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
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 the culprit.
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.
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 deficiency.
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 drugs.
Prevent future episodes: colchicine, probenecid,
sulfinpyrazone, and allopurinol.
Prevent or treat tophi: probenecid, sulfinpyrazone, and
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.