Gout

GOUT
(clinical pharmacy)
Pawan maharjan
Introduction
• Gout is a disease characterized by recurrent acute attack of urate crystal
induced arthritis.
• It is disorder of purine metabolism in which the blood uric acid level is
raised either due to over production or impaired excretion.
• Hyperuricaemia is cause of gout as excess uric acid get deposited in
different joint as urate crystal.
• Normal plasma uric acid 3.4–7.2 mg/dl for men and for female 2.4–6.1
mg/ dl).
• Uric acid, a product of purine metabolism, has low water solubility,
especially at low pH.
• When blood uric acid levels are high, it precipitates and deposits in
joints, kidney and subcutaneous tissue as sodium urate.
• Characterized by pain, inflammation in joints.
TYPES OF GOUT according to ETIOLOGY
• Primary gout: It is usually due overproduction or under
excretion of uric acid without any other secondary cause or
disease condition.
• Secondary gout: It occur due secondary disease or due to use
of medicines
a) Leukaemias, lymphomas, polycythaemia especially when
treated with chemotherapy or radiation: due to enhanced
nucleic acid metabolism and uric acid production.
(b) Drug induced-thiazides, furosemide, pyrazinamide,
ethambutol, levodopa, reduce uric acid excretion by kidney
Classification of gout according clinical
presentation
• Asymptomatic hyperuicemia
• Acute intermittent gout (gouty arthritis)
• Inter critical gout
• Chronic tophaceous gout
Classificaiton..
• Asymptomatic: In this, there is hyperuricemia but there
is not any symptom. Drug treatment is not required.
Non pharmacological treatment is enough.
• Acute intermittent: There is episode of acute attack.
Symptom may be confined to a single joint or multiple
joints and other systemic symptom.
– Initial attack usually occur at night or in early morning,
swollen, hot and tender joints.
– Intially such attack last for 3-14 days, latter affect may more
joints. Systemic symptom such as fever, chills, malaise and
pruritis might also seen
Classifcaiton…
• Intercritical gout: It is symptom free period interval
between attack. In most patient, second attack occur within
1 year but sometime delayed for 5 yr as well.
• In this phase also there is hypeuricaemia.
• Chronic tophaceous gout: Usually develop after 10 yr of
acute intermittent gout.
• Tophaceous gout occurs when uric acid crystals form masses
of white growths that develop around the joints and tissues.
There is formation of tophi which is visible under sking.
• Tophaceous gout might lead to permanent damage of joint.
Predisposing factor/risk factor
• Heredity
• Renal failure
• Alcohol use
• Psoriasis
• Obesity
• Hypertension
• Organ transplantation.
Pathogenesis of Gout
Pathophysiology
• Gouty arthritis develop when monosodium urate crystal
deposited in synovium of joint
• These urate crystal stimulate release of numerous
inflammatory mediator in synovial membrane.
• The influx of neutrophil is important for development of
acute crystal induced synovitis.
• Overall there will be inflammation of joint .
• If untreated tophi or tophacous deposit eventually lead to
joint deformity and disability.
• Similarly it might also lead renal impairment , urothialisis ,
nephropathy.
Symptom
• Sytemic: Fever, malaise
• Muscoskeletal: Articular joint pain,
metatarsophalangeal joint is most common.
• Skin: erythema, warmth, pruritis
• Genito urinary tract: renal colic , calculi
Diagnosis
• Blood test: increase uric acid level, CBC, ESR
• Synovial fluid finding: needle shape crystal of
monosodium urate.
Differential diagnosis
• RA
• Osteoarthritis
Pharmacotherapy
Therapeutic Goal
Symptomatic relief (termination of, pain
inflammation)
Prevention of future attack
Prevention of complication such as tophi, calculi,
nephropathy, join desctruction
Restoring normal function of affected joints
Non pharmacological mgmt
• Ice packs
• Immobilzation of joint
• Alcohol and tobacco abstinence
• Dieatry modification: Decrease in protein diet,
carbodhydrate diet.
• VIT C. (daily 500 mg vit consumption for a
month can reduce uric acid by 0.5mg/dl)
• Drink plenty water
Classification of medicines
1) Acute attack of gout
i) NSAID: Commonly used NSAIDs are Indomethacin 50 mg bd/tds, Naproxen 500 mg BD/TDS,
ketoralc 60 mg IM. They are not recommended for long term use due to toxicity
Aspirin is not use Why….??
ii) Colchicine: It Binds to fibrillar protein tubulin and inhibits granulocyte migration into the
inflamed joint, hence it stop the inflammatory process.
Dose: 1.2mg initially followed by 0.6 mg q 2hrly until pain relief occur. Max dose: 6mg/24 hrly.
iii)Corticosteroids: Use in patient who cannot tolerate NSAID/colchine therapy.

Oral Prednisolone 40-60 mg for 3-5 days then taper for a week.
Intraarticualr corticosteroid injection: Benefit for those who have one or two large joint affected.
Good option for elderly or PUD.
Triamcinoloe 10-40 mg
Dexamethasone 2-10 mg alone or combination with lidocaine
Side effect of corticosteroid…?

Pharmacological mgmg
2) Intercritical gout treatment: non pharmacological treatment such as increase
water intake
i) Uricosuric agent: Probencid, sulfypyrazone
• Probencid improve kidney ability to remove uric acid from blood. Dose:
250mg BD for 1 week then 500 mg Bid for 1-2 weeks
• It should not iniated in acute gout attack
• Some other medicine that promote uric acid excretion: losartan, fenofibrate
• Side effect..?
ii) Synthesis inhibitors: Allopurinol, febuxostat. These drug inhibit xanthine
oxidase enzyme hence inhibit synthesis of uric acid.
Allopurinol dose: 100-300 mg OD
Febuxostat: 40-80- mg OD.
Side effect..?
Pharmacological mgmt
3) Chronic tophaceous gout :
Generally used medicine are
allopurinol/febuxostat and probencid.
Also useful in elderly with HTN.
Newer therapy: Uricase, Rasbuircase.

Complication
• Renal failure
• Nephrothialis
• Joint deformity
Thank you

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GOUT

iii)Corticosteroids: Use in patient who cannot tolerate NSAID/colchine therapy.

Side effect of corticosteroid…?

Newer therapy: Uricase, Rasbuircase.

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