Overview.
Gout is an inflammatory arthritis caused by monosodium urate crystal deposition in joints and soft tissues. It affects approximately 4% of adults and is the most common inflammatory arthritis, especially in men. Acute flares cause excruciating joint pain, redness, and swelling — classically in the big toe. Long-term, untreated hyperuricaemia leads to recurrent flares, tophi, joint damage, and kidney stones. Urate-lowering therapy targeting serum urate <6.0 mg/dL prevents flares and dissolves crystal deposits.
When serum urate exceeds its solubility threshold (~6.8 mg/dL), monosodium urate crystals precipitate in joints and periarticular tissues. These crystals trigger an intense neutrophilic inflammatory response — the gout flare. Between flares, crystals remain deposited silently (intercritical gout). Over years, crystal burden increases, forming tophi (visible deposits) and causing erosive joint damage.
Prevalence: ~4% of US adults (~9.2 million). Male:female ratio approximately 4:1 (oestrogen is uricosuric). Prevalence increasing due to obesity, metabolic syndrome, and dietary factors. Risk increases steeply with age and serum urate level.
Medical name: Gout (Crystal Arthropathy)
Symptoms.
Early warnings
- Asymptomatic hyperuricaemia (>6.8 mg/dL) on routine blood work
- Single episode of acute joint pain and swelling (especially big toe)
- Recurrent kidney stones (uric acid stones)
- Family history of gout
Classic symptoms
- Acute monoarthritis: sudden severe pain, redness, swelling in one joint (big toe/MTP1 = podagra in 50%)
- Peak pain within 12-24 hours of onset
- Joint so tender that even bedsheet contact is unbearable
- Attacks last 7-14 days and resolve spontaneously
- Can affect ankles, knees, wrists, fingers, elbows
- Tophi: painless, chalky nodules around joints and ears (chronic tophaceous gout)
- Between attacks: completely asymptomatic (intercritical gout)
Progression
Untreated gout progresses through stages: asymptomatic hyperuricaemia → first acute flare → intercritical periods (months to years) → recurrent flares (increasing frequency) → chronic tophaceous gout (permanent joint damage, tophi, chronic pain). With urate-lowering therapy maintaining serum urate <6.0 mg/dL, crystal deposits dissolve over 6-24 months and flare frequency drops to near zero.
Risk factors.
- Male sex (female risk rises post-menopause as oestrogen declines)
- Obesity and metabolic syndrome
- Chronic kidney disease (impaired urate excretion)
- Diuretic use (thiazides, loop diuretics)
- High-purine diet (organ meats, shellfish, red meat)
- Alcohol (especially beer and spirits)
- Fructose and sugar-sweetened beverages
- Genetic predisposition (URAT1 transporter variants)
- Organ transplant (cyclosporine use)
- Low-dose aspirin (inhibits urate excretion)
Lab interpretation.
Key biomarkers
- Serum Uric Acid — >6.8 mg/dL between attacks; paradoxically may be NORMAL during acute flare (inflammation increases excretion). Target <6.0 mg/dL on ULT. (primary)
- CRP — Markedly elevated during acute flare (>50 mg/L common). Returns to baseline between attacks. (secondary)
- Creatinine / eGFR — Must be checked — CKD is both a cause and consequence of hyperuricaemia. Allopurinol dosing depends on renal function. (secondary)
Diagnostic criteria
- Gold standard: monosodium urate crystals identified on joint aspiration (negatively birefringent under polarised light)
- Clinical diagnosis: acute monoarthritis with hyperuricaemia, rapid onset, podagra, redness — supported by ACR/EULAR criteria
- Dual-energy CT (DECT) can detect urate crystal deposits non-invasively — useful when aspiration is not feasible
- Serum urate >6.8 mg/dL supports diagnosis but may be normal during flare (recheck 2-4 weeks after)
- Must exclude septic arthritis in any acute hot, swollen joint — joint aspiration with Gram stain/culture
Recommended panels
When & next steps.
When to test
- Acute monoarthritis (sudden painful, swollen, red joint)
- Recurrent episodes of self-limiting acute arthritis
- Visible tophi (chalky nodules near joints)
- Recurrent kidney stones
- Asymptomatic hyperuricaemia found on routine blood work
- Family history of gout with joint symptoms
If suspected
- Joint aspiration (synovial fluid analysis) if feasible — gold standard
- Serum uric acid (note: may be normal during flare; recheck 2-4 weeks after)
- CRP (supports inflammatory arthritis; helps monitor flare resolution)
- CBC (elevated WBC during flare is common)
- Creatinine/eGFR (renal function affects treatment choice and dosing)
- If aspiration not possible: clinical diagnosis using ACR/EULAR criteria or DECT imaging
If confirmed
- Acute flare: colchicine (within 12 hours of onset), NSAIDs (naproxen, indomethacin), or corticosteroids
- Urate-lowering therapy (ULT): start after second flare, or first flare with tophi/CKD/stones
- Allopurinol: first-line ULT; start low (100mg/day), titrate to target urate <6.0 mg/dL (<5.0 mg/dL with tophi)
- Febuxostat: second-line if allopurinol intolerant (cardiovascular safety monitoring required)
- Colchicine prophylaxis (0.5-0.6mg/day) for first 3-6 months of ULT to prevent initiation flares
- Lifestyle: weight loss, limit alcohol/fructose/purines, hydration
- Monitor urate every 3-6 months until target reached; annually when stable
FAQs.
Why was my uric acid normal during my gout attack?
This is a well-known paradox — during acute inflammation, the kidneys temporarily increase urate excretion, dropping serum levels. Up to 40% of acute gout attacks have 'normal' uric acid. Always recheck 2-4 weeks after the flare resolves for an accurate baseline.
Do I need to take medication for life?
Urate-lowering therapy is generally lifelong. Stopping allows urate to rise and crystals to reform. However, once urate is maintained below 6.0 mg/dL for 2+ years, crystal deposits dissolve and flares become rare. Many patients remain flare-free indefinitely on stable low-dose allopurinol.
Is gout just about diet?
Diet plays a role but is rarely the sole cause. Genetics and renal excretion account for ~90% of urate levels; diet typically affects uric acid by only 1-2 mg/dL. Lifestyle modification (weight loss, alcohol reduction, hydration) complements but rarely replaces urate-lowering therapy for recurrent gout.
Can a hot, swollen joint be something other than gout?
Yes — and this distinction is critical. Septic arthritis (joint infection) presents identically and is a medical emergency. Any acute hot, swollen joint with fever should be aspirated urgently to exclude infection. Never assume gout without ruling out infection, especially in a first presentation.