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Diagnosis and Management of Gout

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Diagnosis and Management of Gout ... or failed NSAID/colchicine therapy - Daily doses of prednisone 40-60mg a day for 3-5days then taper 1-2 weeks ... – PowerPoint PPT presentation

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Title: Diagnosis and Management of Gout


1
Diagnosis and Management of Gout
  • Sadeq AL-Shmesawy

2
Objectives
  • To review the etiology and pathophysiology of
    gout
  • To recognize predisposing factors for gout
  • To review diagnostic criteria and evaluation for
    gout
  • To select appropriate treatment for a patient
    presenting with gout.

3
Gout
  • Introduction
  • Etiology Primary vs secondarygout
  • Epidemiology Age, gender and race
  • Pathophysiology
  • Predisposing factors
  • Associated conditions
  • Presentation History, PE, Lab, and Radiology
    work-up
  • Differential Diagnosis
  • Treatment Summary pharmacologic
    Non-pharmacologic.

4
Definition
  • Gout is a heterogeneous disorder that results in
    the deposition of uric acid salts and crystals in
    and around joints and soft tissues or
    crystallization of uric acid in urinary tract.
  • Uric acid is the normal end product of the
    degradation of purine compounds.
  • - Major route of disposal is renal excretion
  • - Humans lack the enzyme uricase to break down
    uric acid into more soluble form.
  • Metabolic Disorder underlying gout is
    hyperuricemia.
  • - Define as 2 SD above mean usually 7.0 mg/dL.
    This concentration is about the limit of
    solubility for (monosodium urate) MSU in plasma.
    At higher levels, the MSU is more likely to
    precipitate in tissues.

5
Pathophysiology
  • Primary gout is caused by inborn defect in purine
    metabolism or inherited defects of the renal
    tubular secretion of urate
  • Secondary gout is caused by acquired disorders
    that result in increased turnover of nucleic
    acids, and by defects in renal excretion of uric
    acid salts, and by the effects of certain drugs.

6
Epidemiology
  • Most common of microcrystalline arthropathy.
    Incidence has increased significantly over the
    past few decades.
  • Affects about 2.1 million worldwide
  • Peak incidence occurs in the fifth decade, but
    can occur at any age
  • Gout is 5X more common in male than
    pre-menopausal females incidence in women
    increases after menopause. After age 60, the
    incidence in women aproaches the rate in men
  • People of South Pacific origin have an increased
    incidence.

incidence in women approaches
7
Classification of hyperuricemia
  • Uric acid overproduction
  • -Accounts for 10 of hyperuricemia
  • -Defined as 800mg of uric acid
  • -Acquired disorders
  • Excessive cell turnover rates such as
    myleoproliferative disorders, Pagets disease,
    hemolytic anemias
  • -Genetic disorders derangements in
    mechanisms that regulate purine neucleotide
    synthesis.
  • Deficiency HGPRT,or superactivity PRPP synthetase
  • Uric acid underexcretion
  • -Accounts for gt90 of hyperuricemia
  • -Diminished tubular secretory rate,
    increased reabsorption, diminished uric acid
    filtration
  • Drugs, other systemic disease that predispose
    people to renal insufficiency

8
Predisposing Factors
  • Psoriasis
  • Poisoning
  • Obesity
  • Hypertension
  • Organ transplantation
  • Surgery
  • Heredity
  • Drugs usage
  • Renal failure
  • Hematologic Disease
  • Trauma
  • Alcohol use

9
Stages of Classic Gout
  • Asymptomatic hyperurcemia
  • - Very common biochemical abnormality
  • - Defind as 2SD above mean value
  • - Majority of people with hyperuricemia never
    develop symptoms of uric acid excess
  • Acute Intermitten Gout (Gouty Arthritis)
  • - Episodes of acute attacks. Symptoms may be
    confined to a single joint or patient may have
    systemic symptoms.
  • Intercritical Gout
  • - Symptom free period intreval between
    attacks. May have hyperuricemia and MSU crystals
    in synovial fluid
  • Chronic Tophaceous Gout
  • - Results from established disease and refers
    to stage of deposition of urate, inflammatory
    cells and foreign body giant cells in the
    tissues. Deposits may be in tendons or ligaments.
  • - Usually develops after 10 or more years of
    acute intermittent gout.

10
Pathogenesis of Gouty Inflammation
  • Urate crystals stimulate the release of numerous
    inflammatory mediators in synovial cells and
    phagocytes
  • The influx of neutrophils is an important event
    for developing acute crystal induced synovitis
  • Chronic gouty inflammation associated with
    cytokine driven synovial proliferation, cartilage
    loss and bone erosion

11
Presenting Symptoms
  • Systemic fever rare but patients may have fever,
    chills and malaise
  • MusculoskeletalAcute onest of monoarticuler
    joint pain. First MTP most common. Usually
    affected in 90of patients with gout. Other
    joints knees, foot and ankles. Less common in
    upper extremities
  • -Postulated that decreased solubility of MSU
    at lower temperatures of peripheral structures
    such as toe and ear
  • Skin warmth, erythema and tenseness of skin
    overlying joint. May have pruritus and
    desquamation
  • GU Renal colic with renal calculi formation in
    patients with hyperuricemia

12
Differential Diagnosis
  • Trauma
  • Infections
  • - septic arthritis, gonococcal arthritis,
    cellulitis
  • Inflammatory
  • - Rheumatic arthritis, Reiters syndrome,
    Psoriatic arthritis
  • Metabolic
  • -pseudogout
  • Miscellaneous
  • - Osteoarthrtis

13
Diagnosis
  • Definitive diagnosis only possible by aspirating
    and inspecting synovial fluid or tophaceous
    material and demonstrating MSU crystals
  • Polarized microscopy, the crystals appear as
    bright birefringent crystals that are yellow
    (negatively birefringent)

14
Synovial Fluid Findings
  • Needle shaped crystals of monosodium urate
    monohydrate that have been engulfed by
    neutrophils

15
Diagnostic Studies
  • Uric Acid
  • - Limited value as majority of hyperuricemic
    patients will never develop gout
  • - Levels may be normal during acute attack
  • CBC
  • - Mild leukocytosis in acute attacks, but may
    be higher than 25,000/mm
  • ESR
  • - mild elevation or may be 2-3x normal
  • 24hr urine uric acid
  • - Only useful in patients being considered for
    uricosuric therapy or if cause of marked
    hyperuricemia needs investigation
  • Trial of colchicine
  • - Positive response may occur in other types
    of arthritis to include pseudogout.

16
Treatment Goals
  • Gout can be treated without complication.
  • Therapeutic goals include
  • - terminating attacks
  • - providing control of pain and inflammation
  • - preventing future attacks
  • - preventing complicaations such as renal
    stones, tophi, and destructive arthropathy

17
Acute Gout Treatment
  • NSAIDs
  • - Most commonly used.
  • - No NSAID found to work better than others
  • - Regimens
  • Indocin 50mg bid-tid for 2-3 days and then taper
  • Ibuprofen 400mg po q4-6 max 3.2g\day
  • Ketorolac 60mg IM or 30 mg IV X1 dose in
    patientslt65
  • - 30mg IM or 15 mg IVin single dose in
    patients gt65yo, or with patients who are renally
    impaired
  • Continue meds until pain and inflammation have
    resolved for 48hr

18
Acute Treatment
  • Colchicine
  • - Inhibits microtubule aggregation which
    disrupts chemotaxis and phagocytosis
  • - Inhibits crystal-induced production of
    chemotatic factors
  • - administered orally in hourly doses of 0.5
    to 0.6mg until pain and inflammation have
    resolved or until GI side effects prevent further
    use. Max dose 6mg/24hr
  • - 2mg IV then 0.5mg q6 until cumulative dose
    of 4mg over 24hr

19
Acute treatment contd
  • Corticosteriods
  • - Patients who cannot tolerate NSAIDs, or
    failed NSAID/colchicine therapy
  • - Daily doses of prednisone 40-60mg a day for
    3-5days then taper 1-2 weeks
  • - Improvemelnt seen in 12-24hr
  • ACTH
  • - Peripheral anti-inflammatory effects and
    induction of adrenal glucocorticoid release
  • - 40-80IU IM followed by second dose if
    necessary
  • Intra-articular injection with steroids
  • - Beneficial in patient with one or two large
    joints affected
  • - Good option for elderly patient with renal
    or PUD or other illness
  • - Triamcicnolone 10-40mg or Dexamethasone
    2-1mg alone or in combination with Lidocaine

20
Non- Pharmacologic Treatments
  • Immobilization of Joint
  • Ice Packs
  • Abstinence of Alcohol
  • - Consumption can increase serum urate levels
    by increasing uric acid production. When used in
    excess it can be converted to lactic acid which
    inhibits uric acid excretion in the kidney
  • Dietary modification
  • - Low cabohydrates
  • - Increase in protein and unsaturated fats
  • - Decrease in dietary purine-meat and seafood.
    Dairy and vegetables do not seem to affect uric
    acid
  • Bing cherries and Vitamin C

21
Prophylaxis
  • Frequent attacks gt3/years, tophi development or
    urate overproduction
  • Avoid use medications that contribute to
    hyperuricemia Thhiazide and loop diuretics,
    low-dose salicylates, niacin, cyclosprine,
    ethambutol
  • - Losartan promotes urate diuresis and may
    even normalize urate levels.
  • This action does not extend to other members
    of the ARB class.
  • - Useful in elderly with HTN and gout
  • Colchicine0.6mg qd-bid
  • - Use alone or in combination with urate
    lowering drugs
  • - Prophylaxis without urate lowering drugs
    may allow tophi to develop

22
Prophylaxis
  • Urate Lowering drugs
  • - Used for documented urate overproduction
  • - Goal is for serum urate concentration to
    6mg/dL or less
  • - Start of therapy can precipitate acute
    attack therefore, may need to use colchicine as
    a long as six months
  • - Xanthine oxidase inhibitors
  • Allopurinol block conversion of xanthine to uric
    acid. Works for underexcretors and overproducers
  • Start typically 300 mg/day and titrate weekly 100
    mg/day until optimal urate levels achieved.
  • Start lower doses with renally impaired patients
  • - Uricosuric drugs
  • Probenecid or sulfinpyrazone increase renal
    clearance of uric acid by inhibiting tubular
    absorption
  • Adverse effects may prohibit use-GI and kidney
    stones
  • Need measurement of 24 hrs urine in anyone for
    whom probenecid therapy is initiated.

23
Newer Therapies
  • Uricase enzyme that oxidizes uric to a more
    soluble form
  • Natural uricase from Aspergillus flavus and
    Candida utilis under investigation
  • Febuxostat New class of xanthine oxidase
    inhibitor
  • More selective than allopurinol
  • Little dependence on renal excretion
  • Losartan-ARB given as 50 mg/dL can be urisuric
    When given with HCTZ, it can blunt the effect of
    diuretic and potentiate its antihypertensive
    action
  • Fenofibrate Studies note when used in combo
    with allopurinol produced additional lowering of
    the urate

24
Complications
  • Renal failure
  • - ARF can be caused hyperuricemia, chronic
    urate nephropathy
  • Nephrolithiasis
  • Joint deformity
  • Recurrent gout

25
References
  • Kipple, JH. Primer on rheumatic disease. 12th ed.
    Arthritis foundation 2001 307- 323.
  • Schumacher HR, Chen LX. Newer therapeutic
    approaches Gout. Rheumatic disease clinics of
    north America 2006 32.
  • Pittman, JR, Bross, MH. Diagnosis and management
    of gout. American family physician 1999 59
  • Monu JU, Pope TL. Gout a clinical and
    radiologic review. Radiologic clinic of north
    America. 2004 42
  • Goldman. Cecil Texbook of medicine. 22nd ed. W.
    B. Saunders company 2004
  • Shen s, Wolfe R. Gout. Emergency medicine
    Clinical reviews. 2004
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