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Arthritis, GoutCrystal-induced arthropathies are induced by cellular reaction to crystal deposition in and around joints. A variety of microcrystals may be deposited and can induce an inflammatory response. The most prevalent forms of crystal-induced arthropathy are gout, calcium pyrophosphate dihydrate deposition, and calcium hydroxyapatite deposition. Gouty arthritis (gout) is a common, painful form of arthritis, caused by monosodium urate monohydrate (MSU) crystals. It results from an elevated blood level of uric acid which can be caused by an overproduction of uric acid or a reduced ability of the kidney to eliminate uric acid. The disorder causes joint inflammation and pain, especially in the joints of the feet and legs. Gout most often affects the base of the big toe (podagra). It also commonly affects other joints: the ankle, knee, wrist and elbow. Urate crystals may form in these joints because the joints are cooler than the central part of the body. Uric acid results from the breakdown of purines. Normally, it is dissolved in the blood and passed through the kidneys into the urine, where it is eliminated. The uric acid level in the blood becomes abnormally high when the kidneys cannot eliminate enough uric acid in the urine. Overproduction or reduced secretion can result in urate crystals being formed and deposited in joints. Combining a high-purine diet with alcohol can worsen matters, because alcohol both increases the production of uric acid and interferes with its elimination by the kidneys. Gouty arthritis is more common in males, postmenopausal women, and people with high blood pressure. Heavy alcohol use, diabetes, obesity, sickle cell anemia, and kidney disease also increases the risk. The condition may also develop in people who take agents which interfere with uric acid excretion. Gout is sometimes confused with other form of arthropathy called pseudogout. Pseudogout is caused by the deposition of calcium pyrophosphate dihydrate (CPPD). The buildup of this salt forms crystals in the joints, which leads to attacks of swelling and pain. Pseudogout mainly affects the elderly. The underlying causes of pseudogout and gout are very different. Uricosuric agents increase renal clearance of uric acid. They can be used to lower the uric acid level in the blood in people who have normal kidney function by increasing the kidney's excretion of uric acid. Xanthine oxidase inhibitors, Allopurinol and Oxypurinol, block the production of uric acid in the body and are especially helpful for people who have high uric level and urate stones or kidney damage. Xanthine oxidase (XO) is an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid, the last two steps in purine metabolism. Colchicine has been the traditional first step for acute attacks since 1939. It is an alkaloid derived from the dried seeds of Colchicum autumnale (known as autumn crocus or meadow saffron). Probenecid (Benemid, Probalan) is used to reduce uric acid levels and decrease the frequency and severity of gout attacks. NSAIDs and corticosteroids can quickly reduce pain and inflammation during gout attacks, but for long-term, the most useful are those that target the build-up of uric acid and prevent deposits of crystals in the joints. References
Last updated: September, 2010 |
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