DISEASES & TREATMENTS
about GOUT and HYPERURICEMIA:
What is gout?
Gout has the unique distinction of being one of the
most frequently recorded medical illnesses throughout history.
It is often related to an inherited abnormality in the body's
ability to process uric acid. Uric acid is a breakdown product
of purines, that are part of many foods we eat. An abnormality
in handling uric acid can cause attacks of painful arthritis (gout),
kidney stones, and blockage of the kidney tubules with uric acid
crystals, leading to kidney failure. On the other hand, some patients
may only develop elevated blood uric acid levels (hyperuricemia)
without arthritis or kidney problems. The term "gout"
traditionally refers to the painful arthritis attacks.
Gouty arthritis is usually an extremely painful attack
of joint inflammation. The joint inflammation is precipitated
by deposits of uric acid crystals in the joint fluid (synovial
fluid) and joint lining (synovial lining). Intense joint inflammation
occurs as white blood cells engulf the uric acid crystals, causing
pain, heat, and redness of the joint tissues. Approximately one
million people in the United States suffer from attacks of gout.
Gout is nine times more common in men than in women. It predominantly
attacks males after puberty, with a peak age of 75. In women,
gout attacks usually occur after menopause.
While hyperuricemia may indicate an increased risk
of gout, the relationship between hyperuricemia and gout is unclear.
Many patients with hyperuricemia do not develop gout, while some
patients with repeated gout attacks have normal or low blood uric
acid levels. Among the male population in the United States, approximately
ten percent have hyperuricemia. However, only a small portion
of those with hyperuricemia will actually develop gout.
What are the risk factors for gouty arthritis?
In addition to the inherited abnormality in handling
uric acid, other risk factors for developing gout include obesity,
excessive weight gain, especially in youth, moderate to heavy
alcohol intake, high blood pressure, and abnormal kidney function.
Certain drugs, such as thiazide diuretics, low-dose aspirin, and
tuberculosis medications (pyrazinamide and ethambutol) can also
cause gout. Certain diseases lead to excessive production of uric
acid in the body. Examples of these diseases include leukemias,
lymphomas, and hemoglobin disorders.
In patients at risk of developing gout, certain conditions
can precipitate acute attacks of gout. These conditions include
dehydration, injury to the joint, fever, excessive dining, heavy
alcohol intake, and recent surgery. Gout attacks triggered by
recent surgery are probably related to changes in the body fluid
balance as patients temporarily discontinue normal oral fluid
intake in preparation for and after the surgery.
What are symptoms of gout?
The small joint at the base of the big toe is the most common site of an acute gout attack. Other joints affected include the ankles, knees, wrists, fingers, and elbows. Acute gout attacks are characterized by a rapid onset of pain in the affected joint followed by warmth, swelling, reddish discoloration, and marked tenderness. Tenderness can be intense so that even a blanket touching the skin over the affected joint can be unbearable. Patients can develop fever with the acute gout attacks. These painful attacks usually subside in hours to days, with or without medication. In rare instances, an attack can last for weeks. Most patients with gout will experience repeated attacks of arthritis over the years.
Uric acid crystals can deposit in tiny fluid-filled
sacs (bursae) around the joints. These urate crystals can incite
inflammation in the bursae leading to pain and swelling around
the joints, a condition called bursitis. In rare instances, gout
leads to a more chronic type of joint inflammation which mimics
In chronic (tophaceous) gout, nodular
masses of uric acid crystals (tophi) deposit in different soft
tissue areas of the body. Even though they are most commonly found
as hard nodules around the fingers, at the tips of the elbows,
and around the big toe, tophi nodules can appear anywhere in the
body. They have been reported in unexpected areas such as in the
ears, vocal cords, or around the spinal cord!
How is gouty arthritis diagnosed?
Gout is suspected when a patient reports a history
of repeated attacks of painful arthritis at the base of the toes.
Ankles and knees are the next most commonly involved joints in
gout. Gout usually attacks one joint at a time, while other arthritic
conditions, such as systemic lupus and rheumatoid arthritis, usually
attack multiple joints simultaneously. The most reliable
test for gout is finding uric acid crystals in the joint fluid
obtained by arthrocentesis. Arthrocentesis is a common office
procedure performed under local anesthesia. Using sterile technique,
fluid is withdrawn (aspirated) from the inflamed joint, using
a syringe and needle. The joint fluid is then analyzed for uric
acid crystals and for infection. Shiny, needle-like uric acid
crystals are best viewed with a polarizing microscope. The diagnosis
of gout can also be made by finding these urate crystals from
material aspirated from tophi nodules and bursitis fluid.
Some patients with a classic history and symptoms
of gout can be successfully treated without undergoing arthrocentesis.
However, establishing a firm diagnosis is still preferable since
other conditions can mimic gout. These include another crystal-induced
arthritis called pseudogout, psoriatic arthritis, rheumatoid arthritis
and even infection.
X-rays can sometimes be helpful, and may show tophi
crystal deposits and bone damage as a result of repeated inflammations.
How is gout treated?
Preventing acute gout attacks is equally as important
as treating the acute arthritis. Prevention of acute gout involves
maintaining adequate fluid intake, weight reduction, dietary changes,
reduction in alcohol consumption, and medications to reduce hyperuricemia.
Maintaining adequate fluid intake helps prevent acute
gout attacks. Adequate fluid intake also decreases the risk of
kidney stone formation in patients with gout. Alcohol is known
to have diuretic effects which can contribute to dehydration and
precipitate acute gout attacks. Alcohol can also affect uric acid
metabolism and cause hyperuricemia.
Dietary changes can help reduce uric acid levels
in the blood. Since purine chemicals are converted by the body
into uric acid, purine rich foods are avoided. Examples of foods
rich in purine include shellfish and organ meats, such as liver,
brains, kidneys, and sweetbreads.
Weight reduction can be helpful in lowering the risk
of recurrent attacks of gout. This is best accomplished by reducing
dietary fat and calorie intake, combined with a regular aerobic
There are three aspects to the medication treatment
of gout. First, pain relievers such as TYLENOL or other more potent
analgesics are used to manage pain. Secondly, anti-inflammatory
agents such as nonsteroidal anti-inflammatory drugs (NSAIDS),
colchicine, and corticosteroids are used to decrease joint inflammation.
Finally, medications are considered for managing the underlying
metabolic derangement that causes hyperuricemia and gout.
NSAIDS such as indomethacin (INDOCIN) and naproxen (NAPROSYN) are effective anti-inflammatory medications for acute gout. These medications are tapered after the arthritis resolves. Common side effects of NSAIDS include irritation of the gastrointestinal system, ulceration of the stomach and intestines, and even intestinal bleeding. Patients who have a history of allergy to aspirin or nasal polyps should avoid NSAIDS because of the risk of an intense allergic (anaphylactic) reaction.
Colchicine for acute gout is most commonly administered
by mouth, but can also be given intravenously. Orally, it is given
hourly or every two hours until there is significant improvement
in pain or the patient develops gastrointestinal side effects
such as severe diarrhea. Other common side effects of colchicine
include nausea and vomiting.
Corticosteroids, such as prednisone, given in short
courses, are powerful anti-inflammatory agents for treating acute
gout. They can be administered orally or injected directly into
the inflamed joint. Corticosteroids can be prescribed to patients
who have accompanying kidney, liver, or gastrointestinal problems.
Long-term chronic use of corticosteroids is discouraged because
of serious long-term side effects.
In addition to medications for acute gout attacks,
other drugs can be taken over prolonged periods to lower blood
uric acid levels. Lowering blood uric acid levels reduces the
risk of recurrent attacks of arthritis, kidney stones, and kidney
disease, and also dissolves hard tophi deposits. Medicines used
to lower blood uric acid level work either by increasing the kidney
excretion of uric acid, or by decreasing the body's production
of uric acid from the purine in foods. Since many patients with
elevated blood uric acid levels may not develop gouty attacks
or kidney stones, the decision for prolonged treatment with uric
acid-lowering drugs should be individualized.
Probenecid (BENEMID) and sulfinpyrazone (ANTURANE)
are medications that are commonly used to decrease uric acid blood
levels by increasing the excretion of uric acid into the urine.
Since these drugs can, in rare instances cause kidney stones,
they should be avoided by those patients with a history of kidney
stones. These medications should be taken with plenty of fluid
so as to promote the rapid passage of uric acid out of the urinary
system in order to prevent stone formation.
Allopurinol (ZYLOPRIM) lowers the blood uric
acid level by preventing uric acid production. It actually blocks
the metabolic conversion from purine in foods to uric acid. This
medication should be used with caution in patients with poor kidney
function, as they are at a particular risk of developing side
effects, including rash and liver damage.
Uric acid-lowering medications, such as allopurinol
(ZYLOPRIM), are generally avoided in patients who are having acute
attacks of gout. For unknown reasons, these medications actually
can worsen the acute inflammation. Therefore, uric acid-lowering
drugs are usually instituted only after complete resolution of
the acute arthritis attacks. If patients are already taking these
medications, they are maintained at the same doses during the
acute attacks. In some patients, increasing the dose of uric acid-lowering
medications can precipitate gout attacks. In these patients, low
doses of colchicine can be given to prevent the precipitation
of acute gout.
Home remedies which can alleviate the symptoms of
acute gout include resting and elevating the inflamed joint. Ice
pack applications can be helpful to reduce pain and decrease inflammation.
Patients should avoid aspirin containing medications because aspirin
prevents kidney excretion of uric acid.
Active research is ongoing in a variety of fields
related to gout and hyperuricemia. The optimal regimens for the
treatment of acute gout attacks and chronic gout conditions still
require further long-term studies. Research scientists will continue
to develop less toxic and more effective medications to battle
this "scourge of the ages."
For more information about GOUT and HYPERURICEMIA, please visit the following sites:
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