Health condition · Clinically reviewed
Gout, acute flares, urate-lowering therapy — and the diet myths.
An inflammatory arthritis from monosodium urate crystals. Modern management treats the flare AND lowers uric acid to prevent recurrence — with much less dietary blame than the internet suggests.
Why trust this guide
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Clinically reviewed
Written by our editorial team and reviewed by a registered UK clinician before publication.
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Sourced from guidance
Every claim is checked against NICE, BSR or peer-reviewed sources you can see at the end.
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Current for 2026
Reflects current UK guidance on flare management and urate-lowering therapy.
Key facts
Gout at a glance.
The essentials, in plain English — what gout is, how it is diagnosed, and how it is treated in the UK today.
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Definition
A crystal arthropathy caused by monosodium urate crystals depositing in and around joints.
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Who gets it
Peak incidence in men over 40; also in postmenopausal women, often on diuretics.
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Classic pattern
Podagra — sudden, exquisitely painful swelling of the first metatarsophalangeal joint — is classic but not universal.
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Diagnosis
Joint aspiration with polarised-light microscopy showing negatively birefringent crystals is the gold standard.
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Long-term care
Urate-lowering therapy — allopurinol first-line — is the cornerstone of preventing recurrence and tophi.
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Triggers that matter
Alcohol (especially beer) and sugary drinks matter more than the traditional dietary blame list.
Why this guide matters
Treat the flare — and lower the urate.
Managing the acute attack is only half the job. Long-term urate-lowering therapy is what stops recurrence and joint damage.
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A flare is not the whole picture
Gout is a chronic disease of urate metabolism — the flare is the visible tip.
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Urate-lowering therapy works
Allopurinol, titrated to a serum-urate target, prevents flares and dissolves tophi.
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The diet story is overplayed
Alcohol and sugary drinks matter far more than most food purines — the guilt is largely misplaced.
How the diagnosis is made
From first flare to a clear plan.
The steps a UK GP will normally follow, in order — so you know what to expect and why.
Phase 1 · Recognising
History, urate and aspiration
Phase 2 · Confirming
Imaging, exclusion and referral
Phase 3 · Managing
Comorbidities and long-term care
- 01
Recognising
Symptom and risk history
Sudden severe joint pain, previous flares, alcohol, diuretics, renal function and cardiovascular risk.
- 02
Recognising
Serum urate
Helpful, but may be normal during an acute flare — a normal urate does not exclude gout.
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Recognising
Joint aspiration + polarised microscopy
The gold standard — needle-shaped, negatively birefringent monosodium urate crystals confirm the diagnosis.
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Confirming
X-ray if chronic
Punched-out erosions and tophi help with long-standing or destructive disease.
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Confirming
Rule out septic arthritis
A hot swollen joint with fever must be aspirated urgently — septic joint is an emergency.
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Confirming
Rheumatology referral
For tophaceous, polyarticular or refractory gout, or intolerance to first-line urate-lowering therapy.
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Managing
Comorbidity check
Blood pressure, lipids, HbA1c and U&E — gout is a cardiometabolic marker, not just a joint problem.
Typical timeline: 1–4 weeks from first flare to a settled plan.
Symptoms
What a gout flare actually looks like.
Sudden onset, exquisite pain, and warmth or redness over the joint — but the pattern of joints involved matters too.
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First MTP acute flare (podagra)
Sudden, exquisite pain and swelling of the big-toe base — the textbook presentation.
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Knee flare
A hot, swollen, tender knee — often the second-most-common joint after podagra.
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Ankle flare
Rapid-onset swelling and warmth around the ankle, often waking you at night.
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Midfoot flare
The tarsal joints can be involved, mimicking a sprain or cellulitis.
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Tophi (chronic)
Firm, chalky lumps of urate around joints, ears or fingers — a sign of long-standing high urate.
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Polyarticular gout
Several joints inflamed at once — more common in long-standing or untreated disease.
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Recurrent flares
Two or more flares per year is a clear trigger to start urate-lowering therapy.
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Hot swollen joint + fever
Call 999 or seek same-day review — septic arthritis must be excluded before assuming gout.
Treatment
How gout is treated in the UK.
Two parallel jobs — settling the current flare, and lowering serum urate so the next one never arrives.
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NSAID for flare
Naproxen or ibuprofen at full anti-inflammatory dose, with a gastric protector — the usual first-line for an acute flare.
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Colchicine (low-dose) for flare
Effective when started early; low-dose regimens reduce diarrhoea and toxicity compared with older schedules.
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Short-course prednisolone
A useful alternative when NSAIDs and colchicine are unsuitable — for example in renal impairment.
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Urate-lowering therapy (allopurinol)
Start low, go slow — titrate to a serum urate target below 300 or 360 µmol/L depending on severity.
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Febuxostat
Second-line when allopurinol is not tolerated or effective; cardiovascular history is considered before prescribing.
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Long-term ULT with prophylaxis
Low-dose colchicine or NSAID for the first months of urate-lowering therapy to prevent early flares.
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Dietary and alcohol advice
Focus on beer, spirits and sugary drinks; whole-food purines have far less impact than traditional advice suggests.
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Address comorbid HTN, obesity, diabetes
Treating cardiovascular risk factors and reviewing diuretics matters as much as the joint itself.
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 rheumatology team knows your history and can tell you which parts apply to you. If in doubt, get seen.
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NICE. Gout: diagnosis and management (NG219).
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British Society for Rheumatology. Management of gout — guideline.
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EULAR. Recommendations for the management of gout.
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UK Gout Society. Patient information resources.
Red flags
When a gout flare needs urgent care.
Most flares can be treated at home with an agreed plan. These are the scenarios where waiting is the wrong call.
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Septic joint (hot, fever)
A hot, swollen joint with fever must be aspirated urgently — call 111 or attend A&E.
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Tophaceous ulceration
A discharging tophus can become infected — same-week clinical review.
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Rapid renal function decline
Urate handling and NSAID use both affect the kidneys — check U&E promptly.
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Cardiovascular event
Gout is a cardiometabolic marker — new chest pain or breathlessness needs urgent assessment.
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Acute kidney injury on NSAID
Stop the NSAID and contact your GP — bloods and hydration review needed.
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Colchicine toxicity
Severe diarrhoea, cytopenia or muscle weakness on colchicine — stop and seek same-day advice.
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Post-transplant gout
Complex to manage on immunosuppressants — specialist input needed.
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Allopurinol hypersensitivity
Rash with fever after starting allopurinol — stop the drug and seek urgent review.
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Post-op flare
Flares are common after surgery — a plan should be in place before elective procedures.
Living with it
A long-term condition, but a very controllable one.
Four things that make the biggest difference day to day — movement, a flare plan, drinks and reviews.
A quiet reminder
Urate targets beat willpower.
A steady serum urate below target does more to prevent flares than any diet ever will.
- 01 Movement
Keep moving between flares
Regular low-impact activity supports joints and cardiometabolic health.
- 02 Flares
Have a rescue plan
Agree an NSAID or colchicine plan with your GP so you can start treatment within hours of a flare.
- 03 Drinks
Rethink beer and sugary drinks
These have the strongest link to flares — food purines matter far less than the internet suggests.
- 04 Reviews
Recheck your urate
On urate-lowering therapy, aim for a target level and review annually once stable.
Frequently asked
Everything we get asked about gout.
Quick answers on diagnosis, allopurinol, diet and when to seek help.
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What causes gout?
Gout is caused by monosodium urate crystals forming in joints when blood urate is persistently high. Genetics, kidney function, alcohol (especially beer), diuretics and cardiometabolic disease all contribute.
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How is gout diagnosed?
The gold standard is joint aspiration with polarised-light microscopy showing needle-shaped, negatively birefringent crystals. Serum urate helps but can be normal during a flare.
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Is allopurinol safe long term?
Yes — for most people. Allopurinol is started at a low dose and titrated to a serum-urate target, with monitoring for rash and blood or kidney changes.
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Do I really need to give up red meat?
Not necessarily. Alcohol (especially beer) and sugary drinks matter far more than the traditional purine-heavy food list. Modest, sensible changes beat restrictive diets.
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Can gout cause permanent joint damage?
Yes — untreated recurrent gout can lead to erosions and tophi. That is why urate-lowering therapy is so important for anyone with frequent flares or tophi.
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When should I start urate-lowering therapy?
Consider it after two or more flares in a year, after a first flare in people with tophi, chronic kidney disease or very high urate, and generally once the acute flare has settled.