Definition: Inflammatory arthritis associated with hyperuricaemia.
There is deposition of sodium urate crystals in:
• Joints: causing arthritis.
• Soft tissues: causing tophi & tenosynovitis.
• Urinary system: causing urate stones & nephropathy.
Uric Acid Metabolism
1. Uric acid production:
From breakdown of nucleoproteins & purines.
2. Uric acid excretion:
• Uric acid is completely filtered by the glomeruli.
• It is completely reabsorbed in the proximal tubules.
• 75% is secreted by the distal tubules.
Etiology of Gout
I. Primary gout:
• Idiopathic hyperuricaemia due to:
1. Increased uric acid production.
2. Diminished uric acid excretion.
• More common in males in the forties.
• Family history in 20% of cases.
II. Secondary gout:
1. Metabolic: Increased uric acid production
A. Enzyme defects:
• Lesch-Nyhan syndrome:
- X-linked recessive disorder.
- Mental retardation.
• G6PD deficiency with glycogen storage disease.
B. Increased cellular destruction:
• Polycythaemia vera.
• Leukemia, especially during treatment.
• Others e.g. carcinoma.
2. Renal: Decreased uric acid excretion.
A. Chronic renal failure.
• Loop & thiazide diuretics.
• Low dose aspirin.
C. Increased lactic acid:
I. Gouty arthritis:
• Monoarticular in 90% of cases.
• The first metatarsophalangeal joint is the first to be affected.
Less commonly the ankle or the knee.
Precipitation: the attack may be precipitated by
• High protein diet.
• High alcohol consumption.
• Trauma, infections & excess exercise.
• Diuretics, salicylates & cytotoxic drugs.
• Sudden decrease of allopurinol or probenecid.
• Severely inflammed joint.
• It is painful, swollen & very tender.
• The overlying skin is red & oedematous.
• Fever may be present.
• Spontaneous recovery occurs within days.
• The attacks are recurrent.
• The joints are free inbetween the attacks.
• Uncommon except in:
- Elderly people with long use of diuretics.
- Chronic renal failure.
• There is chronic arthralgia with attacks of acute arthritis.
• The affection is polyarticular.
• It may be associated with tophi or nephropathy.
II. Gouty tophi:
• In chronic gouty arthritis & marked hyperuricaemia.
- Over the external ear.
- Around the joints.
- Smooth yellowish nodules.
- May ulcerate & discharge chalky material.
Deposits of urates in the subcutaneous tissues.
III. Gouty kidney:
there may be
• Urate stones: may cause hydronephrosis.
• Pyelonephritis: due to decreased resistance.
• Renal hypertension: may cause atherosclerosis.
• Chronic renal failure: may occur.
• Acute renal failure: due to severe hyperuricaemia.
IV. Other associations:
3. Diabetes mellitus, type 2.
4. Ischaemic heart disease.
V. Asymptomatic hyperuricaemia:
This is 10 times more common than gout.
1. Serum uric acid: more than 7 mg/dl.
2. Synovial fluid: contains urates.
3. X-ray: for kidneys & joints.
4. Biopsy from tophi.
I. Treatment of acute attacks:
1. Complete rest:
Of the patient & the affected joint.
2. Local measures:
Local application of ice or lead lotion.
• Indomethacin (Indocid):
50 mg tds for 2 days, then half the dose for 1week.
• Diclofenac (Voltaren):
The same dose as indomethacin.
1mg/6 hours for 1 week. It is stopped if diarrhoea occurs.
IM or intra-articular injections: in severe cases.
II. Long term therapy:
A. General measures:
1. Weight reduction.
2. Avoid foods & drinks containing high purines.
3. Avoid excess alcohol.
4. Good fluid intake.
5. Avoid thiazide diuretics & salicylates.
1. Allopurinol (Zyloric):
• It is a xanthine oxidase inhibitor.
• It decreases uric acid synthesis.
• It may precipitate acute athritis so:
- It is started 4 weeks after the acute attack.
- Used with colchicine to prevent acute attacks.
• It is indicated in:
- Frequent acute attacks.
- Tophi or chronic gouty arthritis.
- Renal stones.
- Marked hyperuricaemia.
- With treatment of malignancy.
• Dose: 300-900 mg/day.
2. Uricosuric drugs:
• Increase renal excretion of uric acid.
• Probenecid: 1 mg/12 hours.
• They must be given with colchecine.
• They are contraindicated in.
- Renal failure.
- Renal stones.
For renal stones & tophi.