What is gout?
Gout is a form of inflammatory arthritis caused by hyperuricaemia — abnormally high uric acid levels in the blood. When uric acid exceeds its solubility limit (around 6.8 mg/dL), it crystallises into monosodium urate crystals that deposit in joints, tendons and surrounding tissues. An acute gout attack occurs when the immune system reacts to these crystals, causing intense inflammation. The classic presentation is sudden, severe pain in the big toe joint (first metatarsophalangeal joint), often waking the patient at night, with redness, swelling and warmth.
Uric acid blood test
| Group | Uric Acid Level | Interpretation |
|---|---|---|
| Men | <7.2 mg/dL | Normal |
| Women | <6.0 mg/dL | Normal |
| Gout risk threshold | ≥6.8 mg/dL | Saturation point — crystals can form |
| Hyperuricaemia | Men >7.2; Women >6.0 | Elevated — gout risk |
Important: uric acid levels may be NORMAL or even LOW during an acute gout attack, because the inflammatory response causes uric acid to redistribute. A normal uric acid during an attack does not rule out gout. Recheck 2–4 weeks after the attack resolves.
Joints commonly affected by gout
| Joint | Frequency | Notes |
|---|---|---|
| Big toe (podagra) | ~70% of first attacks | Classic presentation |
| Ankle | Common | Often second attack site |
| Knee | Common | Large joint attacks can mimic septic arthritis |
| Wrist / fingers | Less common | More common in chronic gout |
| Elbow | Less common | Tophi (crystal deposits) visible here |
What causes high uric acid?
Overproduction of uric acid
Purine-rich diet (red meat, organ meats, seafood, beer), alcohol excess (alcohol both increases uric acid production and reduces renal excretion), rapid cell turnover (haematological malignancies, tumour lysis syndrome after chemotherapy), and rare enzyme deficiencies.
Underexcretion of uric acid
Accounts for 90% of gout cases. Causes: kidney disease (reduced excretion), dehydration, diuretics (especially thiazides and loop diuretics), low-dose aspirin, cyclosporine, hypertension, metabolic syndrome and hypothyroidism.
Diet changes to lower uric acid
- Limit red meat, organ meats (liver, kidney) and shellfish (highest purine content)
- Avoid beer and spirits; moderate wine consumption
- Drink at least 2 litres of water daily (dilutes uric acid)
- Increase low-fat dairy (milk, yoghurt) — shown to lower uric acid
- Eat cherries or tart cherry juice — evidence supports modest uric acid reduction
- Avoid high-fructose corn syrup (soft drinks, fruit juices)
- Maintain a healthy weight — obesity doubles gout risk
Medications for gout
| Medication | Use | Notes |
|---|---|---|
| NSAIDs (ibuprofen, indomethacin) | Acute attack treatment | First-line for acute attacks |
| Colchicine | Acute attack + prevention | Very effective when started early |
| Corticosteroids | Acute attack if NSAIDs/colchicine contraindicated | Used when kidney disease prevents NSAIDs |
| Allopurinol | Long-term uric acid lowering | Started 2–4 weeks after acute attack resolves; target uric acid <6.0 mg/dL |
| Febuxostat | Uric acid lowering (alternative to allopurinol) | Used if allopurinol not tolerated |
Questions to ask your doctor
- Should I start uric acid-lowering therapy (allopurinol)?
- What uric acid target should I aim for?
- Which foods are highest in purines that I should avoid?
- Is my diuretic worsening my gout?
- Do I need a joint aspiration to confirm gout and rule out infection?