1 / 61

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

lotus
Download Presentation

GOUT

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  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

More Related