Gout

Gout

• Gout is a type of microcrystal synovitis caused by monosodium urate crystal deposition in joints.
• It results from abnormal uric acid metabolism.
• This chronic disease can lead to tophi (skin deposits) and potential urate stone formation in the urinary tract.

Epidemiology

• Gout is the most common inflammatory arthritis in men and post-menopausal women.
• It's rare in pre-menopausal women due to enhanced uric acid excretion by estrogen.
• Incidence is increasing with rising obesity and metabolic syndrome.

Causes

• Decreased Uric Acid Excretion (90% cases): Conditions like renal failure, lactic acidosis, lead poisoning, alcohol consumption, and certain medications (e.g., thiazides, loop diuretics, aspirin) can decrease uric acid excretion.
• Increased Uric Acid Production: Conditions like myeloproliferative disorders, psoriasis, and high-purine diets can increase uric acid production.
• Dietary Intake: Foods high in purines (red meat, shellfish, high fructose) contribute to increased uric acid levels.
• Metabolic Syndrome: Obesity, diabetes, hypertension, dyslipidemia contribute to the development and progression of gout.

Pathophysiology

• Uric acid levels depend on dietary purines and endogenous metabolism.
• Xanthine oxidase plays a key role in converting hypoxanthine to xanthine to uric acid.
• Imbalance in the synthesis and excretion of uric acid leads to crystal deposition in joints.

Clinical Features

• Acute Gout: Characterized by severe pain, tenderness, swelling, redness, and warmth in joints, predominantly the first metatarsophalangeal joint (podagra). Typically self-limiting within 5-14 days, worsening in early morning.
• Chronic Gout: Symptoms include joint deformities, asymmetrical arthritis, functional impairment, and tophi (nodules on extensor surfaces). Renal complications (kidney stones and interstitial nephritis) can also occur.

Investigations

• Serum Uric Acid: May be normal during an acute attack.
• Joint Fluid Analysis: Diagnostic for needle-shaped monosodium urate crystals.
• Imaging: Normal X-rays during acute attacks; chronic gout can show erosions and punched-out lesions.
• Other Tests: Complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), renal function, and lipid profile are used for comprehensive evaluation.

Treatment

• Acute Gout: First-line treatment is colchicine (0.5mg 2-4 times a day). Non-steroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are also used, as well as ice packs, and joint aspiration when appropriate. Biologic agents (e.g., anakinra) are reserved for resistant cases.
• Chronic Gout: Treatment focuses on lifestyle modifications—reducing alcohol intake, weight loss, and limiting purine-rich foods. Urate-lowering therapy is also a cornerstone of management.

Urate-Lowering Therapy

• Allopurinol: First-choice drug that inhibits xanthine oxidase.
• Febuxostat: Is used for those who cannot tolerate allopurinol.
• Uricosuric Drugs (e.g., Probenecid): Avoided in renal impairment.