Approach to gout

1. Approach to gout Professor/Mohammed Bamashmos (MD) Professor Mohammedالصح

2. Definition • Gout is defined as a peripheral arthritis resulting from the deposition of sodium urate crystals in one or more joints.

3. Epidemiology • Prevalence of gout is around 1% although hyperuricemia occurs in 5% population • More common in developed countries • Due to familial disposition, incidence may be as high as 80% in families affected by disorder. • More common in male. Male to female ratio 10:1

4. Pathogenesis • Hyperuricemia is the major determinant of gout • Uric acid level in blood depends on the balance between purine synthesis, ingestion of diatery purine, and elimination of urate by kidney and intestine. • Uric acid synthesis: Uric acid is the last step in breakdown pathway of purines. The last two step, the conversion of hypoxanthine to xanthine and xanthine to uric acid is catalysed by enzyme xanthine oxidase. • Uric acid excretion- UA is completely filtered by glomerulus, 98-100 % is then reabsorbed in PCT, and 50% secreted by DCT.

8. Pathogenesis contd…. • Causes of hyperuricemia • Impaired excretion of uric acid (90%) • CRF • Drug therapy eg thiazide, low dose aspirin • Lead toxicity • Increased lactic acid production from alcohal, starvation, exercise.

9. Pathogenesis contd…. • B. Increased production of uric acid I. Inceased turnover of cells (10%) due to • Myeloproliferative disorder eg polycythemia vera • Lymphoproliferative disorder eg leukemia • Others eg carcinoma, severe psoriasis II. Inborn error of metebolism leading to purine overproduction (<1%)

10. Clinical feature • Hyperuricaemia causes 4 clinical syndrome • Acute urate synovitis : Acute gout • Chronic polyarticular gout • Chronic tophaceous gout • Urate renal stone formation

11. Clinical feature • Acute gout • Typically affects middle aged male • Sudden onset of agonizing pain, swelling and redness of first MTP Joint. • The attack usually precipitated by too much food, alcohol, dehydration or by start of diuretics. • Untreated attack last for @7 days. • Usually recovers with desquamation of overlying skin. • In 25% joint other than great toe is affected

13. Clinical feature • Chronic polyarticular gout • Can occur in elderly, on long standing diuretic therapy or in renal failure. • Usual presentation is pain and swelling of multiple joints

14. Clinical feature • Chronic tophaceous gout • Sodium urate forms smooth white deposits (tophi) in skin and around joints. • Can occur in ear, fingers, or in achillis tendon • There is chronic pain, Large deposits can ulcerate. • Often associated with renal impairment and long term use of diuretics.

15. Chronic tophaceous gout

18. Investigations • Serum urate: usually raised (>600 mcmol/l) • Joint fluid microscopy: most specific and diagnostic but technically difficult. • RFT: as signs of renal impairment.

23. Treatment • NSAIDs • Naproxen 750 mg stat, 500mg 8-12 hourly • Diclofenac 100 mg stat 50 mg 6-8 hourly • Indomethacin 75mg stat 50 mg 6-8 hourly Patients with renal impairment or APD should be treated with colchicine or intraarticular steroid • Colchicine: 1mg stat 0.5mg 6-12 hourly. Can cause diarrhoea.

24. Treatment • Diatery advice • Reduce alcohal intake esp. beer • Avoid meat, fish, spinach, couliflower, green peas, etc Regular exercise Weight reduction

25. Treatment • Treatment to reduce serum urate level • If attacks are frequent, severe or associated with renal impairment allopurinol should be started. • Should not be started with in a month of acute attack and should be started under cover of NSAIDs or colchicine. • Allopurinol (300mg OD ) blocks the enzyme xanthine oxidase and reduce the serum urate level.

26. Thank you