gout & pseudogout gout typically follows years of asymptomatic hyperuricemia serum urate...
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GOUT &
PSEUDOGOUT
HOWARD L. FEINBERG, D.O.,F.A.C.O.I., F.A.C.R.
ACOI BOARD REVIEW 2018(No Disclosures)
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GOUTHyperuricemia is not
gout
Gout typically
follows years of
asymptomatic
hyperuricemia
Serum urate
increased by
alcohol, height, body
weight, age, blood
pressure, BUN,
creatnine
13.6/1000 in men
6.4/1000 in women
estrogen causes
increased uric acid
excretion
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CLASSIFICATION CRITERIA
Step 1: Entry Criteria – swelling pain and
redness in a peripheral joint or bursa
Step 2: Sufficient criterion (if met does not
require other criteria) – MSU crystals in a
symptomatic joint or bursa
Step 3: Apply criteria if step 2 is not met
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CLASSIFICATION CRITERIA(Requires 9 points)
Characteristics (1-3 points)
– Erythema over joint
– Can’t bear touch
– Inability to walk or use joint
Time Course (one episode
1 point, recurrent 2 points)
– <24 hours
– Resolves in <14 days
– Complete resolution
between episodes
Evidence of Tophus (4
points)
Serum Urate
– <4 (-4 points)
– 6-8 (2 points)
– 8 – 10 (3 points)
– > 10 (4 points)
MSU negative (-2 points)
Imaging
– Urate deposit evidence (4
points)
– Typical damage evidence
(4 points)
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ASSOCIATED
CONDITIONS
Obesity
Ethanol
Diabetes Mellitus
Hypertriglyceridemia
Hypertension
Hypothyroidisim
Atherosclerosis
Metabolic Syndrome
Pregnancy
Acute Illness
Dehydration
Psoriasis
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NEGATIVE
ASSOCIATIONS
Rheumatoid Arthritis
SLE
Ankylosing Spondylitis
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CLINICAL
Asymptomatic Hyperuricemia
Acute Gout
Intercurrent Period
Acute Gout
Chronic Gout
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PRESENTATION
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PATHOLOGYMonosodium Urate
Crystals are formed
when the bodies
capacity to store uric
acid is surpassed
Uric acid is a
byproduct of purine
metabolism
Serum saturation
6.7mg/dl
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TOPHI
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RADIOGRAPHIC
FINDINGS
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Hyperuricemia
Primary Hyperuricemia
Hyperuricemia which is
not caused by or
secondary to another
disorder.
Idiopathic
underexcretion - 90%
overproduction - 10%
Secondary
Hyperuricemia
Hyperuricemia which
occurs as a result of a
drug effect or is
secondary to another
disease
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OVERPRODUCTION
PRIMARY HYPERURICEMIA
HGPRT Deficiency (Hypoxanthine Guanine Phosphoribosyltransferase Deficiency)
PRPP Synthetase Superactivity(Phosphoribosylpyrophosphate synthetase superactivity)
G-6-P-D Deficiency
Fructose-1-Phosphate Aldolase Deficiency
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OVERPRODUCTION
SECONDARY HYPERURICEMIA
Diet
Myeloproliferative
Disorders
Lymphoproliferative
Disorders
Accelerated ATP
Degradation
Glycogen Storage
Disease (type I, III,
V, VII)
Severe Muscle
Exertion
Hemolytic Disease
Psoriasis
G-6-PD Deficiency
Fructose-1-
Phosphate Aldolase
Deficiency
HGPRT Deficiency
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Under Excretion1o Hyperuricemia
– Idiopathic
2o Hyperuricemia– inhibition of tubular
urate secretion (DKA,
lactic acidosis, Maple
Syrup Urine Disease,
Alcoholic Ketosis)
– enhanced tubular
reabsorbtion
(dehydration, diuretics)
Unknown Mechanism
– Hypertension
– Lead
– Hyperparathyroid
– Drugs
Cyclosporine
ASA
Ethambutol
Pyrazidamide
Ethanol
Nicotinic Acid
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Combined Overproduction &
Underexcretion
Glucose - 6- Phosphatase Deficiency
Fructose -1-phosphate aldolase deficiency
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INDICATIONS FOR
TREATMENT
Acute Gout
Tophi
Uric Acid Stones
Uric Acid Nephropathy
Interstitial Nephritis
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TREATMENT GOALS
Stop acute attacks
Resolve Tophi
Prevent joint damage
Decrease uric acid below 6.0
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TREATMENTAcute
– colchicine
– Indomethacin
– Other NSAID
– Steroid
– Pain Medication
– ACTH
– Joint Injection
– Anakinra (Kineret)
Interleukin-1 receptor
antagonist
Chronic
– Allopurinol
– Febuxostat
– Probenecid
– NSAID
– Colchicine
– Sulfinpyrazone
– Pegloticase (Krystexxa)
– Anakinra ? (Kineret)
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CALCIUM
PYROPHOSPHATE
Common name Pseudogout
Occurs exclusively in and around joints
May be asymptomatic or cause disease
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CLINICAL
PRESENTATIONSAcute
– similar to gout
– may have fever, leukocytosis, elevated ESR
Chronic
– similar to OA
– symmetrical
– mainly in knees, wrists, hips
– isolated patellofemoral disease
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CLINICAL
PRESENTATIONS
Polyarticular-may mimic Rheumatoid
Arthritis
Oligoarticular-usually elderly
Pyrophosphate Arthropathy
– Early-mimics Osteoarthritis
– Late-Charcot Joint
Precocious Osteoarthritis
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CHONDROCALCINOSIS
Rheumatoid 5%
– 10% RF positive
Gout 25%
OA 50%
Asymptomatic 20%
Present in– 4% of adult population
– 50% over age 90
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EPIDEMIOLOGYHereditary -
autosomal
dominant
Post Traumatic
Sporadic-rare
under age 40
Osteochondro-
dysplasia
2o To Metabolic
Disease– hemachromatosis
– hyperparathyroid
– hypothyroid
– amyloid
– hypomagnesemia
– hypophosphatemia
– Rickets
– Familial hypocalcuric
hypocalcemia
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RADIOGRAPHIC
FINDINGSChondrocalcinosis
Crowned Dens
– neck pain due to
crystal deposits
surrounding dens
Cord compression
Wrap Around
Patella
Erosive OA
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DIAGNOSISDefinite– crystals in joint
Probable– other calcium crystals in joint
Possible– X-Ray findings
– Typical joint distribution
– History
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CALCIUM
PYROPHOSPHATE
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PATHOLOGYNormal serum phosphate
Normal phosphate excretion
Elevated levels of inorganic
phosphate in synovial fluid
NTPPPHase = Cause (Nucleoside triphosphate pyrophosphohydrolase)
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TREATMENTNSAID
Colchicine
Steroids
Physical Therapy
Surgery
Joint Injections
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APATITE -LIKE
CRYSTALS
Carbonate substituted apatite
Octacalcium Phosphate (OCP)
Tricalcium phosphate (TCP)
Dicalcium phosphate dihydrate (brushite)
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APATITE - LIKE
DISEASEBursitis
Tendonitis
Arthritis
Renal Failure
epiphyseal
dysplasia
destructive OA
Crystals not visible
on microscopy
Alizaren Red-stain
red
von Kossa-stain
black
precise ID requires
x-ray diffraction
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Contact Information
Howard Feinberg, D.O., F.A.C.O.I., F.A.C.R.
1310 Club Drive
Vallejo, CA 94592