Uric acid is the end product of purine metabolism in the body. When uric acid levels in the blood (serum urate) rise above their saturation point — generally above 360–420 µmol/L (6–7 mg/dL) — crystals of monosodium urate form in joints and surrounding tissues. This is gout: a painful, episodic and highly treatable form of inflammatory arthritis.
What a raised uric acid result means
Hyperuricaemia (elevated serum urate) is present in roughly 20% of adults — far more than the 4% who have symptomatic gout. Most people with elevated uric acid never develop gout crystals. The decision to treat asymptomatic hyperuricaemia is individual and depends on the degree of elevation and associated risks.
A serum urate above 480 µmol/L (8 mg/dL) is associated with a markedly increased risk of gout attacks and urate kidney stones. Most guidelines recommend urate-lowering therapy after a confirmed gout attack, recurrent attacks, or evidence of tophaceous gout.
Symptoms of a gout attack
- Sudden, severe joint pain — often waking the patient from sleep
- Classically affects the big toe (first metatarsophalangeal joint) — known as podagra — but also the ankle, knee, wrist and elbow
- Intense swelling, warmth and redness around the joint
- Skin over the joint may be shiny and appear almost bruised
- Exquisite tenderness — even the weight of a bedsheet can be intolerable
- Attacks typically peak within 24–36 hours and resolve spontaneously within 7–14 days without treatment
What raises uric acid
| Factor | Why it raises urate |
|---|---|
| Purine-rich foods (red meat, organ meat, shellfish, anchovies) | Purines are metabolised to uric acid |
| Alcohol — especially beer and spirits | Alcohol accelerates purine breakdown; beer contains purines directly |
| Fructose (sugary drinks, fruit juice) | Fructose metabolism generates uric acid as a by-product |
| Dehydration | Reduces renal urate excretion, concentrating serum urate |
| Diuretic medications ('water tablets') | Compete with urate for renal excretion |
| Chronic kidney disease | Reduced urate clearance |
| Rapid weight loss or fasting | Increased nucleic acid breakdown; ketones compete with urate |
Treatment: acute attacks and long-term management
Acute attacks are treated with NSAIDs (ibuprofen, indomethacin), colchicine, or corticosteroids depending on the patient's other conditions. Starting urate-lowering therapy during an active attack can prolong the flare — it is generally begun after the attack has resolved.
Allopurinol is the first-line urate-lowering agent. The target serum urate on treatment is below 360 µmol/L (6 mg/dL) — below the saturation point — to dissolve existing crystals and prevent new ones. Dose is titrated gradually, and regular serum urate monitoring guides adjustment.
Dietary change: what actually helps
Diet can reduce serum urate by 60–90 µmol/L — meaningful but rarely sufficient as a sole treatment for established gout. The most impactful changes are reducing alcohol (especially beer), eliminating sugary drinks, limiting red meat and shellfish, and staying well-hydrated. Plant-based purines (lentils, beans, spinach) appear to have a much smaller effect on urate than animal-based ones.
Coffee (2–4 cups per day) is associated with reduced urate levels and gout risk in observational studies — possibly due to competitive xanthine oxidase inhibition. Cherries and cherry extract have modest supporting evidence for reducing attack frequency.
"Gout is one of the most completely treatable conditions in rheumatology — when it isn't treated, it's usually because patients don't realise treatment is so effective."
Omar Khalil, Health Educator, Looms