What is gout and how is it managed?

Understanding Gout: A Simple Guide for First-Year PA Students

Gout is a common inflammatory arthritis caused by too much uric acid in the body, which forms needle-shaped crystals that deposit in joints and cause sudden, severe pain—most famously in the big toe. 1

What Is Gout?

Gout is a metabolic disease built on a foundation of excess uric acid (hyperuricemia), defined as serum urate greater than 6.8-7.0 mg/dL 1. Think of it this way:

• The basic problem: Your body has too much uric acid floating around in the blood 1
• What happens next: When uric acid levels get too high, it crystallizes into monosodium urate monohydrate crystals in joints and tissues 1
• The result: These sharp, needle-shaped crystals trigger intense inflammation, causing the classic gout attack 1

How Common Is It?

Gout affects approximately 3.9% of U.S. adults (about 8.3 million people), making it one of the most common rheumatic diseases 1. The prevalence is rising due to increasing rates of obesity, hypertension, metabolic syndrome, type 2 diabetes, chronic kidney disease, and widespread use of diuretic medications 1.

Clinical Presentation: What Does Gout Look Like?

Acute Gout Attack

The classic presentation is sudden, severe pain in a single joint that develops rapidly 1:

• Most common site: The first metatarsophalangeal joint (big toe)—occurs in 50% of initial attacks 2, 3
• Other common sites: Foot, ankle, midtarsal joints, knee, wrist, fingers, and elbow 3
• Gender differences: Men typically present with toe involvement; women more commonly have elbow or finger joint involvement 4
• Timing: Pain develops rapidly, often overnight, with maximum intensity within 24 hours 1
• Appearance: The joint becomes red, hot, swollen, and exquisitely tender 1

Disease Stages

Gout progresses through distinct phases 1:

1. Acute intermittent gout: Sudden attacks separated by pain-free periods 1
2. Intercritical period: Asymptomatic intervals between attacks (can last days to years) 3
3. Chronic tophaceous gout: Develops with untreated disease; characterized by persistent joint inflammation and visible tophi (deposits of urate crystals in tissues) 1

Tophi

Tophi are pathognomonic (uniquely characteristic) features of gout 1:

• What they are: Solid aggregates of monosodium urate crystals deposited in tissues 3
• Common locations: Helix of the ear, olecranon bursa, over interphalangeal joints, and periarticular tissues 1, 3
• Significance: Their development correlates with both the degree and duration of hyperuricemia 3

Diagnosis

The gold standard is identifying needle-shaped monosodium urate crystals with strong negative birefringence under polarized microscopy in synovial fluid 2, 3. However, clinical diagnosis is often made based on:

• Presence of hyperuricemia 4
• Rapid development of pain, tenderness, and swelling in a characteristic joint 4
• Family history 4
• Response to treatment 2

Management: A Two-Pronged Approach

1. Treating Acute Attacks

For acute gout, choose corticosteroids, NSAIDs, or colchicine—treatment should be initiated within 24 hours of symptom onset for optimal results 1:

First-Line Options (all equally effective) 1:

• NSAIDs: Full FDA-approved doses (naproxen, indomethacin, or sulindac are FDA-approved for gout) 1
• Colchicine: Use LOW-DOSE colchicine (1.2 mg, then 0.6 mg one hour later) 1
  • Critical point: Low-dose colchicine is as effective as high-dose but causes fewer gastrointestinal side effects 1
  • Must be started within 36 hours of symptom onset 1
• Corticosteroids: Oral prednisone 0.5 mg/kg/day for 5-10 days, or intra-articular injection, or intramuscular triamcinolone acetonide 60 mg 1

Important: Do NOT stop ongoing urate-lowering therapy during an acute attack 1

2. Long-Term Management: Lowering Uric Acid

When to Start Urate-Lowering Therapy (ULT)

Do NOT initiate ULT after a first gout attack or in patients with infrequent attacks 1. Start ULT in patients with 1:

• Recurrent gout attacks (≥2 per year)
• Chronic tophaceous gout
• Urolithiasis (kidney stones)
• Renal function impairment
• Frequent or severe acute gout

Urate-Lowering Medications

Allopurinol is the first-line urate-lowering therapy for most patients 4, 5:

• Mechanism: Xanthine oxidase inhibitor that blocks uric acid formation 6, 7
• Dosing: Start low and titrate up to achieve target uric acid levels 1
• Advantages: Reduces both serum and urinary uric acid; works even with renal impairment 6

Alternative options 7, 4:

• Febuxostat: Another xanthine oxidase inhibitor for patients who cannot tolerate allopurinol 4, 5
• Probenecid: Uricosuric drug (increases uric acid excretion in urine); use in patients with normal renal function and no history of kidney stones 7
• Pegloticase: Reserved for severe, refractory cases; requires parenteral administration 8, 4

Prophylaxis Against Flares When Starting ULT

Critical concept: Starting urate-lowering therapy paradoxically INCREASES gout flares initially because mobilizing urate from tissue deposits changes serum levels 1, 8.

Therefore, always provide prophylaxis when initiating ULT 1:

• Options: Low-dose colchicine (0.6 mg once or twice daily) or NSAIDs 1, 5
• Duration: At least 6 months, or at least 3 months after uric acid reaches target in patients without tophi 2, 5
• Evidence: Prophylaxis reduces risk of acute gout attacks by at least 50% 1

3. Lifestyle Modifications

Every patient with gout should receive lifestyle advice 9:

• Weight loss if overweight or obese 9, 2
• Limit alcohol intake, especially beer and spirits 9, 2
• Avoid sugar-sweetened drinks and high-fructose corn syrup 9, 2
• Reduce intake of purine-rich foods (organ meats, shellfish) 2
• Encourage low-fat dairy products (may have protective effects) 9, 2
• Encourage vegetable consumption 2

Common Comorbidities

Gout rarely exists in isolation—patients often have 1, 3:

• Hypertension
• Obesity and metabolic syndrome
• Type 2 diabetes
• Chronic kidney disease
• Cardiovascular disease
• Dyslipidemia

Medication consideration: Thiazide and loop diuretics increase uric acid levels and can precipitate gout 1. The angiotensin receptor blocker losartan increases urinary uric acid excretion and may be beneficial 2.

Key Pitfalls to Avoid

1. Don't start urate-lowering therapy during an acute attack—treat the acute inflammation first, then consider long-term management 1
2. Don't forget prophylaxis—failing to provide prophylaxis when starting ULT leads to increased flares and poor adherence 1, 5
3. Don't use high-dose colchicine—low-dose is equally effective with fewer side effects 1
4. Don't stop ULT during a flare—continue it and treat the acute attack separately 1
5. Don't treat asymptomatic hyperuricemia—elevated uric acid without symptoms is not an indication for treatment 1

Treatment Goals

The ultimate goal is to lower serum uric acid below the saturation point (below 6.8 mg/dL) to prevent crystal formation and dissolve existing deposits 1. This requires long-term commitment to both pharmacologic therapy and lifestyle modifications 1, 2.