gout arthritis 2011

8/3/2019 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.

gout arthritis 2011

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