Gout
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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. Therefore, pseudogout is treated somewhat differently and
is not reviewed in this booklet.
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. The disease can progress through
four stages:
- Asymptomatic (without symptoms) hyperuricemia--In this stage,
a person has elevated levels of uric acid in the blood but no other symptoms.
A person in this stage does not usually require treatment.
- Acute gout, or acute gouty arthritis--In this stage, hyperuricemia
has caused the deposit of uric acid crystals in joint spaces. This leads
to a sudden onset of intense pain and swelling in the joints, which also
may be warm and very tender. An acute attack commonly occurs at night
and can be triggered by stressful events, alcohol or drugs, or the presence
of another illness. Early attacks usually subside within 3 to 10 days,
even without treatment, and the next attack may not occur for months
or even years. Over time, however, attacks can last longer and occur
more frequently.
- Interval or intercritical gout--This is the period between acute
attacks. In this stage, a person does not have any symptoms and has normal
joint function.
- Chronic tophaceous gout--This is the most disabling stage of
gout and usually develops over a long period, such as 10 years. In this
stage, the disease has caused permanent damage to the affected joints
and sometimes to the kidneys. With proper treatment, most people with
gout do not progress to this advanced stage.
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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 men than in women and more common in 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.
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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.
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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.
- Hyperuricemia
- Presence of uric acid crystals in joint fluid
- More than one attack of acute arthritis
- Arthritis that develops in 1 day, producing a swollen, red,
and warm joint
- Attack of arthritis in only one joint, usually the toe, ankle,
or knee
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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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- To help prevent future attacks, take the medicines your doctor prescribes.
Carefully follow instructions about how much medicine to take and when
to take it. Acute gout is best treated when symptoms first occur.
- Tell your doctor about all the medicines and vitamins you take. He
or she can tell you if any of them increase your risk of hyperuricemia.
- Plan followup visits with your doctor to evaluate your progress.
- Maintain a healthy, balanced diet; avoid foods that are high in purines;
and drink plenty of fluids, especially water. Fluids help remove uric
acid from the body.
- Exercise regularly and maintain a healthy body weight. Lose weight
if you are overweight, but do not go on diets designed for quick or extreme
loss of weight because they increase uric acid levels in the blood.
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Scientists are studying which NSAIDs are the most effective
gout treatments, and they are analyzing new compounds to develop safe,
effective medicines to lower the level of uric acid in the blood and to
treat symptoms. They also are studying the structure of the enzymes that
break down purines in the body to achieve a better understanding of the
enzyme defects that can cause gout.
Scientists are studying the effect of crystal deposits on cartilage
cells for clues to treatment. They also are looking at the role of calcium
deposits in pseudogout in the hope of developing new treatments. The role
genetics and environmental factors play in hyperuricemia also is being
investigated.
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National Institute of Arthritis and Musculoskeletal and
Skin Diseases (NIAMS)
American College of Rheumatology/Association of Rheumatology
Health Professionals
Arthritis Foundation
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