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🦶 Men's Health

Gout — Long-Term Management

Beyond the acute attack — controlling uric acid for life.

Gout is the most common inflammatory arthritis, caused by the accumulation of uric acid crystals in joints. After the first attack, most people have another within 2 years without treatment. Long-term urate-lowering therapy, diet modification, and trigger avoidance prevent recurrent attacks, joint damage, and kidney stones.

Signs and Symptoms

✓ Acute attacks: sudden, severe pain — often rated 10/10 — redness, warmth, swelling
✓ Most common joint: the big toe (podagra) — also ankle, knee, wrist
✓ Attacks often begin at night or early morning
✓ Skin over the joint becomes tight and shiny during an attack
✓ Hyperuricaemia (high uric acid) between attacks — usually asymptomatic
✓ Tophi — chalky white uric acid deposits under skin around joints (in chronic gout)
✓ Kidney stones — uric acid stones in people with chronic high uric acid
✓ Joint damage and deformity in untreated chronic gout

Risk Factors

When to Seek Help

NowAcute attack with fever and extreme pain — confirm gout versus joint infection (septic arthritis), which requires urgent antibiotic treatment.
SoonFirst or recurrent gout attack — uric acid testing and long-term management plan to prevent recurrence and complications.
RoutineIf on urate-lowering therapy — check uric acid level every 6 months until target achieved; annually thereafter.

Tests & Diagnosis

🧪 Serum Uric Acid (SUA)
Confirms hyperuricaemia — target below 360 µmol/L (6 mg/dL) on treatment; below 300 µmol/L (5 mg/dL) in severe or tophaceous gout. Note: uric acid may be normal during an acute attack.
🧪 Joint Aspiration and Crystal Analysis
The definitive diagnostic test — demonstrates monosodium urate crystals under polarised light microscopy. Distinguishes gout from pseudogout and septic arthritis.
🧪 X-ray of Affected Joints
In established gout — shows punched-out erosions adjacent to tophi. Normal in early disease.
🧪 Kidney Function (eGFR)
Chronic hyperuricaemia and gout can damage kidneys. Baseline and annual monitoring. Affects choice of urate-lowering therapy dose.
🧪 Full Blood Count and Liver Function
Baseline before starting allopurinol — and monitoring on treatment.

Treatment Options

1
Acute Attack — Treat Immediately
Anti-inflammatory medications started within the first 12–24 hours of an attack significantly shorten its duration: colchicine (most specific for gout), NSAIDs (ibuprofen, indomethacin), or oral steroids. Colchicine at a low dose (0.5mg twice daily for 3–5 days) is now preferred.
2
Allopurinol — Long-Term Urate Lowering
The standard urate-lowering medication — reduces uric acid production. Started at a low dose (50–100mg) and increased gradually to achieve target uric acid below 360 µmol/L. Must be taken daily for life. Do not start during an acute attack.
3
Febuxostat — Alternative Urate Lowering
More potent than allopurinol — used when allopurinol is not tolerated or target uric acid is not achieved. Requires monitoring in people with cardiovascular disease.
4
Diet and Lifestyle Modification
Reduce: red meat, organ meats, shellfish, beer, spirits, fructose drinks. Increase: low-fat dairy (reduces uric acid), water (at least 2 litres daily), cherries (modest but real effect). Lose weight. Reduce alcohol.
5
Prophylactic Anti-inflammatory Cover
When starting allopurinol — low-dose colchicine or NSAID for the first 3–6 months prevents the acute attacks that often occur as uric acid levels change. This is important and often omitted.

Frequently Asked Questions

If I take allopurinol, can I eat whatever I want?
Allopurinol significantly reduces uric acid but does not completely negate the effect of diet and alcohol. Continuing to eat large amounts of red meat, shellfish, and drink beer will still trigger attacks even on medication. Diet modification enhances medication effectiveness.
Why should I not start allopurinol during an acute attack?
Starting allopurinol during an attack causes rapid changes in uric acid levels that can prolong or worsen the current attack. Wait 2–4 weeks after the attack has fully resolved, then start at a low dose with prophylactic anti-inflammatory cover.
My uric acid is high but I have never had gout — do I need treatment?
Asymptomatic hyperuricaemia (high uric acid without gout attacks) is not routinely treated. However, lifestyle modification is recommended. Treatment is considered when uric acid is very high (above 540 µmol/L) or in people with significant kidney disease.
Can gout be cured?
Yes — with consistent urate-lowering treatment to below the target uric acid level, tophi dissolve over months to years and attacks become increasingly rare or cease entirely. This requires lifelong medication and regular monitoring.
Is gout a sign of kidney disease?
Gout and kidney disease are closely linked — both cause and consequence of each other. Chronic gout can damage the kidneys (urate nephropathy). Kidney disease reduces uric acid excretion and worsens gout. Annual kidney function monitoring is essential.

Related Pages

Osteoarthritis Knee GuideWhat Is eGFR?Gout Uric Acid Men's Health

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