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Health Questions & Answers #73 ~ [Issue 0306-4]  Wellness Weekly
 Mar 29, 2006 08:17 PST 

Q & A #1:
What Is Gout?

Gout is one of the most painful rheumatic diseases. It results from
deposits of needle-like crystals of uric acid in connective tissue,
in the joint space between two bones, or in both. These deposits lead
to inflammatory arthritis, which causes swelling, redness, heat,
pain, and stiffness in the joints. The term arthritis refers to more
than 100 different rheumatic diseases that affect the joints,
muscles, and bones, as well as other tissues and structures. Gout
accounts for approximately 5 percent of all cases of arthritis.

Pseudogout is sometimes confused with gout because it produces
similar symptoms of inflammation. However, in this condition, also
called chondrocalcinosis, deposits are made up of calcium phosphate
crystals, not uric acid.

Uric acid is a substance that results from the breakdown of purines,
which are part of all human tissue and are found in many foods.
Normally, uric acid is dissolved in the blood and passed through the
kidneys into the urine, where it is eliminated. If the body increases
its production of uric acid or if the kidneys do not eliminate enough
uric acid from the body, levels of it build up in the blood (a
condition called hyperuricemia). Hyperuricemia also may result when a
person eats too many high-purine foods, such as liver, dried beans
and peas, anchovies, and gravies. Hyperuricemia is not a disease and
by itself is not dangerous. However, if excess uric acid crystals
form as a result of hyperuricemia, gout can develop. The excess
crystals build up in the joint spaces, causing inflammation. Deposits
of uric acid, called tophi (singular: tophus), can appear as lumps
under the skin around the joints and at the rim of the ear. In
addition, uric acid crystals can collect in the kidneys and cause
kidney stones.

For many people, gout initially affects the joints in the big toe.
Sometime during the course of the disease, gout will affect the big
toe in about 75 percent of patients. It also can affect the instep,
ankles, heels, knees, wrists, fingers, and elbows.

Q & A #2:
What Causes Gout?

A number of risk factors are related to the development of
hyperuricemia and gout:

- Genetics may play a role in determining a person's risk, since up
to 18 percent of people with gout have a family history of the disease.
- Gender and age are related to the risk of developing gout; it is
more common in women and adults than in children.
- Being overweight increases the risk of developing hyperuricemia and
gout because there is more tissue available for turnover or
breakdown, which leads to excess uric acid production.
- Drinking too much alcohol can lead to hyperuricemia because it
interferes with the removal of uric acid from the body.
- Eating too many foods rich in purines can cause or aggravate gout
in some people.
- An enzyme defect that interferes with the way the body breaks down
purines causes gout in a small number of people, many of whom have a
family history of gout.
- Exposure to lead in the environment can cause gout.

Some people who take certain medicines or have certain conditions are
at risk for having high levels of uric acid in their body fluids. For
example, the following types of medicines can lead to hyperuricemia
because they reduce the body's ability to remove uric acid:

- Diuretics, which are taken to eliminate excess fluid from the body
in conditions like hypertension, edema, and heart disease, and which
decrease the amount of uric acid passed in the urine;
- Salicylates, or anti-inflammatory medicines made from salicylic
acid, such as aspirin;
- The vitamin niacin, also called nicotinic acid;
- Cyclosporine, a medicine used to suppress the body's immune system
(the system that protects the body from infection and disease) and
control the body's rejection of transplanted organs; and
- Levodopa, a medicine used to support communication along nerve
pathways in the treatment of Parkinson's disease.

Q & A #3:
Who Is Likely To Develop Gout?

Gout occurs in approximately 840 out of every 100,000 people. It is
rare in children and young adults. Adult men, particularly those
between the ages of 40 and 50, are more likely to develop gout than
women, who rarely develop the disorder before menopause. People who
have had an organ transplant are more susceptible to gout.

Q & A #4:
How Is Gout Diagnosed?

Gout may be difficult for doctors to diagnose because the symptoms
may be vague, and they often mimic other conditions. Although most
people with gout have hyperuricemia at some time during the course of
their disease, it may not be present during an acute attack. In
addition, having hyperuricemia alone does not mean that a person will
get gout. In fact, most people with hyperuricemia do not develop the
disease.

To confirm a diagnosis of gout, a doctor may insert a needle into an
inflamed joint and draw a sample of synovial fluid, the substance
that lubricates a joint. A laboratory technician places some of the
fluid on a slide and looks for monosodium urate crystals under a
microscope. Their absence, however, does not completely rule out the
diagnosis. The doctor also may find it helpful to examine chalky,
sodium urate deposits (tophi) around joints to diagnose gout. Gout
attacks may mimic joint infections, and a doctor who suspects a joint
infection (rather than gout) may check for the presence of bacteria.

Q & A #5:
How Is Gout Treated?

With proper treatment, most people with gout are able to control
their symptoms and live productive lives. Gout can be treated with
one or a combination of therapies. The goals of treatment are to ease
the pain associated with acute attacks, to prevent future attacks,
and to avoid the formation of tophi and kidney stones. Successful
treatment can reduce both the discomfort caused by the symptoms of
gout and long-term damage of the affected joints. Treatment will help
to prevent disability due to gout.

The most common treatments for an acute attack of gout are high doses
of nonsteroidal anti-inflammatory drugs (NSAIDs) taken orally (by
mouth) or corticosteroids, which are taken orally or injected into
the affected joint. NSAIDs reduce the inflammation caused by deposits
of uric acid crystals but have no effect on the amount of uric acid
in the body. The NSAIDs most commonly prescribed for gout are
indomethacin (Indocin) and naproxen (Anaprox, Naprosyn), which are
taken orally every day. Corticosteroids are strong anti-inflammatory
hormones. The most commonly prescribed corticosteroid is prednisone.
Patients often begin to improve within a few hours of treatment with
a corticosteroid, and the attack usually goes away completely within
a week or so.

When NSAIDs or corticosteroids do not control symptoms, the doctor
may consider using colchicine. This drug is most effective when taken
within the first 12 hours of an acute attack. Doctors may ask
patients to take oral colchicine as often as every hour until joint
symptoms begin to improve or side effects such as nausea, vomiting,
abdominal cramps, or diarrhea make it uncomfortable to continue the drug.

For some patients, the doctor may prescribe either NSAIDs or oral
colchicine in small daily doses to prevent future attacks. The doctor
also may consider prescribing medicine such as allopurinol (Zyloprim)
or probenecid (Benemid) to treat hyperuricemia and reduce the
frequency of sudden attacks and the development of tophi.
	
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