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  1. 1. www.themegallery.com
  2. 2. Introduction: Introduction Diagnosis Purine metabolism Diagnosis Management
  3. 3. Introduction: <ul><li>Gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia. </li></ul><ul><li>It affects 1–2% of adults in developed countries& is the most common inflammatory arthritis in men. </li></ul><ul><li>Epidemiological data are consistent with a rise in prevalence of gout. </li></ul><ul><li>Diet / genetic polymorphisms of renal transporters of urate seem to be the main causal factors of primary gout. </li></ul><ul><li>Gout & hyperuricaemia are associated with HT, DM, metabolic syndrome, renal & CVD. </li></ul><ul><li>NSAIDs& colchicine remain the most widely recommended drugs to treat acute attacks. </li></ul><ul><li>Oral corticosteroids could be an alternative to these drugs. </li></ul>
  4. 4. Introduction: <ul><li>Interleukin 1β is a pivotal mediator of acute gout&could become a therapeutic target. </li></ul><ul><li>When serum uric acid is lowered below monosodium urate saturation point, the crystals dissolve & gout can be cured. </li></ul><ul><li>Patient education, appropriate lifestyle advice, treatment of comorbidities are an important part of management. </li></ul>
  5. 10. 1977 ACR criteria for acute gout <ul><li>The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following 12 clinical, lab radio features </li></ul>
  6. 11. 1977 ACR criteria for acute gout <ul><li>1. More than one attack of acute arthritis </li></ul><ul><li>2. Maximum inflammation developed within 1 day </li></ul><ul><li>3. Monoarthritis attack </li></ul><ul><li>4. Redness observed over joints </li></ul><ul><li>5. First metatarsophalangeal joint painful or swollen </li></ul><ul><li>6. Unilateral first metatarsophalangeal joint attack </li></ul><ul><li>7. Unilateral tarsal joint attack </li></ul><ul><li>8. Tophus (proven or suspected) </li></ul><ul><li>9. Hyperuricemia </li></ul><ul><li>10. Asymmetric swelling within a joint on x ray/exam </li></ul><ul><li>11. Subcortical cysts without erosions on x ray </li></ul><ul><li>12. Monosodium urate monohydrate microcrystals in joint fluid during attack </li></ul><ul><li>13. Joint fluid culture negative for organisms during attack </li></ul>
  7. 17. Gout: acute attack trt Cochicin. NSAIDs steroids 0·5 mg three times daily Favored if no C/Is&for 1–2 ws. Paranteral &oral pred Rest/Ice Steoides Colchicin/ NSAIDs
  8. 18. Toxic effects of colchicine: Macrolides cyclosporine verapamil RF/HF Elderly Toxic effects of colchicine Statins
  9. 19. Urate - lowering therapy: Tophi Uric acid stones Indicated in: Recurrent attacks Chronic arthropathy
  10. 20. Non-drug Management: Stop diuretics Dietary changes Include: Stop alcohol weight loss
  11. 21. Dietary advices: Fructose Red meat/sea food. Avoid: Beer Spirits
  12. 22. Starting urate -lowering drugs: - Started 1-2 weeks after resolution of the acute attack. - Colchicin or NSAIDs for 3-6 months. Should be treated without interruption of urate-lowering therapy. Urate lowering drugs: Prevention of acute flares during maintenance trt: Flares
  13. 23. Urate-lowering drugs: Allopurinol: <ul><li>XOI. </li></ul><ul><li>The dose increased until a uric acid conc of 3-3.5 or maximum of 300-800 mgm are achieved. </li></ul><ul><li>Dose is reduced in patients with RF. </li></ul><ul><li>Side-effects are rare& include cutaneous intolerance, in 2%,usually in 3 weeks with mortality of 20%. </li></ul>
  14. 24. Cutaneous S/Es of Allopurinol increased with: RF Co-diurtics use Re Chalenge High dose
  15. 25. Urate-lowering drugs: Rasburicase <ul><li>Off –label monthly infusions of rasburicase have been eff ective in patients with severe gout not treatable with allopurinol. </li></ul><ul><li>A pegylated uricase—less antigenic& longer half-life—is under development. </li></ul><ul><li>FDA-approved for Tumor Lysis Syndrome </li></ul><ul><li>High cost. </li></ul>
  16. 26. Urate-lowering drugs: Febuxostat <ul><li>Febuxostat is a novel XOI; 80-120 mg/ day are more effective than allopurinol 300 mg/day. </li></ul><ul><li>Dose adjustment is not necessary in mild renal failure. </li></ul><ul><li>Side-eff ects include raised liver enzyme activity and a small increase in the rate of serious cardiovascular events, precludes use in patients with ischaemic or CHF. </li></ul>
  17. 27. Uricosuric agents <ul><li>Probenecid, sulfinpyrazone,benzbromarone </li></ul><ul><li>Can be used as second-line therapy for patients with underexcretion of uric acid. </li></ul><ul><li>Fluid intake should be increased/ urine pH maintained above 6 to prevent development of uric acid stones. </li></ul><ul><li>Benzbromarone, a powerful uricosuric drug, is more active than allopurinol taken at the maximum allowed dose for patients with moderate renal failure. </li></ul><ul><li>Hepatotoxic. </li></ul>
  18. 28. Gout & RF: <ul><li>Interaction between allopurinol/azathioprine/ 6-MP </li></ul><ul><li>Mycophenolate mofetil has no effect on uricaemia &not metabolised by XO, can be used in place of ciclosporin or tacrolimus, which both raise serum urate. </li></ul>
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