by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
Click here: Second Opinion Arthritis Treatment Kit
Gout is a form of arthritis. The term “gout” is the name for the metabolic disease marked by excessive uric acid deposits in the joints.
Gout causes severe pain in joints. Patients with chronic gout may have repeated episodes of gouty arthritis. The arthritis is caused by an acute inflammatory attack triggered by uric acid crystals. White blood cells flood the area and ingest the crystals. As crystals are "gobbled up" by white cells, they cause the release of multiple intracellular enzymes that aggravate inflammation.
Gout is caused by a defect in metabolism which results in an overproduction of uric acid; there is also a reduced ability of the kidney to eliminate uric acid. Risk is increased in males, postmenopausal women, and people with hypertension. Heavy alcohol use, diabetes, obesity, sickle cell anemia, and kidney disease also increase risk.
The condition may also develop in people are on mediciations which interfere with uric acid excretion.
Symptoms of an attack come on suddenly, usually involving only one or a few joints. When the joint affected is the big toe, this condition is called "podagra". The pain frequently starts during the night and is often described as throbbing, crushing, or excruciating. The affected joints show warmth, redness, and tenderness. The pain tends to subside within several days. Chronic gout attacks, however, occur more often.
If several attacks of gout occur each year this may cause joint deformity and limitation of motion in affected joints. Uric acid deposits called tophi develop in cartilage tissue, tendons, and soft tissues. These tophi usually develop only after a patient has suffered from the disease for many years. Deposits also can occur in the kidneys, leading to chronic kidney disease and kidney failure.
Tests that indicate gouty arthritis include:
•Joint fluid analysis that detects uric acid crystals
•Elevated serum uric acid level
•Joint x-rays which show damage consistent with gouty arthritis
Acute attacks are managed with any number of medications including low doses of colchicine, non-steroidal anti-inflammatory drugs, or steroids.
Chronic gouty arthritis is treated with drugs like probenecid, allopurinol, and febuxostat (Uloric). Patients should drink plenty of water or other fluids to decrease the risk of kidney complications.
Colchicine can be added as prophylaxis to prevent further acute attacks. This drug can be discontinued when uric acid levels are stable (usually after 6 months), but it can also be continued at low doses to help prevent further attacks.
Non-steroidal anti-inflammatory drugs also are used either for acute attacks or for prophylaxis while a patient is started on uric acid lowering therapy.
Patients who develop tophaceous gout where uric acid deposits are numerous can be treated with Krystexxa. This drug mobilizes uric acid and converts it to allantoin, an inert ingredient that is excreted easily.
Gout may occur in association with other types of arthritis such as pseudogout- a condition due to calcium pyrophosphate crystals- and psoriatic arthritis- the arthritis associated with psoriasis. Symptoms are generally worse in people who develop the disease before age 30.
• Kidney stones
• Kidney failure
• Joint deformities
• Loss of mobility
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