Gout is the most common form of inflammatory arthritis in the UK, affecting approximately 1–2% of adults, with prevalence increasing significantly with age. It is also one of the most treatable joint conditions — with effective acute management and long-term urate-lowering therapy, attacks can be prevented almost entirely. The dramatic, exquisitely painful nature of an acute gout attack makes it one of the most distinctive conditions in medicine.
The Biology of Gout
Gout is caused by hyperuricaemia — chronically elevated serum uric acid (above approximately 360 μmol/L) — leading to the deposition of monosodium urate (MSU) crystals in joints and surrounding tissues. Uric acid is the final breakdown product of purines (components of DNA and RNA, found in high concentrations in certain foods). Most uric acid is excreted by the kidneys; gout develops when production exceeds excretion. The classic acute gout attack occurs when crystals are shed into the joint space, triggering an intense inflammatory response — the NLRP3 inflammasome is activated, producing a massive IL-1β-driven inflammatory cascade that produces the exquisite pain, warmth, redness, and swelling characteristic of an acute attack.
Classic Presentation
First MTP joint (base of the big toe) is affected in approximately 50% of first attacks — known as podagra. Other common sites: ankles, knees, wrists, fingers. The attack typically: develops rapidly (reaching maximum intensity within 6–12 hours), is often nocturnal in onset, produces pain rated as among the most severe experienced, and resolves completely over 5–14 days without treatment. Without treatment of hyperuricaemia, attacks recur with increasing frequency and severity, joints become chronically inflamed, and tophi (urate crystal deposits) accumulate.
Acute Attack Management
The three options for acute gout are NSAIDs, colchicine, and corticosteroids — all prescribed by a GP. OTC NSAIDs (ibuprofen at maximum OTC doses) can provide meaningful relief for mild-moderate attacks if taken immediately at onset. Rest, elevation, and ice application also help. Starting allopurinol during an acute attack can prolong the attack — it should be started only once the attack has fully resolved.
Dietary Management
High-purine foods to limit: organ meats (liver, kidneys, sweetbreads) — highest impact; oily fish (anchovies, herrings, sardines, mackerel) in large quantities; shellfish (particularly mussels, scallops). Moderate-purine foods: red meat, poultry, most other fish — moderate restriction for those with frequent attacks. Alcohol: beer and spirits significantly raise uric acid through both purine content and reduced renal uric acid excretion. Wine has less effect but should still be moderated. Sugar-sweetened drinks and fructose: fructose increases uric acid production via purine metabolism — sugary drinks and fruit juice are significantly associated with gout risk. Protective foods: low-fat dairy (particularly skimmed milk and low-fat yoghurt) reduces uric acid levels through orotic acid and casein mechanisms — genuinely and substantially protective. Coffee (both regular and decaf) also reduces uric acid. Cherries and cherry extract have evidence for reducing attack frequency and acute inflammation.
Frequently Asked Questions About Gout
Should I take allopurinol long-term?
Yes — if you have recurrent gout attacks (2+ per year), tophi, chronic gouty arthropathy, or uric acid kidney stones. Allopurinol (or febuxostat if allopurinol is not tolerated) reduces serum urate to below the crystallisation threshold, preventing further attacks and dissolving existing tophi over time. The target serum urate is below 360 μmol/L (ideally below 300 μmol/L for those with tophi). The medication is taken daily, indefinitely, and is very effective. Many people stop it incorrectly after a period without attacks, then experience recurrence.
Can diet alone control gout?
Dietary modification alone typically reduces serum urate by approximately 60–90 μmol/L — meaningful but often insufficient to bring urate below the crystallisation threshold in established gout. Dietary changes are most effective as adjuncts to urate-lowering medication, and are more effective at preventing attacks in those with borderline hyperuricaemia than in those with significantly elevated levels.
Why do gout attacks often occur at night?
Several mechanisms contribute: body temperature drops during sleep, reducing uric acid solubility (the same amount of uric acid forms crystals more easily at lower temperature); joint fluid is reabsorbed during recumbency, increasing local uric acid concentration; and respiratory rate and depth decrease, producing mild hypercapnia and reduced pH, both of which reduce uric acid solubility.
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