Gout
By Shravya & Helen
Gout is…
An inflammatory arthritis associated with hyperuricaemia and intra-articular sodium urate crystals
Gout is prevalent…
• Mainly in deveoped countries• In Europe and USA it is approx 0.2%
– Presence of hyperuricaemia is 5%
• In men more than women (10:1)• Rarely presents before young adult or
premenopausal females• Prevalence in older females is increasing with
increased diuretic groups• Hyperuricaemia common in certain ethnic
groups- Maoris
Gout presents ...
• Typically in middle-aged male with sudden, agonising pain, swelling and redness of first MTP (60%)
• Can also be seen in ankle, foot, small joints of hand, wrist, elbow or knee
• Untreated, lasts ~7 days• Recovery associated with desquamation of overlying skin• In severe attacks, overlying cellulitis males gout difficult to
distinguish clinically from infective cellulitis• Chronic polyarticular seen mainly in elderly with long-
standing diuretic use• May see tophi (smooth white sodium urate deposits) in skin
and around joints.– Also on pinna, fingers & Achilles tendon
Differentials include…
• Septic arthritis
• Haemarthrosis
• Pseudogout
• Palindromic RA
• Cellulitis
Causes of Gout…
• Hereditary• Dietary purine
increase• Alcohol excess• Diuretics• Leukaemia• Cytotoxics (tumour
lysis)• Renal impairment
• Gout is also a marker for conditions such as:– Hypertension– IHD– Metabolic syndrome
Pathogenesis
• Hyperuricaemia is a major determinant for developing gout
• Blood Uric acid levels depend on
– balance b/w purine synthesis and ingestion og dietary purines
– Elimination of urate by kidney & intestine
• Uric acid is produced in the last step in breakdown of purines
– Uric acid is completely filtered by the glomerulus
– It is then mostly reabsorbed in the proximal tubule and 50% secreted by the distal tubule
– Low-dose aspirin blocks urate secretion
– High-dose aspirin also blocks reabsorption increased net excretion
– Insulin resistance enhanses urate resorption• 90% of pts with gout have impaired excraition of urate
Investigations• Synovial Fluid Analysis –
typical negatively birefringent needle-shaped MSU crystals
→ Can be extra or intracellular
→ Not sensitive
• Leucocytosis/ESR/CRP - raised during acute attack
• Serum Uric Acid levels - ↑ Not specific in acute attack
• Radiography – Hallmarks of gout are normal mineralization, joint space preservation, sharply marginated erosions with sclerotic borders, overhanging edges, and asymmetric polyarticular distribution Tophi seen in late gout
Treatment• NSAIDS – naproxen or indomethacin
C/I: corticosteroids (prednisolone)• Colchicine – 2nd Line; used prophylactically;
C/I - GFR<10 mL/min; hepatic dysfunction, biliary obstruction, or inability to tolerate diarrhea S.E doserelated - nausea, vomiting, abdominal pain, diarrhea, anaemia, neutropenia
• Allopurinol – 1st line, prevents the production of uric acid; C/I - azothioprine S.E - diarrhea, nausea, RASH, itching, drowsiness, can cause LIVER TOXICITYfatal
• Probenecid
• Surgery – late or untreated gout orthopaedic attention
• Avoid alcohol
• Arthrosclerosis and Gout associated advice low-cholesterol diet
• Untreated gout can lead to severe joint destruction and renal impairment