What is articular gout, also known as gouty arthritis, and how is it treated in adult males with a family history of the disease, obesity, or certain dietary habits, and who may have a history of kidney disease, diabetes, or cardiovascular disease?

What is Articular Gout?

Articular gout (gouty arthritis) is an inflammatory arthritis caused by the deposition of monosodium urate (MSU) crystals in joints and surrounding tissues, resulting from chronic hyperuricemia (serum urate >6.8 mg/dL), and is the most common form of inflammatory arthritis in adults. 1, 2

Pathophysiology and Disease Spectrum

Gout represents a spectrum of disease built on excess body urate burden 1:

• Hyperuricemia (serum urate >6.8 mg/dL) creates supersaturated extracellular fluid where MSU crystals form and deposit in joints, tendons, bursae, and other tissues 1, 2
• Acute gouty arthritis presents as self-limited attacks of severe synovitis ("gout flares") triggered by inflammatory responses to MSU crystals 1
• Chronic gouty arthritis develops when recurrent attacks lead to persistent joint inflammation involving one or more joints 1
• Tophaceous gout occurs with pathognomonic tophi (collections of MSU crystals) in articular, periarticular, bursal, bone, auricular, and cutaneous tissues 1

Clinical Presentation

The American College of Rheumatology guidelines emphasize that gout should be considered in any acute arthritis in an adult 3:

• Classic presentation: Rapid onset (<24 hours) of severe pain and swelling with overlying erythema, most commonly affecting the first metatarsophalangeal joint 1, 3
• Atypical presentations: Can involve hand, wrist, finger, elbow, ankle, knee, or multiple joints simultaneously (polyarticular gout defined as ≥4 joints) 1, 3
• Suggestive features: Male gender, previous similar episodes, associated cardiovascular disease, and hyperuricemia 3

Critical diagnostic pitfall: Serum uric acid may be normal during acute attacks, so hyperuricemia alone cannot diagnose or exclude gout 1, 3

Risk Factors and Comorbidities

The European League Against Rheumatism (EULAR) guidelines mandate systematic assessment for risk factors and comorbidities in every gout patient 1:

Modifiable risk factors requiring evaluation 1:

• Obesity and overweight status
• Alcohol consumption (especially beer and spirits)
• Medications: diuretics, low-dose aspirin, cyclosporine, tacrolimus
• Diet: non-diet sodas, excessive meat and shellfish intake

Associated comorbidities that must be screened 1, 4, 5:

• Chronic kidney disease (increases gout risk 4.95-fold) 3
• Hypertension
• Cardiovascular disease and heart failure
• Diabetes mellitus and metabolic syndrome
• Dyslipidemia
• Obesity

These comorbidities negatively impact quality of life, long-term prognosis, and complicate treatment decisions 5

Diagnostic Approach

The gold standard is synovial fluid aspiration with MSU crystal identification (sensitivity 84%, specificity approaching 100%) 3:

• EULAR strongly recommends synovial fluid analysis in every patient with undiagnosed inflammatory arthritis, especially atypical presentations, to exclude septic arthritis 1, 3
• Demonstration of MSU crystals allows definitive diagnosis 1

When aspiration is not feasible, imaging can detect MSU crystal deposition 1, 3:

• Ultrasound: 74% sensitivity, 88% specificity for double contour sign at cartilage surfaces (highly specific for urate deposits) 3
• Dual-energy CT: 85-100% sensitivity, 83-92% specificity 3
• Plain radiographs: Limited value for acute flares but can show chronic changes 1

Treatment Strategy

Acute Attack Management

The American College of Rheumatology guidelines mandate that acute gout attacks should be treated with pharmacologic therapy initiated within 24 hours of onset 1:

First-line options (all appropriate, choice depends on contraindications) 1:

• NSAIDs: Full anti-inflammatory doses
• Corticosteroids: Oral, intravenous, or intra-articular
• Colchicine: Appropriate if started within 36 hours of symptom onset

Severe or refractory attacks: Combination therapy can be employed 1

Critical management principle: Established urate-lowering therapy (ULT) should be continued without interruption during acute attacks 1

Long-Term Urate-Lowering Therapy

The overarching principle is reducing serum urate below saturation threshold to prevent crystal formation and dissolve existing deposits 1, 6, 2:

• Target serum urate: <0.36 mmol/L (6 mg/dL) for non-tophaceous gout, <0.30 mmol/L for tophaceous gout 6
• Allopurinol (xanthine oxidase inhibitor): Reduces both serum and urinary uric acid by inhibiting uric acid formation; plasma half-life 1-2 hours for allopurinol, 15 hours for active metabolite oxipurinol allowing once-daily dosing 7
• Febuxostat: Alternative xanthine oxidase inhibitor, usable in mild-moderate renal impairment 5
• Dose adjustments required in chronic kidney disease for most agents 5

Prophylaxis During ULT Initiation

Pharmacologic anti-inflammatory prophylaxis is recommended for all patients when ULT is initiated 1:

• First-line: Oral colchicine with appropriate dose adjustment for chronic kidney disease and drug interactions 1
• Alternative: Low-dose NSAID therapy unless contraindicated 1
• Duration: Continue prophylaxis if clinical gout activity persists or serum urate target not yet achieved 1

Rationale: ULT initiation causes early increase in acute attacks due to remodeling of urate crystal deposits, contributing to non-adherence 1

Special Considerations for High-Risk Populations

In patients with multiple comorbidities (kidney disease, cardiovascular disease, diabetes) 5:

• NSAIDs can cause acute renal toxicity or worsen chronic kidney disease and should be avoided 5
• Colchicine and ULT require dosage adjustments in renal impairment, potentially limiting efficacy 5
• Febuxostat may be used in mild-moderate renal impairment, but insufficient data exists for creatinine clearance <30 mL/min 5

For refractory cases: IL-1 inhibitors (canakinumab) are FDA-approved for gout flares in adults who cannot receive or tolerate NSAIDs and colchicine, have not responded to these treatments, or cannot receive repeated steroids 8

Key Management Pitfalls to Avoid

• Never diagnose gout on hyperuricemia alone - serum urate may be normal during acute attacks 1, 3
• Never interrupt established ULT during acute attacks - this worsens outcomes 1
• Never delay treatment beyond 24 hours of acute attack onset 1
• Never use NSAIDs in patients with significant chronic kidney disease - risk of acute renal toxicity 5
• Never skip prophylaxis when initiating ULT - paradoxical flare increase leads to treatment abandonment 1