Scope of this summary
Adults with suspected or established monosodium-urate crystal arthritis, including acute flare and long-term urate lowering. Septic arthritis, asymptomatic hyperuricemia, tumor lysis, pediatric disease and pregnancy require separate decisions.
sources for this section:ACR Gout
The Bottom Line
- Confirm uncertain gout with synovial-fluid crystal analysis when feasible, especially for a first, atypical or high-risk hot joint; serum urate can be normal during a flare and does not exclude infection.
- Treat a flare early with colchicine, an NSAID or glucocorticoid selected from kidney, gastrointestinal, cardiovascular, infection and interaction risk; use low-dose rather than high-dose colchicine.
- Strongly recommend urate-lowering therapy for tophaceous gout, radiographic damage from gout or frequent flares, and conditionally consider it in the specific first-flare or infrequent-flare situations defined by ACR.
- Use allopurinol as preferred first-line urate-lowering therapy, including chronic kidney disease, start low and titrate using serial serum urate to a target below 6 mg/dL rather than leaving a fixed low dose.
- Provide anti-inflammatory prophylaxis for at least three to six months when initiating urate lowering, extending it when flares continue, and educate that early flares do not mean treatment failure.
sources for this section:ACR Gout
Practical clinical workflow
1
Assess joint distribution, onset, fever, skin break, prior crystals, medicines, alcohol, diet, kidney disease and stones; aspirate and culture when septic arthritis is plausible.
2
Choose immediate anti-inflammatory treatment and provide a future flare plan, accounting for renal function, anticoagulation, interactions and previous response.
3
Review indication for urate lowering and modifiable contributors; test HLA-B*5801 before allopurinol in patients of Southeast Asian or African American ancestry as conditionally recommended.
4
Start low-dose allopurinol or an alternative when appropriate, titrate to serum urate below 6 mg/dL and monitor adherence, flares, renal function and toxicity.
5
Address weight, alcohol, high-fructose intake and comorbid hypertension, cardiovascular and kidney disease without implying lifestyle alone replaces urate-lowering therapy when indicated.
sources for this section:ACR Gout
Safety boundaries and escalation
- A hot joint with fever, bacteremia risk or immunosuppression is septic arthritis until reasonably excluded; crystals and infection can coexist.
- Allopurinol hypersensitivity with rash, fever, mucosal involvement, facial edema or organ injury is an emergency and the drug must not be casually restarted.
- Colchicine toxicity risk rises with kidney or liver impairment and CYP3A4 or P-glycoprotein interactions; verify the current FDA label and dosing.
- NSAIDs and glucocorticoids can worsen bleeding, kidney, heart failure, glucose and infection risk; select flare therapy from the whole patient rather than a default recipe.
sources for this section:ACR Gout
Localization
Use the ACR treat-to-target guideline, US ancestry-specific HLA-B*5801 recommendation and current FDA labels. Insurance coverage affects agent access but should not replace shared clinical decisions.
sources for this section:ACR Gout
Source documents
Use the linked source documents for complete recommendations, evidence grading, exclusions and implementation detail.
- American College of Rheumatology2020 American College of Rheumatology Guideline for the Management of GoutDOI 10.1002/acr.24180 路 published 2020-05-11 路 accessed 2026-08-20view source
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