What is the appropriate management for a 48-year-old male with knee joint pain and hyperuricemia (elevated uric acid level)?

Management of 48-Year-Old Male with Knee Pain and Hyperuricemia

Immediate Diagnostic Confirmation Required

Before initiating any treatment, you must confirm the diagnosis of gout by joint aspiration and identification of monosodium urate crystals under polarized light microscopy. 1

• The uric acid level of 8.4 mg/dL indicates hyperuricemia (above the saturation point of 6.8 mg/dL), but this alone does not confirm gout, as many patients with elevated uric acid never develop gout 1, 2
• Serum uric acid can paradoxically be normal or even low during an acute gout attack due to its behavior as a negative acute phase reactant 1
• Joint aspiration with crystal identification remains the gold standard for definitive diagnosis 1
• If joint aspiration is not feasible, ultrasound or dual-energy CT can detect urate crystal deposition, though the "double contour sign" alone is insufficient to mandate treatment 1

If This is an Acute Gout Attack (Confirmed or Highly Suspected)

Treat the acute inflammation immediately with NSAIDs, corticosteroids, or low-dose colchicine (0.5 mg three times daily) as first-line options. 1, 3

• NSAIDs are the most convenient and well-accepted first-line option in the absence of contraindications 1
• Low-dose colchicine (0.5 mg three times daily) is equally effective as high-dose regimens but causes significantly fewer gastrointestinal side effects 1, 3
• Intra-articular corticosteroid injection is effective and safe if a single joint is involved 1
• Do not initiate urate-lowering therapy during an acute attack if the patient is not already on it 3

Decision on Urate-Lowering Therapy

If This is the First Episode Only:

Do not initiate urate-lowering therapy after a single gout attack unless specific high-risk features are present. 1

• The 2020 ACR guidelines conditionally recommend against starting urate-lowering therapy for asymptomatic hyperuricemia or after a single flare 1
• Exceptions where you should initiate therapy after the first attack: chronic kidney disease stage ≥3, serum uric acid >9 mg/dL, or history of urolithiasis 1
• With uric acid of 8.4 mg/dL and no mention of these risk factors, wait for a second attack before starting urate-lowering therapy 1

If This is a Recurrent Attack or Patient Has Risk Factors:

Initiate allopurinol starting at 100 mg daily, with gradual upward titration every 2-5 weeks to achieve serum uric acid <6 mg/dL. 1, 4, 5

• Allopurinol is the preferred first-line urate-lowering agent due to efficacy, safety, tolerability, and cost 1, 4
• Start at 100 mg daily and increase by 100 mg increments every 2-4 weeks until serum uric acid is below 6 mg/dL 1, 4, 5
• The therapeutic goal is to maintain serum uric acid below 6 mg/dL (360 μmol/L) to promote crystal dissolution and prevent new crystal formation 1, 6
• Maximum FDA-approved dose is 800 mg daily, and doses above 300 mg can be used even with mild-moderate renal impairment with appropriate monitoring 1, 6

Mandatory Flare Prophylaxis When Starting Urate-Lowering Therapy

All patients starting urate-lowering therapy must receive prophylactic anti-inflammatory medication for at least 6 months. 1, 4

• Use low-dose colchicine (0.5-1.2 mg daily) or low-dose NSAIDs as first-line prophylaxis 1, 4
• Low-dose corticosteroids are an alternative if colchicine and NSAIDs are contraindicated 1
• Continue prophylaxis until serum uric acid has been normalized and the patient has been free from acute attacks for several months 1, 5

Monitoring Strategy

Check serum uric acid every 2-5 weeks during dose titration, and assess renal function before initiating therapy and periodically thereafter. 4, 3, 5

• Adjust allopurinol dose based on serum uric acid levels, not just on a fixed schedule 1, 5
• Monitor for signs of allopurinol toxicity including rash, pruritus, and elevated liver enzymes 6
• Maintain serum uric acid <6 mg/dL long-term to prevent recurrent attacks and tophi formation 6, 4

Lifestyle Modifications (Essential Component)

Counsel the patient on weight loss if obese, dietary modifications, and reduced alcohol consumption, especially beer. 1

• These non-pharmacologic interventions are core aspects of gout management 1
• Address associated comorbidities including hyperlipidemia, hypertension, hyperglycemia, obesity, and smoking 1
• Encourage fluid intake sufficient to yield at least 2 liters of daily urinary output 5

Critical Pitfalls to Avoid

• Never treat asymptomatic hyperuricemia alone without confirmed gout or specific high-risk features 1, 5
• Never start allopurinol at 300 mg daily—always begin at 100 mg and titrate slowly to reduce hypersensitivity risk 1, 6, 5
• Never initiate urate-lowering therapy during an acute attack in a treatment-naive patient—this can paradoxically worsen the flare 3
• Never fail to provide flare prophylaxis when starting urate-lowering therapy—this is a major cause of treatment failure and non-adherence 1, 4