by Stephen Gislason MD
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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 gouthave been associated with drinking and high living; apenance 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 characteristics are
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.
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 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 allopurinol.
Prevent the formation of uric acid kidney stones: allopurinol
Colchicinehas 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.
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