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GOUT

GOUT. Wayne Blount, MD, MPH Professor, Emory Univ. S.O.M. OBJECTIVES. Identify diagnostic criteria for gout Identify 3 treatment goals for gout Name the agents used to treat the acute flares of gout and the chronic disease of gout. Why Worry About Gout ?. Prevalence increasing

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GOUT

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  1. GOUT Wayne Blount, MD, MPH Professor, Emory Univ. S.O.M.

  2. OBJECTIVES • Identify diagnostic criteria for gout • Identify 3 treatment goals for gout • Name the agents used to treat the acute flares of gout and the chronic disease of gout

  3. Why Worry About Gout ? • Prevalence increasing • May be signal for unrecognized comorbidities : ( Not to point of searching) Obesity (Duh!) Metabolic syndrome DM HTN CV disease Renal disease

  4. URATE, HYPERURICEMIA & GOUT • Urate: end product of purine metabolism • Hyperuricemia: serum urate > urate solubility (> 6.8 mg/dl) • Gout: deposition of monosodium urate crystals in tissues

  5. HYPERURICEMIA & GOUT • Hyperuricemia caused by Overproduction Underexcretion • No Gout w/o crystal deposition

  6. THE GOUT CASCADE • Urate • Oevrproduction Underexcretion • Hyperuricemia • ________________________________________ • Silent Gout Renal Associated • Tissue manifestations CV events & • Deposition mortality

  7. GOUT: A Chronic Disease of 4 stages • Asymptomatic hyperuricemia • Acute Flares of crystallization • Intervals between flares • Advanced Gout & Complications

  8. ACUTE GOUTY FLARES • Abrupt onset of severe joint inflammation, often nocturnal; Warmth, swelling, erythema, & pain; Possibly fever • Untreated? Resolves in 3-10 days • 90% 1st attacks are monoarticular • 50% are podagra

  9. SITES OF ACUTE FLARES • 90% of gout patients eventually have podagra : 1st MTP joint

  10. Sites • Can occur in other joints, bursa & tendons

  11. INTERVALS SANS FLARES • Asymptomatic • If untreated, may advance • Intervals may shorten • Crystals in asx joints • Body urate stores increase

  12. FLARE INTERVALS • Silent tissue deposition & Hidden Damage

  13. ADVANCED GOUT • Chronic Arthritis • X-ray Changes • Tophi Develop • Acute Flares continue

  14. ADVANCED GOUT • Chronic Arthritis • Polyarticular acute flares with upper extremities more involved

  15. TOPHI • Solid urate deposits in tissues

  16. TOPHI • Irregular & destructive

  17. TOPHI RISK FACTORS • Long duration of hyperuricemia • Higher serum urate • Long periods of active, untreated gout

  18. RADIOLOGIC SIGNS

  19. X-RAYS

  20. X-RAYS

  21. DIAGNOSING GOUT • Hx & P.E. • Synovial fluid analysis • Not Serum Urate

  22. SERUM URATE LEVELS • Not reliable • May be normal with flares • May be high with joint Sx from other causes

  23. GOUT RISK FACTORS • Male • Postmenopausal female • Older • Hypertension • Pharmaceuticals: Diuretics, ASA, cyclosporine

  24. GOUT RISK FACTORS • Transplant • Alcohol intake Highest with beer Not increased with wine • High BMI (obesity) • Diet high in meat & seafood

  25. SYNOVIAL FLUID ANALYSIS (Polarized Light Microscopy) • The Gold standard • Crystals intracellular during attacks • Needle & rod shapes • Strong negative birefringence

  26. SYNOVIAL FLUID

  27. DIFFERENTIAL DIAGNOSIS • Pseudogout: Chondrocalcinosis, CPPD • Psoriatic Arthritis • Osteoarthritis • Rheumatoid arthritis • Septic arthritis • Cellulitis

  28. Gout vs. CPPD • Similar Acute attacks • Different crystals under Micro; Rhomboid, irregular in CPPD

  29. Gout vs CPPD

  30. RA vs Gout • Both have polyarticular, symmetric arthritis • Tophi can be mistaken for RA nodules

  31. RA vs Gout

  32. REDNECK MEDICAL TERMS • “BENIGN” : WHAT YOU BE AFTER YOU BE EIGHT

  33. TREATMENT GOALS • Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation • Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause

  34. ENDING ACUTE FLARES • Control inflammation & pain & resolve the flare • Not a cure • Crystals remain in joints • Don’t try to lower serum urate during a flare • Choice of med not as critical as alacrity & duration EBM

  35. Acute Flare Med Choices • NSAIDS • Colchicine • Corticosteroids

  36. MED Considerations • NSAIDS : Interaction with warfarin Contraindicated in: Renal disease PUD GI bleeders ASA-induced RAD

  37. MED Considerations • Colchicine : Not as effective “late” in flare Drug interaction : Statins, Macrolides, Cyclosporine Contraindicated in dialysis pt.s Cautious use in : renal or liver dysfunction; active infection, age > 70

  38. MED Considerations • Corticosteroids : Worse glycemic control May need to use mod-high doses

  39. TREATMENT GOALS • Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation • Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause

  40. PROTECTION VS. FUTURE FLARES • Colchicine : 0.5-1.0 mg/day • Low-dose NSAIDS • Both decrease freq & severity of flares • Prevent flares with start of urate-lowering RX Best with 6 mos of concommitant RX EBM • Won’t stop destructive aspects of gout

  41. TREATMENT GOALS • Rapidly end acute flares Protect against future flares Reduce chance of crystal inflammation • Prevent disease progression Lower serum urate to deplete total body urate pool Correct metabolic cause

  42. PREVENT DISEASE PROGRESSION • Lower urate to < 6 mg/dl : Depletes Total body urate pool Deposited crystals EBM • RX is lifelong & continuous • MED choices : Uricosuric agents Xanthine oxidase inhibitor

  43. PREVENT THIS

  44. URICOSURIC AGENTS • Probenecid, (Losartan & fenofibrate for mild disease) • Increased secretion of urate into urine • Reverses most common physiologic abnormality in gout ( 90% pt.s are underexcretors)

  45. XANTHINE OXIDASE INHIBITOR • Allopurinol : • Blocks conversion of hypoxanthine to uric acid • Effective in overproducers • May be effective in underexcretors • Can work in pt.s with renal insufficiency

  46. WHICH AGENT ? Allopurinol Uricosuric Issue in renal disease X X Drug interactions X X Potentially fatal hypersen- sitivity syndrome X Risk of nephrolithiasis X Mutiple daily dosing X

  47. WHICH AGENT • Base choice on above considerations & whether pt is an overproducer or underexcretor : Need to get a 24-hr. urine for urate excretion: < 700 --- underexcretor (uricosuric) > 700 --- overproducer (allopurinol)

  48. NEW AGENTS • RX gaps : • Can’t always get urate < 6 • Allergies • Drug interactions • Allopurinol intolerance • Worse Renal disease

  49. URICASE ENZYMES(Stay Tuned) • Catabolize urate to allantoin: More soluble, excretable form • Currently approved for hypoeruricemia in tumor lysis syndrome • Some concerns: fatal immunogenicity & unknown long-term effects

  50. CASE STUDIES

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