Cut fructose-sweetened soft drinks.

  3. 03 Medicines

    Review the drugs that lift urate

    Thiazide and loop diuretics, low-dose aspirin, ciclosporin and tacrolimus all push urate up. Losartan modestly lowers it.

  4. 04 Stay on ULT

    Do not stop between attacks

    Urate-lowering therapy only works if you keep taking it. Stopping when you feel well is the commonest reason gout returns.

Frequently asked

Everything we get asked about gout.

Quick answers on attacks, allopurinol targets, diet and staying on treatment.

  • What is gout?

    Gout is an inflammatory arthritis caused by monosodium urate crystals depositing in and around joints. It usually presents as sudden, severe attacks of a hot, red, swollen joint, most classically the base of the big toe.

  • How is gout diagnosed?

    The gold standard is joint aspiration with polarised light microscopy showing negatively birefringent needle-shaped urate crystals. Serum urate above 360 micromol/L supports the diagnosis but can be normal in an acute attack, so it is usually rechecked 4 to 6 weeks later. Ultrasound and dual-energy CT can help in specialist settings.

  • What triggers a gout attack?

    Common triggers include alcohol (particularly beer), fructose-sweetened drinks, red meat and seafood, dehydration, starting or stopping urate-lowering therapy, diuretics and other medicines, surgery and acute illness. Underlying hyperuricaemia is the real driver.

  • How is an acute attack treated?

    Rest, ice and prompt anti-inflammatory treatment at the first twinge. Options are NSAIDs, colchicine 500 mcg two to three times daily (capped at 6 mg per course) or a corticosteroid by mouth, injection or into the joint. Choice depends on kidney function, other medicines and comorbidities.

  • Do I need lifelong urate-lowering treatment?

    Current NICE and BSR guidance offer urate-lowering therapy after even a single attack, particularly with tophi, renal disease, recurrent flares or a high starting urate. Allopurinol is first-line, titrated to a target below 360 micromol/L (below 300 in tophaceous disease). Colchicine cover for 3 to 6 months at the start reduces flares.

  • Can diet alone control gout?

    Diet and lifestyle help, but rarely fix the problem on their own once you have had attacks or tophi. They lower urate by a small amount, whereas allopurinol reliably brings urate below target. Think of diet as an important partner to medication, not a replacement.

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