Gout = Inflammatory Arthritis
Gout is a painful inflammatory arthritis caused by uric acid crystals
forming in the joints. Attacks of gout often start suddenly during sleep and
feel like a joint is "on fire."
Gout occurs acutely as intermittent attacks of inflammatory arthritis with
severe joint pain, swelling, redness and warmth of affected joint. In some
individuals, it can be a progressive, crippling chronic disease that also
damages the kidneys. Gout affects more than one million Canadians and Americans.
Painful attacks of joint pain can occur at any age, but the first attack often
affects men between the ages of 40 and 50. Gout is 20 times commoner in men than
women; however, the number of postmenopausal women who have gout is increasing.
Obesity, high blood pressure and atherosclerotic heart disease are often
associated. A familial pattern is observed in up to15% of cases.
Historically, attacks of gout have been associated with drinking and high
living; a penance for indulgent lifestyles. Most modern gout suffers, however
are more temperate folk and have a genetic tendency to gout or are predisposed
for a variety of other reasons. They do not have to be party animals, voracious
eaters or alcoholics to suffer gout, although overindulgence in the wrong food
and drink will definitely aggravate the tendency. Gout affects more than one
million Canadians and Americans. Painful attacks can occur at any age, but the
first attack often affects men between the ages of 40 and 50. Gout is 20 times
more common in men than women; however, the number of postmenopausal women who
have gout is increasing.
A Gout attack is a severe inflammatory arthritis usually in one joint; the
severe joint pain and swelling
red or purple skin around the joint
extreme tenderness -the area may be so tender that even the touch of a bed
sheet may be unbearable.
Uric Acid Crystals Cause Inflammation
The pain and swelling of gout are caused by uric acid crystals that form in
the joint. Uric acid is a waste product of purine metabolism. Uric acid is
dissolved in the blood and is excreted through the kidneys into the urine. In
people with gout, the uric acid level increases and uric acid crystals are
deposited in joints and other tissues. These needle-shaped crystals trigger an
immune response that produces intense local inflammation with severe pain,
tenderness and swelling. After several years of increased serum uric acid, uric
acid crystals can build up in the joint(s) and surrounding tissues. They form
deposits that are sometimes apparent as firm lumps (tophi) under the skin. Tophi
often are found in or near severely affected joints, on or near the elbow, over
the fingers and toes, and in the outer edge of the ear. Uric acid crystals can
also form stones in the kidneys, in the ureters and in the bladder. Stones form
when the uric acid concentration in the urine is too high - this is cause by low
water intake, diuretics, and overly acidic urine. A diet rich in purines may be
Uric Acid Production
Uric acid substance is a product of the chemical breakdown of the purine
bases that compose the genetic material, DNA and RNA. As cells die and release
DNA from their chromosomes, purines are converted into uric acid which is
excreted in the urine and, to a lesser extent, the intestinal tract. The
concentration of uric acid in the blood is related to the balance between uric
acid production and excretion. The normal level in children is 4 ? 2 mg/dl. At
puberty, the level increases in males by 1 mg/dl, but it does not increase in
females; the normal range is 3 to 7 mg/dl in adult males and 2 to 6 mg/dl in
adult females. At concentrations greater than 6.5 to 7.0 mg/dl in water, urate
precipitates in the form of sodium urate crystals. When blood levels are above
10 mg/dl, the chance of an acute attack of gout is greater than 90 percent.
Only 10% of people with hyperuricemia are over-producers of uric acid caused
by diseases of the blood and bone marrow, inherited enzyme abnormalities and
metabolic alterations due to obesity. In patients who overproduce uric acid
because of a deficiency of hypoxanthine-guanine phosphoribosyltransferase, gout
attacks may begin before puberty.
Increased destruction of body cells leads to increased uric acid production;
examples are malignancies, particularly lymphoreticular cancers, hemolytic
anemia, polycythemia, leukemias and nonmalignant conditions of increased
cellular proliferation (e.g., psoriasis). Uric acid production will also
increase with the accelerated breakdown of adenosine triphosphate (ATP) in
glucose-6-phosphatase deficiency, tissue ischemia and myophosphorylase
Decreased urinary excretion of urate most often contributes to
hyperuricemia. Patients with urate clearances of 6 to 7 ml per minute are more
likely to have hyperuricemia after a purine load than those with clearances of
12 to 14 ml per minute. The assessment of renal handling of urate may be part of
medical investigation designed to provide information about urate production,
renal function, urine flow and the contribution of dietary purine intake to
serum and urine urate.
Gout medications are used to:
- Relieve the pain and swelling of an acute attack: nonsteroidal
anti-inflammatory drugs (NSAIDs), colchicine, codeine, Demerol, corticosteroid
- Prevent future episodes: colchicine, probenecid, sulfinpyrazone, and
- Prevent or treat tophi: probenecid, sulfinpyrazone, and allopurinol.
- Prevent the formation of uric acid kidney stones: allopurinol
has been used to treat gout for over 2,400 years. It relieves the pain and
swelling of acute attacks. It works best if taken immediately after the onset of
an attack. When taken by mouth, colchicine can cause diarrhea, nausea, and
abdominal cramps. Colchicine is less popular now than in the past because of its
slow onset of action and frequent gastrointestinal side effects. Colchicine
interferes with neutrophil phagocytosis and chemotaxis -early events in the
production of joint inflammation and is most effective when started soon after
the onset of an attack of gouty arthritis. The beneficial effect of colchicine
declines the longer treatment is delayed.
Nonsteroidal anti-inflammatory drugs
(NSAIDs) are used to relieve the pain and swelling of an acute attack. They
usually begin working within 24 hours. These medications are as effective as
colchicine but may have less frequent side effects. Side effects from NSAIDs may
include stomach upset, headache, skin rashes, and sometimes ulcers.
Medications that Reduce the Rate of Uric Acid Production
Allopurinol (Lopurin, Zurinol, Zyloprim) reduces the amount of uric acid in
the blood and urine by slowing the rate of production of uric acid. It is the
best medicine for people who have kidney problems or kidney stones caused by
uric acid. Occasional side effects include skin rash and stomach upset.
Infrequently, allopurinol can cause a allergic reaction - skin rash, hives,
itching, fever, nausea, and muscle pain are typical symptoms.
Medications that Help Eliminate Uric Acid
Some drugs lower the uric acid level by increasing the amount of uric acid
passed in the urine. They help dissolve tophi and prevent uric acid deposits in
joints. Probenecid (Benemid, Parbenem, Probalan) and sulfinpyrazone (Anturane).
Common side effects include nausea, skin rash, stomach upset, or headaches.
Increase water intake to about 10 x 8 ounce glasses per day.
Avoid aspirin with these drugs because it blocks their effects on the
kidneys. At first, probenecid or sulfinpyrazone may increase the risk of kidney
stones by increasing the uric acid content in the urine. Adding baking soda to
the water will make the urine more alkaline, increase the solubility of uric
acid and help to reduce the risk of urinary tract stones. Probenecid,
sulfinpyrazone, and allopurinol also may cause more frequent gout attacks at
first. You may have to take colchicine or an NSAID for the first few months of
preventive drug therapy to prevent a gout attack.