gout arthritis 2011
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Gout
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Gout
Gout is defined as a peripheral arthritis
resulting from the deposition of sodium urate
crystals in one or more joints.
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Gout
Gout encompasses a group of disorders thatoccur alone or in combination and include (1)hyperuricemia, (2) attacks of acute, typically
monarticular, inflammatory arthritis, (3)tophaceous deposition of urate crystals in andaround joints, (4) interstitial deposition ofurate crystals in renal parenchyma, and (5)
urolithiasis
Copyright 1998 McGraw-Hill. All rights reserved.
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Gout
Affects less than 0.5% of the population
Due to familial disposition, incidence may be
as high as 80% in families affected by disorder.
Stoffey et al, Emed 2002
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Gout
Typical sequence involves progression
through:
asymptomatic hyperuricemia
acute gouty arthritis
interval or intercritical gout
chronic or tophaceous gout
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Pathophysiology
Urate saturates in plasma at 7 mg/dL Assuming pH, temp, Na are WNL
MSU deposits in less vascular tissue Cartilage
Tendons/ligaments There is a predilection for peripheral
joint/tissue
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Pathophysiology
Primary gout: Overproducers: 10%
Under-excretors: 90%
Secondary gout: Excess nucleoprotein turnover (lymphoma, leukemia)
Increased cell proliferation/death (psoriasis) Rare genetic disorder Lesch-Nyan Syndrome
pharmaceuticals
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Signs and Symptoms
Acute attack: Over hours frequently nocturnal
Excruciating pain
Swelling, redness and tenderness
Podagra: 1st MTP classic presentation
May effect knees, wrist, elbow, and rarely SI and hips.
Chronic:
Destructive tophacous Much greater chance if untreated
Rarely presents as a chronic
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Signs and Symptoms
Renal lithiasis
Uric acid nephropathy
Urate nephropathy
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Diagnosis
Based on history and physical
Confirmed by arthrocentesis Urate crystals: needle-shaped negatively birefringent
either free floating or within neutrophils &
macrophages.
Uric acid level non specific.
30% may show normal level Urine collection:
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Microscopic Diagnosis
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Gout Arthritis
Gout can also occur as a
result of
overproduction of uric
acid Gout is an attack of uric
acid deposits in joints
Usually found in joints
of feet and legs
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What is Gout Arthritis
Purines are not
properly processed in
our body
Excreted throughkidneys and urine
Hyperuricemia- build-
up of uric acid in body
and joint fluid
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The Four Stages of Gout
Asymptomatic
Acute
Intercritical
Chronic
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ASYMPTOMATIC
A- meaning without
indicates that there are
no symptoms associated
Patient will be unawareof what is happening
Gout can only be
determined with the
help of a physician
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ACUTE
Sever and sudden
onset
Involve one or a few
joints
Frequently starts
nocturnally
Joint is warm, red,
and tender
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INTERCRITICAL
More concentration of
uric acid crystals
Typically no need for
drug intervention at the
time.
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CHRONIC
Continuous or
persistent over a long
period of time
Treatment required Not easily or quickly
resolved
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SYMPTOMS
Joint pain Affects one or more joints : hip, knee, ankle,
foot, shoulder, elbow,wrist, hand, or other joints Great toe, ankle and knee are most common
Swelling of Joint Stiffness
Warm and red Possible fever
Skin lump which may drain chalky material
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Diagnosing Gout
X-rays
Arthrocentesis-
extraction of joint fluid
Examination of joint
Patient medical history
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Epidemiology
Prevalence of hyperuricemia
2.3 41.4% in various populations.
Corresponds with serum creatinine /BUN levels, body weight, height, age,
blood pressure, and alcohol intake. (Taiwan)
Body bulk (as estimated by body weight, surface area, or body mass index)has proved to be one of the most important predictors of hyperuricemia in
people of widely differing races and cultures.
Incidence of Gout
Varies depending on population studied 1.8 /1000 3.2/1000
RR for blacks slightly higher (1.3)
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1977 ACR criteria for acute gout
The presence of characteristic urate crystals in the joint fluid, or a tophus proved to containurate crystals by chemical means or polarized light microscopy, or the presence of 6 of thefollowing 12 clinical, laboratory, and radiographic phenomena:
1. More than one attack of acute arthritis
2. Maximum inflammation developed within 1 day
3. Monoarthritis attack
4. Redness observed over joints
5. First metatarsophalangeal joint painful or swollen
6. Unilateral first metatarsophalangeal joint attack
7. Unilateral tarsal joint attack
8. Tophus (proven or suspected)
9. Hyperuricemia
10. Asymmetric swelling within a joint on x ray/exam
11. Subcortical cysts without erosions on x ray 12. Monosodium urate monohydrate microcrystals in joint fluid during attack
13. Joint fluid culture negative for organisms during attack
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Classification of Hyperuricemia and Gout
Primary Hyperuricemia and Gout with NoAssociated Condition
Uric acid undersecretion(80%90%)
Idiopathic
Urate overproduction (10%20%)
Idiopathic
HGPRT deficiency
PRPP synthetase overactivity
Secondary Hyperuricemia and Gout withIdentifiable Associated Condition
Uric acid undersecretion
Renal insufficiency
Polycystic kidney disease
Lead nephropathy
Drugs(Diuretics,Salicylates (lowdose), Pyrazinamide, Ethambutol,Niacin, Cyclosporine, Didanosine )
Urate overproduction
Myeloproliferative/ Lymphoproliferativediseases / Hemolyticanemias/ Polycythemia vera/Othermalignancies
Psoriasis/Glycogen storage disease Dual mechanism
Obesity, ETOH,Hypoxemia andhypoperfusion
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Outcomes in Gout
Clinical outcomes 60% of untreated gout have attacks within 1 yr , 78% have recurrence
in 2 yrs, only 7% have no attacks in 10 yrs.
Chronic tophaceous gout develops after 10 -20 yrs of untreated gout.
Incidence decreased from 14% in 1949> 3% in 1972.(Oduffy et al)------colchicine effect
Hyperuricemia control superior to self medication alone. Humanistic outcomes
Treatment outcomes decrease QOL in pts with gout.
Adherence to allopurinol only 56%. (Riedel et al , managed care study)
Economic outcomes
Direct burden annually is 27.4 million USD. (men only) Patients with acute gout miss 3-5 days of work annually.
Average cost-effectiveness ratio for patients using urate-loweringdrugs is $487 to $983 compared with a cost of $5070 to $6571 forthose not using these agents.
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Diagnosis Clinical :
In men , initial attack monoarticular 1st MTP joint(50% of cases)
Other jts involved instep/knees/wrists/ olecranon bursa. Often begins atnight. Usually abrupt , severely painful.
Later attacks polyarticular , assoc with systemic signs., most often initialpresenting complaint in women. (hands/tarsal jts/knees)
Precipitants Minor trauma , ETOH, diuretic Rx, Surgery, severe medical
illness, hypouricemic Rx. Tophi Classically , helix/ antihelix ,but rare ; more common , hands, feet,
olecranon bursa. Complications : ulceration/infection.
Laboratory:- GOLD STANDARD SF Analysis WBC ct 2000-100 000/ml
MSU crystals- needle shaped , negatively birefringent.
Serum Uric acid level important in monitoring treatment .(42% - normallevels)
24 hr uric acid collectionuseful in young pts with gout/ + fam h/o
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Diagnosis
Radiologic
X RAY :
Punched out erosions
only 45% of pts have
them, takes 6 yrs todevelop
Martels sign
CT/MRI/US/Bone scan
Sensitive , non specific
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Treatment
Acute gouty arthritis: Anti- inflammatory drugs ( if s.creat < 2mg/dl, no PUD)
Colchicine preferred in pts without confirmed diagnosis of gout. Endpoints improvement in jt symptoms/ GI symptoms/ 10 doses taken.
NSAIDs if diagnosis confirmed. Any NSAID can be used . Newer agents Etoricoxcib 120 OD comparable to indomethacin 50 TID.
In c/o renal failure /PUD - IM ACTH , oral /iv prednisone.
Avoid adjusting dosage of urate lowering agents.
Prophylaxis : Only indicated if patient is started on urate lowering Rx.
Colchicine( 1-3 pills a day)/ NSAID( in colchicine intolerant).
Does not alter crystal deposition and development of tophi.
Continue till serum urate levels stabilize and no attacks for 3 6 mths.
If long term prophylactic colchicine given, check CBC ,CK every 6 mths.
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Treatment (contd)
Control of hyperuricemia Differing opinions regarding initiation esp. around 1st
attack. Clear evidence if erosions + on X-ray / chronic tophaceous
gout/ >2 gout attacks per year.
Goal : s. urate levels < 6 mg%. Serial s. uric acid at least once every 6 mths upon
initiation. Choice of agents :
Xanthine oxidase inhibitor
Uricosuric agents. Equal efficacy in pts with normal renal function and
who excrete < 800 mg/day of uric acid.
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Treatment (contd)
Xanthine oxidase inhibitors
Allopurinol- only prescription drug available.
Renally excreted, therefore adjust dose if s.creat > 2mg% or CrCl
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Treatment (contd)
Adjuvant Rx Control obesity ,ETOH intake, hyperlipidemia ,HTN
Losartan / fenofibrate weakly uricosuric
Diet moderation in purine intake. Makes a difference of up to 1mg %
in s. uric acid. Beer, other alcoholic beverages.
Anchovies, sardines in oil, fish roes, herring.
Yeast.
Organ meat (liver, kidneys, sweetbreads)
Legumes (dried beans, peas)
Meat extracts, consomm, gravies.
Mushrooms, spinach, asparagus, cauliflower
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Treatment (contd)
Newer agents
PEG- uricase
Febuxostat
Asymptomatic hyperuricemia Investigate cause
No recommendations for Rx.
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