Gout is the most common inflammatory arthritis in adults — caused by the deposition of monosodium urate (MSU) crystals in joints and periarticular tissues due to chronically elevated serum uric acid (hyperuricaemia). The classic presentation is a sudden, excruciating arthritis of the big toe (podagra), typically waking the patient from sleep with extreme pain, redness, warmth and swelling. Even without treatment, gout flares usually resolve spontaneously in 7-14 days. If untreated and uric acid remains elevated, attacks become more frequent, affect more joints, and eventually cause permanent joint damage and tophi (visible subcutaneous urate deposits).

What causes gout and what worsens it?

Root cause: hyperuricaemia (elevated serum uric acid >360 μmol/L). 90% of hyperuricaemia is due to reduced renal excretion of uric acid; 10% from increased production. Risk factors: Dietary: high-purine foods (red meat, shellfish, organ meat, beer); high-fructose corn syrup; alcohol (especially beer and spirits). Medications: thiazide and loop diuretics (major risk — raise uric acid by reducing renal excretion); low-dose aspirin; ciclosporin (transplant recipients). Medical conditions: chronic kidney disease; obesity; hypertension; heart failure; myeloproliferative disorders. Dehydration acutely precipitates flares.

How is gout diagnosed?

Gold standard: joint aspiration (arthrocentesis) + polarised light microscopy showing negatively birefringent, needle-shaped monosodium urate crystals in the synovial fluid. This is pathognomonic of gout. Clinical diagnosis: appropriate for classic podagra presentation without aspiration — particularly if no access to polarised microscopy. Serum uric acid: importantly, serum UA can be NORMAL or even low during an acute flare (crystals precipitate when UA falls); do NOT rule out gout based on a normal UA during an attack. Measure UA ≥2 weeks after the flare resolves for accurate baseline. Dual-energy CT (DECT): can image urate deposition directly.

How is an acute gout flare treated?

Treat as early as possible — ideally within 24 hours of onset: NSAIDs (naproxen 500mg BD, indomethacin — most rapidly effective if no contraindications; avoid in CKD, PUD, anticoagulation). Colchicine (0.5mg 2-3 times daily × 4-7 days — preferred in CKD, antithrombotic therapy; reduce dose in CKD; interacts with ciclosporin and clarithromycin). Prednisolone (30-35mg once daily × 5 days — if NSAIDs and colchicine contraindicated). Local corticosteroid injection: most effective for monoarthritis. Do NOT start or stop urate-lowering therapy during an acute flare (traditionally; evidence that continuing/starting ULT is acceptable).

When should urate-lowering therapy be started?

ULT is indicated for: recurrent gout (≥2 flares per year); tophaceous gout; gout with chronic kidney disease; gout with uric acid urolithiasis; any gout with joint damage. Start low, titrate slow: allopurinol 100mg/day initially → increase by 100mg monthly → until target serum urate <360 μmol/L (<6 mg/dL) achieved; <300 μmol/L for tophaceous gout. Important: always cover ULT initiation with colchicine 0.5mg once or twice daily (or low-dose NSAID) for 3-6 months — to prevent flares from urate mobilisation. Check HLA-B*5801 before allopurinol in Han Chinese, Thai, Korean patients — carriers have high risk of severe allopurinol hypersensitivity (SJS/TEN).

How does GMJ News cover gout?

GMJ News covers WHO gout burden, the acute podagra flare, MSU crystal diagnosis, allopurinol and ULT targets, colchicine prophylaxis, dietary modification, pegloticase for severe gout, gout as cardiovascular risk factor, and CPPD distinction. Gout — the most common inflammatory arthritis — is directly relevant to PHIG's NCD programme and clinical rheumatology practice in Georgia.

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Q: How does GMJ News cover gout?

GMJ News covers WHO gout burden, the acute podagra flare, MSU crystal diagnosis, allopurinol and ULT targets, colchicine prophylaxis, dietary modification, pegloticase for severe gout, gout as cardiovascular risk factor, and CPPD distinction. Gout — the most common inflammatory arthritis — is directly relevant to PHIG's NCD programme and clinical rheumatology practice in Georgia.

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

Summary Statistics Glossary GMJ news FAQ Documents Organizations Research

Gout — caused by deposition of monosodium urate (MSU) crystals in joints from hyperuricaemia — is the most common inflammatory arthritis in men in high-income countries, affecting approximately 41 million people globally and causing the exquisitely painful, pathognomonic acute flare at the first metatarsophalangeal joint (podagra — “the disease of kings”) that wakes patients from sleep with sudden severe pain, redness and swelling (WHO). Crucially, gout is no longer merely an articular disease: it is independently associated with higher rates of myocardial infarction, stroke and chronic kidney disease — and urate-lowering therapy with allopurinol (first-line, target serum urate <360 μmol/L) combined with dietary modification has been shown to reduce not just flares but also cardiovascular risk.

Key messages

Most common inflammatory arthritis in men — 41M globally

Gout is the most common inflammatory arthritis in men in high-income countries, affecting approximately 41 million people globally. It is driven by hyperuricaemia (elevated serum uric acid) causing monosodium urate crystal deposition in joints (WHO).

Podagra — the pathognomonic acute flare

The classic gout flare: sudden, excruciating pain, redness, warmth and swelling at the first metatarsophalangeal joint (the big toe — podagra), waking the patient from sleep. Onset is abrupt (maximal intensity within hours). Without treatment, even severe flares usually resolve spontaneously in 7-14 days.

Polarised light microscopy — the gold standard diagnosis

Definitive diagnosis: joint aspiration + polarised light microscopy demonstrating negatively birefringent needle-shaped monosodium urate (MSU) crystals. Serum uric acid can be paradoxically NORMAL during an acute flare (crystals precipitate when uric acid falls suddenly). Do not rule out gout based on a normal uric acid during an acute attack.

Allopurinol first-line — target serum urate <360 μmol/L

Urate-lowering therapy (ULT): allopurinol (xanthine oxidase inhibitor) is first-line — start at low dose (100mg/day), titrate to target serum uric acid <360 μmol/L (<6 mg/dL); <300 μmol/L for tophaceous gout. Febuxostat is an alternative for allopurinol-intolerant patients. Starting ULT during an acute flare does not worsen the flare.

Gout is a cardiovascular disease equivalent

Gout is independently associated with 25-60% increased risk of myocardial infarction and stroke, and accelerates chronic kidney disease progression. Addressing gout is now considered part of cardiovascular risk management — not merely a rheumatological issue.

Colchicine prophylaxis for 3-6 months when starting ULT

Starting allopurinol mobilises urate from deposits and can paradoxically precipitate acute flares. Low-dose colchicine (0.5mg once or twice daily) or low-dose NSAID should be prescribed for 3-6 months when initiating or up-titrating ULT, to prevent mobilisation flares.

Key statistics

41M

people with gout globally (WHO estimate)

WHO

most common inflammatory arthritis in men in HICs

WHO/EULAR

<360 μmol/L

target serum uric acid with ULT (<6mg/dL) — EULAR/ACR target

EULAR/ACR

25-60%

higher MI/stroke risk with gout — cardiovascular association

Lancet/Rheumatology

Negative birefringent

needle-shaped MSU crystals on polarised microscopy — gold standard diagnosis

ACR/EULAR

3-6 months

colchicine/NSAID prophylaxis recommended when starting ULT

EULAR/ACR

Gout — joints affected in order of frequency

Source: EULAR/ACR. First MTP (podagra) is classic first attack; ankle, knee follow. Polyarticular gout in established disease.

Glossary of key terms

Hyperuricaemia
WHO/EULARElevated serum uric acid (>360 μmol/L or >6 mg/dL in most guidelines; some use >420 μmol/L or 7 mg/dL). Causes: decreased renal excretion (90% — genetic variants in URAT1, GLUT9 transporters; diuretics; CKD; dehydration); increased production (10% — high-purine diet; alcohol; enzyme defects e.g. Lesch-Nyhan syndrome; myeloproliferative disorders). Most people with hyperuricaemia never develop gout.

Monosodium urate (MSU) crystals
ACR/EULARMonosodium urate crystals form when serum uric acid supersaturates → crystallisation in cooler, lower-pH articular and periarticular tissues. MSU crystals are needle-shaped, negatively birefringent (yellow when parallel to the slow vibration direction of red compensator on polarised light microscopy). Crystals trigger NLRP3 inflammasome activation → IL-1β release → intense acute neutrophilic inflammation.

Tophaceous gout
WHO/RheumatologyChronic gout with visible tophi — subcutaneous deposits of MSU crystals surrounded by granulomatous inflammation, appearing as firm white nodules over bony prominences (olecranon, Achilles tendon, ears, fingers). Tophi cause chronic joint damage, joint erosions and deformity. Aggressive ULT (target uric acid <300 μmol/L) dissolves tophi over months to years.

Pegloticase (Krystexxa)
FDA/EMAPegylated recombinant uricase — converts uric acid to highly soluble allantoin. Dramatically lowers serum uric acid (sometimes to near-zero). IV infusion every 2 weeks. Reserved for severe refractory tophaceous gout unresponsive to allopurinol/febuxostat. Limitations: immunogenicity (anti-drug antibodies develop in approximately 40% → loss of efficacy); infusion reactions; very expensive. Co-prescribing methotrexate or azathioprine to reduce immunogenicity improves outcomes.

Diet and lifestyle
EULAR/WHOHigh-purine foods to reduce: red meat (beef, pork, lamb), organ meat (liver, kidney), shellfish, anchovies, sardines. High-fructose corn syrup — a major modern gout driver via hepatic uric acid production. Alcohol — particularly beer (high-purine) and spirits. Beneficial: adequate hydration; dairy products (milk proteins promote uric acid excretion — uricosuric); vitamin C (modest uricosuric effect); cherries/cherry juice (anti-inflammatory effect, modest uric acid reduction). Weight loss reduces serum uric acid.

CPPD (calcium pyrophosphate deposition)
EULAR/RheumatologyA distinct crystal arthropathy — calcium pyrophosphate dihydrate (CPPD) crystals — not to be confused with gout (MSU). Also called pseudogout. CPPD crystals are rhomboid-shaped, positively birefringent (blue parallel to slow vibration direction). Classically affects the knee (chondrocalcinosis on X-ray). Associated with hyperparathyroidism, haemochromatosis, hypomagnesaemia. Treatment: NSAIDs, colchicine; no urate-lowering therapy.

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