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Hey Doc, Ive Got the Gouch Diagnosis and Management of Gout

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A woman does not take the gout unless her menses are stopped. ... 84% had at least one episode of podagra. 90% had podagra or attack involving the foot ... – PowerPoint PPT presentation

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Title: Hey Doc, Ive Got the Gouch Diagnosis and Management of Gout


1
Hey Doc, Ive Got the Gouch! Diagnosis and
Management of Gout
  • Valerie Berger, M.D.
  • January 15, 2001

2
History
  • Earliest evidence of gout is on an Egyptian mummy
  • The Works of Hippocrates, 460-357BC
  • A woman does not take the gout unless her menses
    are stopped.
  • A youth does not get gout before sexual
    intercourse.
  • In gouty affections inflammation subsides within
    40 days.

3
History
  • Natures revenge for debauchery
  • Most of the Roman emperors suffered from gout

4
History
  • The term gout comes from the 10th century Latin
    word gutta meaning a drop
  • The first classic, clinical description of gout
    by Thomas Snydenham, 1683
  • Leeuwenhoek
  • 1848 Alfred Garrod identifies urate crystals in
    the blood

5
History
  • The advent of colchicine
  • Eber Papyrus mentions colchicine, dates to 1500BC
  • Derived from the Autumn crocus
  • Routine use was stopped from the Middle Ages
    until the mid 1700s because it was thought to be
    poisonous.

6
History
  • Universally accepted in the 19th century after
    the French standardized the potency
  • Ben Franklin
  • King George IV
  • Louis XVIII

7
History
  • Late 1800s brought the first uricosurics, but
    not widely used secondary to side effects
  • 1950s - The first tolerable uricosurics and
    xanthine oxidase inhibitors

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9
Pathology
  • Gout is associated with elevated serum uric acid
  • Uric acid is the end product of purine metabolism
  • Created by one of two pathways

10
Pathology
  • De Novo Pathway
  • Uric acid created from non-purine precursors
  • Salvage Pathway
  • Uric acid created from the recapture of nucleic
    acid from breakdown products.

11
Pathology
12
Pathology
  • Enzymatic deficiencies and increased nucleic acid
    turnover account for only 10 of gout patients.
  • Remaining 90 are primary gout due to an
    unknown defect limiting the ability to excrete
    uric acid.

13
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14
Pathology
  • Uric acid normally dissolves in plasma
  • Poorly soluble in synovial fluid and precipitates
    out as MSU crystals

15
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16
Pathology
  • Acute attack is not related to the presence of
    crystals in the joint, but rather to a cascade of
    events that occurs after activation of synovial
    macrophages.

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19
Epidemiology
  • Framingham Study, 1967
  • 1st large population study
  • prospective over 12 years
  • uric acid levels
  • x-ray findings
  • clinical symptoms

20
Epidemiology
  • 5,127 subjects (2,283 men and 2,844 women)
  • Age 30-59 at time of enrollment
  • Biennial exam
  • average of 7 physical exams preformed

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22
Epidemiology
  • Age had no effect on the mean serum uric acid
    level in men
  • But in women, there was an increase in mean uric
    acid levels between the ages of 40 and 50

23
Epidemiology
  • Average age of onset of gout
  • 47.7 in men
  • 54.1 in women
  • Prevalence of gout was 1.5 of the population
  • 2.8 of men
  • 0.4 of women

24
Epidemiology
  • What is the relationship between hyperuricemia
    and gout?
  • What is an abnormal uric acid level?
  • Gout screening
  • How low does the uric acid need to be?

25
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26
Epidemiology
  • There was no specific level at which uric acid
    was abnormal
  • Many patients who are hyperuricemic do not have
    symptoms
  • Since there was no definitive cut off, uric acid
    levels gt6mg/dl in men and gt5.6mg/dl in females
    were arbitrarily picked as abnormal values

27
Epidemiology
  • Clinical features
  • 25 had only one attack during the study
  • The average number of attacks was 5
  • 23 of men and 10 of women had gt5 attacks
  • No difference in the mean uric acid levels in
    those with gt10 attacks versus the gouty
    population as a whole

28
Epidemiology
  • Clinical features
  • 84 had at least one episode of podagra
  • 90 had podagra or attack involving the foot
  • Only 13 ever had an attack involving the upper
    extremities.

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30
Diagnosis
  • No standard classification of gout until 1977
  • Wallace, et al. did a chart review of 700
    patients from Rheumatology clinics
  • gout
  • psuedogout
  • rheumatoid arthritis
  • septic arthritis

31
Diagnosis
  • More than one attack
  • Maximum inflammation in one day
  • Monoarthritis
  • Redness
  • First MTP involved
  • Unilateral first MTP
  • Unilateral tarsal attack
  • Tophus
  • Hyperuricemia
  • Asymmetric swelling
  • Subcortical cysts
  • MSU crystals in joint fluid
  • Joint fluid culture negative

32
Diagnosis
  • The gold standard for diagnosis of gout is joint
    aspiration and crystal identification
  • Chart review revealed that not all gout patients
    had a tap
  • 50 of gout pts
  • 25 of RA pts
  • 80 of psuedogout pts
  • 70 of septic arthritis pts

33
Diagnosis
  • Is this because gout affected joints are
    difficult to tap?
  • Crystals were only found in 84.4 of those
    patients with gout
  • Can the diagnosis gout be made strictly by
    history?

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36
Diagnosis
  • 6 out of 12 positive criteria provides best
    sensitivity and specificity
  • 6 out of 12 positive criteria plus identification
    of crystals identifies 97.8 of patients with
    gout.

37
Diagnosis
  • Do I need a twenty four hour urine if I think my
    patient has gout?

38
Diagnosis
  • 24 hour urines help discriminate between
    over-excreters and under-excreters among
    those patients with hyperuricemia

39
Diagnosis
  • Over-excreters
  • enzymatic deficiencies
  • high metabolic turnover states
  • excrete more than 800mg of uric acid/24hrs
  • account for 10 of patients with gout
  • Under-excreters
  • Unknown defect
  • excrete less than 800mg of uric acid/24hrs
  • account for 90 of patients with gout

40
Diagnosis
  • gt800mg uric acid excretion
  • Needs further workup to uncover etiology of
    hyperuricemia.
  • Treated exclusively with xanthine oxidase
    inhibitor (allopurinol)
  • lt800mg uric acid excretion
  • No further work up needed
  • May be treated with a uricosuric (probenecid) or
    xanthine oxidase inhibitor (allopurinol)

41
Diagnosis
  • 24 hour urine collection problems
  • messy
  • storage
  • preservative
  • precipitation of crystals

42
Diagnosis
  • 1979 Simkin, et al. evaluated the utility of a
    spot urine for uric acid levels versus a 24 hour
    collection.
  • 19 physicians and health care workers collected
    24 hour samples.
  • Compared these to several mid-morning spot urines
    from the controls, from 10 normal patients, and
    36 men with gout and normal renal function.

43
Diagnosis
  • No significant difference in the mid-morning spot
    urine values and the 24 hour values.
  • Mean uric acid excretion among the normal men was
    0.4/-0.095mg/dl
  • Of the men with gout, only 8 excreted greater
    than 0.7mg/dl

44
Diagnosis
  • Conclusions
  • Crystal identification is the best
  • If crystals cannot be obtained, use the history
  • Determination of uric acid excretion is not
    mandatory unless underlying pathology is
    suspected (young age, signs of malignancy) or
    long-term antihyperuricemic agents are needed

45
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46
Stages of Gout
  • Asymptomatic Hyperuricemia
  • Acute Attack
  • Intercritical Period
  • Chronic Gout

47
Asymptomatic Hyperuricemia
  • Do nothing unless they become symptomatic

48
Acute Attack
  • NSAIDS
  • Indomethacin
  • 150mg followed by 50mg q6-8 hours times 6-8 doses
  • then decrease to 25 mg q6-8 hours.
  • Symptoms usually resolve in 5-7 days

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51
Acute Attack
  • The VA study
  • 10 men given 800mg Motrin q8 hrs
  • Dose decreased to 400mg q8 hrs after pain relief
  • Questioned regarding pain relief, dyspepsia,
    nausea and vomiting.

52
Acute Attack
  • All men had significant reduction in pain at 24
    hours
  • All had complete relief at 72 hours
  • No side effects reported

53
Acute Attack
  • Sparked flury of other studies looking at every
    new NSAID that hit the market
  • Basic conclusion from all of them is any short
    acting NSAID is effective in terminating an
    attack
  • 800mg ibuprofen q6-8hrs
  • However, there are side effects, primarily GI and
    renal

54
Acute Attack
  • Colchicine
  • 0.6mg q1-2hrs times 16 doses
  • Take until pain relief or side effects occur
  • GI upset
  • Diarrhea

55
Acute attack
  • Before 1987 there was no RCT proving that
    colchicine actually altered the course of acute
    gout.
  • 42 pts with gout randomized to receive 1mg of
    colchicine followed by 0.5mg q2hrs until relief
    or toxicity, or placebo

56
Acute Attack
  • 2/3 of colchicine group reported pain relief
    versus 1/3 of placebo
  • All patients receiving colchicine developed
    toxicity
  • 91 reported developing it before relief of pain
  • Study limited by inpatient population, small
    numbers and a mean 38hr delay between onset of
    symptoms and enrollment

57
Acute Attack
  • Colchicine is effective in aborting an attack
  • Side effects must be contended with
  • Best used at the first sign of an impending attack

58
Acute Attack
  • Intra-articular corticosteroid injections
  • Can aspirate fluid at the same time
  • Good option for those who cant take NSAIDS or
    tolerate colchicine

59
Acute Attack
  • Systemic Steroids
  • 30-60mg Prednisone tapered over 7-10 days
  • again good for patients who cant tolerate NSAIDS
    or colchicine

60
Acute Attack
  • ACTH
  • Less commonly used
  • 40-80 units IM twice a day for two days then
    daily for 2-3 days.

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62
Intercritical Gout
  • Joint aspiration will often find uric acid
    crystals, but no accompanying inflammation
  • Typically no need for drug intervention at this
    time

63
Intercritical Gout
  • Antihyperuricemic therapy indicated if
  • Multiple attacks per year
  • Multiple joints are involved at one time
  • Extreme hyperuricemia (gt12mg/dl)
  • Evidence of bone or joint destruction

64
Intercritical Gout
  • Colchicine
  • 0.6mg qd, bid, or tid
  • May be used in the short term to prevent an acute
    attack when starting probenecid or allopurinol

65
Intercritical Gout
  • Uricosurics
  • Probenecid and sulfinpyrazone
  • Used to lower serum uric acid levels
  • Promotes uric acid excretion by blocking renal
    tubular reabsorption
  • Best in patients with normal renal function and
    uric acid excretion lt800mg/day

66
Intercritical Gout
  • Probenecid
  • Starting dose is 0.5g twice a day
  • Then increase to a total 1.5g per day up to a max
    of 2g per day in divided doses
  • GI distress, hypersensitivity rxn, precipitation
    of stones and an acute attack
  • Never start in an acute flare
  • Use NSAIDS and colchicine to stop any inflammation

67
Intercritical Gout
  • Xanthine Oxidase Inhibitors
  • Reduces serum uric acid by inhibiting the
    production of it
  • Allopurinol
  • Can be used in both under and over-excreters
  • Safe in patients with creatinine clearance lt50
    of normal

68
Intercritical Gout
  • Allopurinol
  • Starting dose is 200mg per day
  • Increase over the next 2-3 weeks until urate
    level decreases
  • Max dose is 800mg/day but doses gt600mg/day
    increase risk of side effects

69
Intercritical Gout
  • Allopurinol
  • Side effects include rash, hepatitis, vasculitis,
    and bone marrow suppression
  • Hypersensitivity reaction
  • TEN
  • fever
  • hepatitis
  • eosinophilia
  • worsening renal function

70
Intercritical Gout
  • Allopurinol
  • More likely to have side effects if renal
    function is poor
  • Can desensitize
  • Dont use in an acute flare
  • Can precipitate an acute attack

71
Intercritical Gout
  • Prevention
  • Trauma
  • Surgery
  • Dehydration
  • Alcohol
  • Certain foods

72
Intercritical Gout
  • Organ meats
  • Wild game
  • Seafood
  • Lentils
  • Peas
  • Asparagus
  • Yeast
  • Beer

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74
Chronic Gout
  • Rare
  • Continuous symptoms despite treatment
  • Morning stiffness, synovial thickening, and joint
    deformity.
  • Gouty erosions on x-ray
  • Tophi

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77
Chronic Gout
  • Continue treatment with antihyperuricemic agents
  • Continue treatment for acute flares.

78
Future Therapy
  • 1988 Chua, et al. published a case report
  • Pt with lymphocytic lymphoma and hypersensitivity
    to allopurinol.
  • Urate was lowered using PEG-uricase

79
Future Therapy
  • Uricase oxidizes uric acid to allantoin which is
    much more soluble than uric acid
  • Humans and birds lack this enzyme
  • Uricase can reduce serum uric acid if given to
    species that lack the enzyme
  • Efficacy diminishes over time due to the
    formation of antibodies

80
Future Therapy
  • Antigenicity may be reduced by the attachment of
    monomethoxypolyethylene glycol (PEG) to the
    uricase
  • 2001 Duke University enrolling subjects with
    severe gout, lymphoid malignancies organ
    transplants to receive PEG-uricase
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