Overview
Definition
An inflammatory arthritis caused by the deposition of monosodium urate (MSU) crystals in joints and soft tissues.
Epidemiology
Most common inflammatory arthritis in adult men. Associated with metabolic syndrome and alcohol consumption.
Etiology & Risk Factors
- Hyperuricemia (uric acid > 6.8 mg/dL). Can be due to underexcretion by the kidneys (90% of cases) or overproduction (10% of cases).
- Triggers: Alcohol (especially beer), purine-rich foods (red meat, seafood), dehydration, thiazide or loop diuretics.
Clinical Symptoms
- Acute Gout Flare: Sudden, excruciating pain, redness, swelling, and warmth in a single joint (Monoarticular)
- Podagra: Involvement of the first metatarsophalangeal (MTP) joint (the big toe) - classic presentation
- Tophi: Hard, painless nodules of urate crystals under the skin or in joints (occurs in chronic/untreated disease)
Clinical Approach
Diagnosis
- Joint Aspiration (Arthrocentesis - Gold Standard): Synovial fluid analysis reveals negatively birefringent, needle-shaped monosodium urate crystals under polarized light
- Serum Uric Acid: Often elevated, but can be NORMAL during an acute flare (do not use to rule out acute gout)
- X-ray: 'Rat-bite' or 'punched-out' erosions with overhanging edges (seen in chronic gout)
Management
- Acute Flare: NSAIDs (Indomethacin, Naproxen) are first-line. Colchicine or Corticosteroids (intra-articular or oral) are alternatives.
- Chronic/Preventative (Urate-Lowering Therapy): Allopurinol (Xanthine oxidase inhibitor) is first-line to lower uric acid. DO NOT start during an acute flare (can worsen it), but do not stop if the patient is already taking it.
- Lifestyle: Weight loss, limit alcohol/purines, stay hydrated
Complications
- Chronic tophaceous gout and joint destruction
- Uric acid kidney stones (nephrolithiasis)
- Urate nephropathy (renal failure)