Gout: Cause, Symptom, Diet and Medication

Gout - popularly called the disease of the rich. It is due to malfunction of purine metabolism.
Gout: Cause, Symptom, Diet and Medication
Gout is a systemic disease which means, condition that occurs throughout the body. It is caused by the accumulation of uric acid in the joints. Uric acid is a substance or chemical which is a natural part of the normal breaking down and building up of food and body tissues. The level in the blood can be measured and shows how much there is in the body overall. A high blood level of uric acid (called hyperuricemia) occurs when the liver produces more uric acid than the body can excrete in the urine, or when a diet high in rich foods produces more uric acid than the kidneys can filter from the blood. When this happens, the uric acid that is normally dissolved in the blood may, from time to time, form microscopic crystals. There is precipitation of sodium urate crystals in the synovial fluid of the joints, leading to severe inflammation and arthritis.

Why it happens:

Uric acid production is related to catabolism or breakdown of nucleotide called purine.
Nucleotides are grouped as purines or pyrimidines. Purine nucleotides are adenine and guanine. Catabolism of the purine nucleotides leads ultimately to the production of uric acid. Uric acid is insoluble and is excreted in the urine as sodium urate crystals.

Most forms of gout are the result of excess purine or of a partial deficiency of the enzyme, called HGPRT which coverts xanthine to uric acid. Most forms of gout can be treated by administering the allopurinol. This compound is a structural analog of hypoxanthine that strongly inhibits xanthine oxidase.

Other diseases related to purine metabolism:

Two other severe disorders, both associated with defects in purine metabolism: Lesch-Nyhan Syndrome and severe combined immunodeficiency disease (SCID) results from the loss of a functional gene responsible for the production of enzyme HGPRT. Patients with this defect exhibit severe symptoms of gout and severe malfunction of the nervous system. Death usually occurs before patients reach their 20th year.

SCID is caused by a deficiency in the enzyme adenosine deaminase (ADA). This is the enzyme responsible for converting adenosine to inosine in the breakdown of the purines. This deficiency selectively leads to a destruction of B and T lymphocytes, the cells that mount immune responses. The net effect of ADA absence is to inhibit DNA synthesis. Since lymphocytes must be able to proliferate dramatically in response to antigenic challenge, the inability to synthesize DNA seriously impairs the immune responses, and the disease is usually fatal in infancy. Another disorder called the von Gierke’s disease also leads to excessive uric acid production.

Signs and Symptoms

Gout usually develops in the joint of the first toe (metatarsal phalangeal joint) or ankle joints. Common symptoms include inflammation, pain, redness, stiffness and swelling.
Cause:
The following are some of the more common causes of gout:
Higher than normal levels of uric acid can be part of the inherited make-up of some families
Obesity
High alcohol intake
High intake of food containing purines
Some of the drugs used to treat high blood pressure.
Less commonly, longstanding kidney disease may result in high blood levels of uric acid.

Food to avoid:

The first step is to avoid food with high levels of purine. Therefore the following foods which are high in purines should be restricted or avoided:
Excessive amounts of red meat.
Shellfish, fish roe and scallops.
Peas. lentils and beans
Alcohol intake should be reduced.
Weight loss may be very important.
Medication for high blood pressure may need to be altered
Fried foods
Roasted nuts
Anchovies
Herring and sardines
Mussels
Mushrooms
Food made from or containing refined white flour

Other preventative measures include the following:

Drink plenty of fluids (especially water)
Exercise regularly
Maintain a healthy diet and healthy body weight
See a physician regularly

By Ipshita Chatterjee
Published: 3/7/2005
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