• It is chiefly a disorder of adult Male 5 % in Female .
• Gout is uncommon before 3rd decade.
• Peak of onset in Males (45 years) usually after 20 - 30 years of sustained hyperuricemia, and in post menopausal females above 60 years.
There are 4 clinical presentations of Gout (Hyperurecemia)
Probably 95% of hyperuricemic subjects never develop gout.
• 90 % of cases of the initial attacks are monoarticular usually in the first metatarsophalangeal joint (podagra)
• Other initial sites:
- Ankles, wrist, heels, finger, knee, elbow.
• It may be precipitated by:
- Trauma .- Surgery - Ingestion of alcohol- Exercise - Diuretics.
• Minority of patients showing acute gout with normal serum uric acid.
• Dramatic relief of pain with colchicine is suggestive.
• In severe attacks, overlying crystal cellulitis makes gout difficult to distinguish clinically from infective cellulitis .
• The typical attack is rapid onset reaching maximum severity 2-6 hours, often waking the patient in the early morning, it is self limiting over 5-14 days. Milder episodes for few days called peptite attacks.
• There is ++ temperature,++ TLC , l' ++ ESR.
• Intercritical periods are asymptomatic periods between attacks.
a- Joints show :
• Polyarthritis.
• Asymmetrical joint affection.
• Exacerbation and remission.
• Late : joint destruction.
b- Tophi
• Tophi are deposits of solid urate crystals that elicit a foreign body reaction of mononuclear cells with
granuloma formation, this occurs after longstanding severe hyperuricemia.
• Tophi deposits occur usually in the skin, around joints and ear lobule, extensor surface of fingers, achilles tendon or in elbows. Large deposition may cause overlying skin to ulcerate and extrude urate crystals.
• Periarticular deposition lead to a halo of radio-opacity on x-ray
C - Chronic gouty nephropathy (see below)
b- Chronic gouty nephropathy (chronic urate nephropathy)
Urate precipitation in renal interstitial tissue-s chronic renal
failure.
c- Uric acid stones
Uric acid precipitation in acidic urine ===> obstructive uropathy.
• Gout is uncommon before 3rd decade.
• Peak of onset in Males (45 years) usually after 20 - 30 years of sustained hyperuricemia, and in post menopausal females above 60 years.
There are 4 clinical presentations of Gout (Hyperurecemia)
I. Asymptomatic hyperuricemia
refers to elevation of serum uric acid prior to the development of arthritis.Probably 95% of hyperuricemic subjects never develop gout.
II. Acute gouty arthritis
• There is painful arthritis.• 90 % of cases of the initial attacks are monoarticular usually in the first metatarsophalangeal joint (podagra)
• Other initial sites:
- Ankles, wrist, heels, finger, knee, elbow.
• It may be precipitated by:
- Trauma .- Surgery - Ingestion of alcohol- Exercise - Diuretics.
• Minority of patients showing acute gout with normal serum uric acid.
• Dramatic relief of pain with colchicine is suggestive.
• In severe attacks, overlying crystal cellulitis makes gout difficult to distinguish clinically from infective cellulitis .
• The typical attack is rapid onset reaching maximum severity 2-6 hours, often waking the patient in the early morning, it is self limiting over 5-14 days. Milder episodes for few days called peptite attacks.
• There is ++ temperature,++ TLC , l' ++ ESR.
• Intercritical periods are asymptomatic periods between attacks.
III. Chronic tophaceous gout
(chronic arthropathy, tophi, nephropathy)a- Joints show :
• Polyarthritis.
• Asymmetrical joint affection.
• Exacerbation and remission.
• Late : joint destruction.
b- Tophi
• Tophi are deposits of solid urate crystals that elicit a foreign body reaction of mononuclear cells with
granuloma formation, this occurs after longstanding severe hyperuricemia.
• Tophi deposits occur usually in the skin, around joints and ear lobule, extensor surface of fingers, achilles tendon or in elbows. Large deposition may cause overlying skin to ulcerate and extrude urate crystals.
• Periarticular deposition lead to a halo of radio-opacity on x-ray
C - Chronic gouty nephropathy (see below)
IV. Renal disease.
a- Uric acid nephropathy due to precipitation of uric acid in renal tubules. especially with myelo or Iympho proliferative diseases during chemotherapy (tumour lysis syndrome)(uric acid> 25 mg/dl) ===> Acute renal failure.b- Chronic gouty nephropathy (chronic urate nephropathy)
Urate precipitation in renal interstitial tissue-s chronic renal
failure.
c- Uric acid stones
Uric acid precipitation in acidic urine ===> obstructive uropathy.