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Gout

Title               

Ñ    Gout

Definition

Ñ    Inflammatory arthropathy

Associated with:

Ñ    Hyperuricaemia

Pathogenesis

Causes

Hyperuricaemia

Hyperuricaemia may be due to:

Increased Production of Uric Acid

Increased de novo synthesis of purines

Ñ    Hypoxanthine-guanine-phophoribosyl transferase (HGPRT) reduction:

This is an X-liked inborn error of metabolism causing the Lesch-Nyhan syndrome

Ñ    Phophoribosyl-pyrophosphae synthetase overactivity

Ñ    G6PD deficiency with glycogen storage disease type I:

Increased production and decreased excretion

Increased purine synthesis due to increased cell turnover

HS

Ñ    Myeloproliferative disorders

Ñ    Lymphoproliferative disorders

IS

Ñ    Psoriasis

Others

Ñ    Cancer

Impaired excretion of uric acid

KUS

Ñ    Chronic renal failure

CVS

Ñ    Hypertension

Drugs

Ñ    Thiazide diuretics

Ñ    Low dose aspirin

Toxins

Ñ    Lead

E&M

Ñ    Primary hyperparathyroidism

Ñ    Hypothyroidism

Ñ    Increased lactic acid production:

Exercise, starvation, alcohol

HS

Ñ    G6PD deficiency

Pathological Process

Ñ    Uric acid crystals accumulate in tissues including the synovium

Ñ    Uric acid crystals coated with apoliporotein E or B

Ñ    This prevents an inflammatory response

Ñ    Changes in uric acid levels or microtrauma may lead to shedding of uncoated crystals

Ñ    This results in an inflammatory response

Clinical Features

Age

Ñ    Prevalence increases with age

Sex

Ñ    Males > Females

Clinical Syndromes

There are four clinical phases of gout:

Ñ    Asymptomatic hyperuricaemia

Ñ    Acute gout

Ñ    Intercritical gout:

Chronic polyarticular gout

Ñ    Chronic tophaceous gout

Asymptomatic hyperuricaemia

Ñ    Crystal deposition in articular cartilage, synovium, capsule, periarticular soft tissue

Ñ    Renal colic may occur

Acute gout

Ñ    Usually presents as severe, agonising pain in the first metatarsophalangeal joint with swelling and redness

Ñ    Atypical attacks may present as tenosynovitis, bursitis, cellulitis

Intercritical gout

Ñ    Asymptomatic intervals between attacks

Ñ    Later attacks may increase and become pauci-articular or poly-articular

Chronic tophaceous gout

Ñ    Skin deposits and joint destruction

Ñ    May rarely involve the eye, eyelids, tongue, larynx, heart

Investigations

Fluids

Blood

Biochemistry

Ñ    Serum urate raised:

The level may fall immediately after an acute attack

Levels should be rechecked several weeks after an acute attack

Joint Fluid Aspirate

Compensated polarised light microscopy

Ñ    Monosodium urate crystals are seen as strongly birefringent (negative sign) needle shaped crystals

Imaging

X-ray

Chronic tophaceous gout

Ñ    Periarticular deposits are seen as a halo of radio-opacity

Ñ    Punched out bone cysts may also be seen

Management

Control

Drugs

Acute attack

Ñ    NSAIDs

Ñ    Colchicine

Ñ    Steroids:

Rarely

Decrease serum urate levels

Ñ    Allopurinol:

Blocks xanthine oxidase, which converts xanthine to urate

Ñ    Probenecid:

Increases urate excretion

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