Gout is a form of acute arthritis that causes severe pain and swelling in the joints.
In humans, uric acid
is the end product of the degradation of purines. Itserves no known physiologic purpose and is regarded as a waste product. The purines from which uric acid is produced originate from three sources:
- Dietary purine
- Conversion of tissue nucleic acid to purine nucleotides
- De novo synthesis of purine bases
Gout is caused by elevated levels of uric acid in the blood. This excess accumulation may result from either overproduction or underexcretion.
Renal underexcreation of uric acid is the primary cause of hyperuricaemia in about 90% of cases while overproduction is the cause in less than 10%.
The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues. The metatarsal-phalangeal joint at the base of the big toe is the most commonly affected. However, it may also affect the heel, ankle, hand, wrist, elbow or present as kidney stones, or urate nephropathy.Uric acid kidney stones occurs in 10% to 25% of patients with gout.
Predisposing factors include excessive urinary excretion of uric acid, acidic urine, and highly concentrated urine.
Dietary purines play an unimportant role in the generation of hyperuricemia.
Drugs that decrease renal clearance of uric acid have been also associated with attacks of gout. these include hydrochlorothiazide, nicotinic acid, Aspirin, Alcohol, pyrazinamide, levodopa, ethambutol, ciclosporin, and cytotoxic drugs.
Treatment of an acute attack:
- Joint rest for 1 to 2 days should be encouraged, and local application of ice may be beneficial.
- Nonsteroidal antiinflammatory drugs (NSAIDs) such as Ibuprofen and Naproxen: Therapy should be initiated with maximum recommended doses for gout at the onset of symptoms and continued for 24 hours after complete resolution of an acute attack. Acute attacks generally resolve within 5 to 8 days after initiating therapy.
- Colchicine is highly effective in relieving acute gout attacks but has a low benefit-toxicity ratio. Colchicine should be reserved for patients with insufficient relief, intolerance, or contraindications to NSAIDs.
- Corticosteroids such as prednisone: Corticosteroids may be used to treat acute attacks of gouty arthritis, but they are reserved primarily for patients with a contraindication or who are unresponsive to NSAID or colchicine therapy.
Prophylactic therapy is important for patients with frequent attacks:
- Uric acid–lowering therapy
- Xanthine oxidase inhibitors (including allopurinol and febuxostat) block uric acid production
- Uricosurics (including probenecid and sulfinpyrazone) increase the excretion of uric acid in the urine
- Nonpharmacologic Therapy: Patients may be advised to reduce their intake of foods high in purines (e.g., organ meats), avoid alcohol, limit caffeinated beverages, increase fluid intake, lose weight if obese and exercise regularly.