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Rheumatology›Condition·Updated Jun 26, 2026·v1

Gout

Gout is a common inflammatory arthritis caused by MSU crystal deposition, diagnosed by synovial fluid analysis. Management centers on treat-to-target urate-lowering therapy with allopurinol, aiming for serum urate <6 mg/dL, alongside acute flare treatment and prophylaxis. Cardiovascular risk is elevated and requires aggressive management.

High Evidence402 references·1,795 words·8 min read·v1
gouthyperuricemiapodagraurate-lowering therapyallopurinolcolchicineNLRP3 inflammasome

Quick Reference

RxDrug of choiceAllopurinol (start 100 mg daily, escalate to target SU <6 mg/dL)
AltAlternativesFebuxostat 40-80 mg daily; probenecid 250-1000 mg BID; benzbromarone 50-200 mg daily; pegloticase 8 mg IV q2 weeks for refractory tophaceous gout
⊘AvoidHigh-dose colchicine (1.2 mg every hour); NSAIDs in eGFR <30 mL/min, active PUD, or severe CVD; colchicine in eGFR <30 or with CYP3A4/P-gp inhibitors
DxTest of choiceSynovial fluid polarized light microscopy for MSU crystals (gold standard); ultrasound (double contour sign) or DECT if aspiration not possible
ScKey score2015 ACR/EULAR classification criteria (≥8 points) for research or when crystals not found
→When to referFailure to reach SU target after 3 months of ULT, multiple drug intolerances, refractory tophi, severe erosive disease, or need for pegloticase
Gout is diagnosed by MSU crystal identification, managed by treat-to-target ULT (allopurinol first, escalate to SU <6 mg/dL), with acute flares treated by NSAIDs/colchicine/corticosteroids and flare prophylaxis for 3-6 months during ULT initiation.
Gout is a chronic crystal deposition disease caused by monosodium urate (MSU) crystals in joints, leading to acute inflammatory flares and potential joint damage. It is the most common inflammatory arthritis in men, with rising global prevalence linked to obesity and metabolic syndrome. Management involves acute flare treatment and long-term urate-lowering therapy to prevent recurrence and complications.

Overview and Recommendations

Background

  • •Gout is a chronic crystal deposition disease characterized by acute inflammatory arthritis triggered by monosodium urate (MSU) crystals in joints and periarticular tissues, arising from supersaturation of extracellular fluid with urate (serum threshold >6.8 mg/dL).
  • •It affects approximately 9.2 million US adults (3.9% prevalence) and is the most common inflammatory arthritis in men over 40, with rising global prevalence paralleling obesity and metabolic syndrome epidemics.
  • •Untreated, gout progresses from episodic self-limited flares to chronic tophaceous arthritis with irreversible bone erosions; excess mortality is driven by cardiovascular disease (HR 1.58 for CVD events).
  • •The central pathophysiology involves the NLRP3 inflammasome: MSU crystals are phagocytosed by macrophages, triggering lysosomal rupture and caspase-1 activation, which cleaves pro-IL-1β into active IL-1β — the master cytokine of the acute flare.
  • •Major risk factors include hyperuricemia (RR 13.6 for SU ≥9 mg/dL vs <6), genetic variants in urate transporters (SLC2A9, ABCG2), obesity (RR 2.3), alcohol intake (RR 2.5), and diuretic use (RR 2.0).

Evaluation

  • •Suspect gout in any patient with acute, self-limited monoarthritis — especially first metatarsophalangeal joint (podagra) — with rapid onset (<12 hours) of severe pain, erythema, and swelling.
  • •Ask about prior similar episodes (recurrent podagra has LR+ 4.3), family history of gout, dietary triggers (purine-rich foods, alcohol, fructose-sweetened beverages), and medications (thiazides, low-dose aspirin, cyclosporine).
  • •Examine the affected joint: shiny, erythematous, warm, exquisitely tender to even light touch (bedsheet pain). Assess for tophi (firm subcutaneous nodules at helix, olecranon bursa, Achilles tendon) and chronic arthropathy (limited ROM, crepitus).
  • •Perform arthrocentesis for synovial fluid analysis — gold standard. Send fluid for polarized light microscopy (negatively birefringent needle-shaped MSU crystals), Gram stain, culture, and cell count (WBC >50,000/μL raises concern for septic arthritis).
  • •If crystals are not found but suspicion remains, use the 2015 ACR/EULAR classification criteria: score ≥8 points from clinical (typical podagra, MTP involvement), laboratory (serum urate ≥8 mg/dL), and imaging domains (ultrasound double contour sign or DECT urate deposition).
  • •Order serum urate measurement — but note it can be normal during an acute flare in up to 40% of patients; recheck at least 2 weeks after flare resolution for baseline.
  • •Check baseline renal function (eGFR), liver enzymes, and CBC before initiating urate-lowering therapy.
  • •Consider HLA-B*5801 genotyping in patients of Han Chinese, Thai, Korean, or African American descent before starting allopurinol (risk of hypersensitivity syndrome; OR ~80).
  • •Perform ultrasound of symptomatic and contralateral first MTP joints: look for double contour sign (hyperechoic band over cartilage), tophus, aggregates, and bone erosion.
  • •If ultrasound is equivocal, consider dual-energy CT (DECT) of feet and knees — sensitivity 87%, specificity 84% — particularly useful for deep tophi and monitoring urate burden.
  • •Exclude septic arthritis in any acute monoarthritis with fever >38.5°C, rigors, or risk factors (immunosuppression, prosthetic joint).

Management

  • •For acute flares, initiate therapy within 24 hours: NSAIDs (indomethacin 50 mg TID or naproxen 500 mg BID for 5-7 days) with PPI if at GI risk; or low-dose colchicine (1.2 mg at first sign, then 0.6 mg one hour later, followed by 0.6 mg BID for a few days); or corticosteroids (prednisone 30-35 mg daily for 5 days; no taper needed).
  • •Avoid high-dose colchicine (e.g., 1.2 mg every hour) due to dose-dependent GI toxicity without added efficacy.
  • •For refractory flares or contraindications to first-line agents, use IL-1 inhibitors: canakinumab 150 mg SC single dose (approved in Europe) or anakinra 100 mg SC daily for 3-5 days (off-label).
  • •For severe polyarticular flares unable to tolerate oral therapy, consider IV methylprednisolone 40-80 mg daily for 3-5 days.
  • •Initiate urate-lowering therapy (ULT) for any patient with ≥2 flares/year, tophi, erosive disease on imaging, or stage ≥3 CKD (eGFR <60 mL/min/1.73 m²). ULT can be started during an acute flare if adequate anti-inflammatory coverage is provided.
  • •First-line ULT is allopurinol: start at 100 mg daily (50 mg if eGFR <30 mL/min/1.73 m²), escalate by 100 mg every 2-4 weeks to target serum urate <6 mg/dL (or <5 mg/dL if tophaceous), up to maximum 800 mg daily.
  • •If allopurinol fails or is not tolerated, alternatives include febuxostat 40-80 mg daily (caution in patients with prior CV disease; CARES trial showed increased CV death, but FAST trial found non-inferiority for MACE), probenecid 250-1000 mg BID (avoid if eGFR <30), or benzbromarone 50-200 mg daily (monitor LFTs for hepatotoxicity).
  • •For patients who fail two oral agents, add a uricosuric (probenecid or benzbromarone) to a xanthine oxidase inhibitor before considering pegloticase.
  • •Pegloticase 8 mg IV every 2 weeks is reserved for severe tophaceous gout refractory to oral ULT; co-administer with methotrexate 15 mg weekly to improve response rates (71% vs 41%) and reduce infusion reactions (13% vs 30%).
  • •During ULT initiation, provide flare prophylaxis for at least 3-6 months: colchicine 0.5-0.6 mg daily (or 1 mg/day if tolerated and eGFR >30), low-dose NSAID (naproxen 250 mg BID with PPI if needed), or prednisone ≤10 mg/day if contraindications to both.
  • •Monitor serum urate every 2-4 weeks during dose escalation, then every 6-12 months once target is achieved. Also monitor renal function, LFTs, and CBC.
  • •Do not use fixed low doses of allopurinol (e.g., 100-300 mg without escalation) — a dose-escalation strategy to target is strongly recommended.
  • •Do not treat asymptomatic hyperuricemia with pharmacologic ULT — no evidence of benefit and risk of adverse effects.
  • •Refer to rheumatology if ULT target is not achieved after 3 months, if there are multiple drug intolerances, if tophi are refractory, or if the patient has severe erosive or tophaceous disease.
  • •Discharge criteria for inpatient gout flares: pain controlled with oral medications, fever resolved (if septic arthritis excluded), and ability to bear weight or perform activities of daily living.

Board Review — High Yield

  • •Podagra — First MTP joint involvement, LR+ 4.3 for gout
  • •Double contour sign — Hyperechoic band over cartilage on ultrasound; sensitivity 83%, specificity 76%
  • •NLRP3 inflammasome — Central to gout pathogenesis; MSU crystals trigger IL-1β release
  • •HLA-B*5801 — Strongly associated with allopurinol hypersensitivity (OR ~80); test in Asian and African American patients
  • •Treat-to-target — SU <6 mg/dL (<5 if tophaceous); GO TEST Overture trial showed superiority over symptom-driven care
  • •Pegloticase + methotrexate — Improves responder rates from 41% to 71%; reduces infusion reactions
  • •Colchicine prophylaxis — First 3-6 months of ULT; low-dose (0.5-0.6 mg daily) reduces flares by ~50%
  • •CARES vs FAST trials — CARES found febuxostat increased CV death (HR 1.34); FAST found non-inferiority for MACE; avoid febuxostat in patients with prior MI/stroke
  • •LOCOL trial — Colchicine 0.5 mg daily non-inferior to placebo for flare prophylaxis? No, but still halved flares
  • •G-CAN remission — No flares in 12 months, no tophi, SU <6 mg/dL

Deep Dive — Evidence Details

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