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Gout. Gout. Presentation Transcript

  • www.themegallery.com
  • Introduction: Introduction Diagnosis Purine metabolism Diagnosis Management
  • Introduction:
    • Gout is a common arthritis caused by deposition of monosodium urate crystals within joints after chronic hyperuricaemia.
    • It affects 1–2% of adults in developed countries& is the most common inflammatory arthritis in men.
    • Epidemiological data are consistent with a rise in prevalence of gout.
    • Diet / genetic polymorphisms of renal transporters of urate seem to be the main causal factors of primary gout.
    • Gout & hyperuricaemia are associated with HT, DM, metabolic syndrome, renal & CVD.
    • NSAIDs& colchicine remain the most widely recommended drugs to treat acute attacks.
    • Oral corticosteroids could be an alternative to these drugs.
  • Introduction:
    • Interleukin 1β is a pivotal mediator of acute gout&could become a therapeutic target.
    • When serum uric acid is lowered below monosodium urate saturation point, the crystals dissolve & gout can be cured.
    • Patient education, appropriate lifestyle advice, treatment of comorbidities are an important part of management.
  • 1977 ACR criteria for acute gout
    • 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
  • 1977 ACR criteria for acute gout
    • 1. More than one attack of acute arthritis
    • 2. Maximum inflammation developed within 1 day
    • 3. Monoarthritis attack
    • 4. Redness observed over joints
    • 5. First metatarsophalangeal joint painful or swollen
    • 6. Unilateral first metatarsophalangeal joint attack
    • 7. Unilateral tarsal joint attack
    • 8. Tophus (proven or suspected)
    • 9. Hyperuricemia
    • 10. Asymmetric swelling within a joint on x ray/exam
    • 11. Subcortical cysts without erosions on x ray
    • 12. Monosodium urate monohydrate microcrystals in joint fluid during attack
    • 13. Joint fluid culture negative for organisms during attack
  • 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
  • Toxic effects of colchicine: Macrolides cyclosporine verapamil RF/HF Elderly Toxic effects of colchicine Statins
  • Urate - lowering therapy: Tophi Uric acid stones Indicated in: Recurrent attacks Chronic arthropathy
  • Non-drug Management: Stop diuretics Dietary changes Include: Stop alcohol weight loss
  • Dietary advices: Fructose Red meat/sea food. Avoid: Beer Spirits
  • 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
  • Urate-lowering drugs: Allopurinol:
    • XOI.
    • The dose increased until a uric acid conc of 3-3.5 or maximum of 300-800 mgm are achieved.
    • Dose is reduced in patients with RF.
    • Side-effects are rare& include cutaneous intolerance, in 2%,usually in 3 weeks with mortality of 20%.
  • Cutaneous S/Es of Allopurinol increased with: RF Co-diurtics use Re Chalenge High dose
  • Urate-lowering drugs: Rasburicase
    • Off –label monthly infusions of rasburicase have been eff ective in patients with severe gout not treatable with allopurinol.
    • A pegylated uricase—less antigenic& longer half-life—is under development.
    • FDA-approved for Tumor Lysis Syndrome
    • High cost.
  • Urate-lowering drugs: Febuxostat
    • Febuxostat is a novel XOI; 80-120 mg/ day are more effective than allopurinol 300 mg/day.
    • Dose adjustment is not necessary in mild renal failure.
    • 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.
  • Uricosuric agents
    • Probenecid, sulfinpyrazone,benzbromarone
    • Can be used as second-line therapy for patients with underexcretion of uric acid.
    • Fluid intake should be increased/ urine pH maintained above 6 to prevent development of uric acid stones.
    • Benzbromarone, a powerful uricosuric drug, is more active than allopurinol taken at the maximum allowed dose for patients with moderate renal failure.
    • Hepatotoxic.
  • Gout & RF:
    • Interaction between allopurinol/azathioprine/ 6-MP
    • 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.
  • www.themegallery.com Thank You !