Gout is an inflammatory arthritis associated with high uric acid levels in blood, and consequent deposition of intra-articular monosodium urate crystals, mainly in the first metatarsophalangeal joint.
Males are more frequently affected than females, and the disease typically appears during adulthood.
Uric acid is the final product of endogenous and dietary purine metabolism in humans, and the level of serum uric acid depends on the balance between purine synthesis, intake of dietary purines, and the excretion of uric acid from the body.
Ingestion of purine rich foods such as organ meats, seafood, beef, mushrooms, diary products, fructose containing drinks, high-saturated fat, and alcohol increase the risk of gout.
Serum uric acid levels can also be increased in various disease conditions, including diabetes, hypertension, dyslipidemia, obesity, and ischemic heart disease.
Increased uric acid production is also seen in disorders of high cell turnover.
These include lymphoproliferative disorders such as leukemia, myeloproliferative disorders such as polycythemia, and various other types of cancers, and psoriasis.
Uric acid production is increased in various inborn errors of metabolism that cause several enzyme deficiencies.
However, they account for only a minority of gout cases.
Impaired excretion of uric acid is the major cause for high uric acid levels and accounts for about 90% cases of gout.
It can be due to chronic kidney disease, dehydration, drugs such as thiazides and low-dose aspirin, led toxicity, high blood pressure, endocrine abnormalities like hypothyroidism and primary hyperparathyroidism, and increased lactic acid production due to starvation and exercise.
Some cases of gout are idiopathic, meaning that they do not have an identifiable underlying cause.
A patient with an acute attack of gout typically presents with sudden onset, agonizing pain, swelling, and redness of the first metatarsophalangeal joint.
It is usually precipitated by one of the above-mentioned factors, especially alcohol and diuretics.
An untreated attack typically lasts for about 7 days.
Recovery is associated with desquamation of the overlying skin.
And in about 25% of cases, a joint other than the first metatarsophalangeal joint is affected.
The more chronic form of gout, called tophaceous gout, is associated with the formation of lesions called tophi in various parts of the body, including the ears, fingers, skin, around joints, and tendons.
It is often associated with renal impairment.
Clinical picture is often diagnostic in gout, as is the rapid response to non-steroidal anti-inflammatory drugs and colchicine.
However, joint fluid microscopy is the most specific diagnostic test.
Serum uric acid levels can be normal or low during an attack.
In addition, it is important to monitor the renal functions during an acute episode of gout.
First line treatment option for gout is non-steroidal anti-inflammatory drugs such as naproxen and diclofenac.
Alternatives such as colchicine can be given if there is a history of renal impairment, active peptic ulcer disease, or if the patient does not respond well to non-steroidal anti-inflammatory drugs.
If there are frequent attacks of gout, and in tophaceous gout, treatment with agents that reduce serum uric acid is indicated.
These include allopurinol, febuxostat, pegloticase, and uricosuric agents.
Additionally, it is important to advise the patients to avoid the triggers of gout and reduce the total calorie intake.
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