Dr. Joseph P. Sibarani

GOUT
dr. Joseph P. Sibarani

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
 May be signal for
unrecognized comorbidities
– Obesity
– Metabolic syndrome
– DM
– HTN
– CV disease
– Renal disease
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
HYPERURICEMIA & GOUT
 Hyperuricemia is caused by
1. Overproduction
2. Underexcretion
 No Gout without crystal deposition

GOUT:
A Chronic Disease of 4 stages
1. Asymptomatic hyperuricemia
2. Acute Gouty Flares
3. Intervals between flares
4. Advanced Gout & Complications

2. 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
Sites of acute flares
 90% of gout
patients eventually
have podagra : 1st
MTP joint
Sites
 Can occur in other

joints, bursa &
tendons
3. INTERVALS BETWEEN
FLARES
 Asymptomatic
 If untreated, may advance
 Intervals may shorten

 Crystals (+) in asymptomatic joints
 Body urate stores increase
3. INTERVALS BETWEEN
FLARES
 Silent tissue
deposition &
Hidden
Damage
4. ADVANCED GOUT
 Chronic Arthritis
 X-ray Changes
 Tophi Develop
 Acute Flares continue

4. ADVANCED GOUT
 Chronic Arthritis
 Polyarticular acute
flares with upper
extremities more
involved
TOPHI
 Solid urate deposits

in tissues
TOPHI
 Irregular &
destructive
TOPHI RISK FACTORS
 Long duration of hyperuricemia
 Higher serum urate
 Long periods of active, untreated gout

RADIOLOGIC SIGNS
X-RAYS
X-RAYS
DIAGNOSING GOUT
 History + Physical examination
 Synovial fluid analysis
 Not Serum Urate..!!

SERUM URATE LEVELS
 Not reliable
 May be normal with flares
 May be high from other causes

GOUT RISK FACTORS
 Male
 Postmenopausal female
 Older age
 Hypertension
 Pharmaceuticals:
– Diuretics,
– ASA,
– Cyclosporine
GOUT RISK FACTORS
 Transplant patients
 Alcohol intake
– Highest with beer
– Not increased with wine
 High BMI (obesity)
 Diet high in meat & seafood
SYNOVIAL FLUID ANALYSIS
(Polarized Light Microscopy)
 The Gold standard
 Crystals intracellular during attacks
 Needle & rod shapes
 Strong negative birefringence

SYNOVIAL FLUID
DIFFERENTIAL
DIAGNOSIS
 Pseudogout: Chondrocalcinosis, CPPD

 Psoriatic Arthritis
 Osteoarthritis
 Rheumatoid arthritis
 Septic arthritis
 Cellulitis
Gout vs. CPPD
 Similar Acute attacks
 Different crystals under Micro;

Rhomboid, irregular in CPPD
Gout vs CPPD
RA vs Gout
 Both have polyarticular, symmetric

arthritis
 Tophi can be mistaken for RA nodules

RA vs Gout
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
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)
Acute Flare Med Choices
 NSAIDS
 Colchicine
 Corticosteroids
MED Considerations
 NSAIDS :
Interaction with
warfarin
Contraindicated in:
Renal disease
PUD
GI bleeders
ASA-induced RAD
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
MED Considerations
Corticosteroids :
 Worse glycemic control
 May need to use mod-high doses

TREATMENT GOALS
Protect against future flares
Reduce chance of crystal inflammation

Lower serum urate to deplete total body
urate pool
Correct metabolic cause
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 drug, Best with
6 months of concommitant RX
EBM
– Won’t stop destructive aspects of gout
TREATMENT GOALS
Protect against future flares
Reduce chance of crystal inflammation

Lower serum urate to deplete total body
urate pool
Correct metabolic cause
PREVENT DISEASE
PROGRESSION
 Lower urate to < 6 mg/dl : Depletes
Total body urate pool & Deposited crystals
EBM
 Drugs prescription is lifelong & continuous
 MEDical choices :
– Uricosuric agents
– Xanthine oxidase inhibitor
PREVENT THIS
URICOSURIC AGENTS
 Probenecid
– Increased secretion of urate into urine
– Reverses most common physiologic

abnormality in gout ( 90% pt.s are
underexcretors)
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
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
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)
NEW AGENTS
 RX gaps :
– Can’t always get urate < 6
– Allergies
– Drug interactions
– Allopurinol intolerance
– Worse Renal disease
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
CASE STUDIES
CASE J.F.
 80 YO W F c/o acute overnight pain &

swelling in R knee
 PE: 5’1’’ & 180 lbs
R knee swollen, warm & erythematous
 PMH : HTN x 5 yrs
 Meds: HCTZ (25 QD) & Aspirin
 SH : 20 PY smoker; 5 wine drinks/wk
WHAT ARE J.F.’s RISK
FACTORS FOR GOUT ?
 HTN
 SMOKER
 Hydrochlorothiazide
 Aspirin
 WINE CONSUMPTION
 OBESITY
 AGE
 POSTMENOPAUSAL
HOW WOULD YOU DX
GOUT ?
A. HX & PE COMPATIBLE
B. CHECK SERUM URATE LEVEL
C. ASSESS SYNOVIAL FLUID
D. TRIAL OF COLCHICINE
E. CHECK X-RAYS
IF YOU DX GOUT, WHAT
RX TODAY? (& Why?)
A. MOTRIN
B. INDOCIN
C. PREDNISONE
D. ALLOPURINOL
E. PROBENECID
F. COLCHICINE
NEXT STEP FOR J.F. ?
A. Modify risk factors

B. Give refills to rx next flare
C. Start colchicine to prevent flares
D. Check serum urate level
E. Start allopurinol
F. Start probenecid
CASE M.B.
 56 YO W M c/o hand stiffness & growths

 PE : 6’2’’ & 205 lbs
Multiple tophi; chronic arthritis
 PMH : DM x 8 yrs; gout x4 yrs, but no flares
x 3 yrs, lost 20# on Atkins diet
 Meds: Glyburide; colchicine (0.6 mg TID)
 Labs: Creat.= 2.0; Urate = 11.4
IN WHAT STAGE OF GOUT
IS M.B. ?
 A. Doesn’t have gout
 B. ASX. Hyperuricemia
 C. Interflare period
 D. Advanced Gout
WOULD YOU CHANGE
MD’S RX ?
 No – Not gout
 No – No flare x 3 yrs.
 Yes - Increase colchicine
 Yes – Add allopurinol
 Yes – Add benemid
WHAT OTHER ISSUES
WOULD YOU CONSIDER ?
 Renal dysfunction
 Weight
 DM
 Glyburide
 Diet
CONCLUSIONS
 Gout is chronic with 4 stages

 Uncontrolled gout can lead to severe
disease
 Separate RX for flares & preventing
advancement
 Many meds for flares
 Treating the disease requires lowering urate
 Get a 24-hr urine for urate excretion
QUESTIONS

Dr. Joseph P. Sibarani

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GOUT

dr. Joseph P. Sibarani

 Identify diagnostic criteria for gout

 Identify 3 treatment goals for gout

 Name the agents used to treat the

 Urate: end product of purine metabolism

 Hyperuricemia: serum urate > urate

 Gout: deposition of monosodium urate

 No Gout without crystal deposition

2. Acute Gouty Flares

3. Intervals between flares

4. Advanced Gout & Complications

 Abrupt onset of severe joint

 Can occur in other

 If untreated, may advance

 Intervals may shorten

 Acute Flares continue

 Solid urate deposits

 Long duration of hyperuricemia

 Higher serum urate

 Long periods of active, untreated gout

 History + Physical examination

 Synovial fluid analysis

 Not Serum Urate..!!

 May be normal with flares

 May be high from other causes

 Crystals intracellular during attacks

 Needle & rod shapes

 Strong negative birefringence

 Pseudogout: Chondrocalcinosis, CPPD

 Similar Acute attacks

 Different crystals under Micro;

 Both have polyarticular, symmetric

 Tophi can be mistaken for RA nodules

 Rapidly end acute flares

 Prevent disease progression

 Control inflammation & pain & resolve

 Drug interaction : Statins, Macrolides,

 Cautious use in : renal or liver

 May need to use mod-high doses

 Prevent disease progression

– Both decrease freq & severity of flares

 Prevent disease progression

– Increased secretion of urate into urine

– Reverses most common physiologic

 Base choice on above considerations &

 Catabolize urate to allantoin:

 Currently approved for hypoeruricemia in

 Some concerns: fatal immunogenicity &

 80 YO W F c/o acute overnight pain &

A. Modify risk factors

 56 YO W M c/o hand stiffness & growths

 A. Doesn’t have gout

 Gout is chronic with 4 stages

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