Gout is a type of arthritis caused by elevated uric acid in the blood and then depositing in the joints. The classic area involved is the big toe, but any joint can be involved. 4% of the adult population is affected, and African-Americans are at the highest risk. Pain usually occurs with intermittent attacks.
Despite a popular misconception that gout is merely an episodic nuisance, it is a serious disease that can significantly affect physical function and quality of life. A 2013 systematic review found that quality of life was significantly reduced in patients with gout. I have seen many acute flares in patients and it does not look fun.
Economic costs include decreased worker productivity and increased absences from work. From 2001 to 2005, an estimated 2 million visits were made to primary care providers due to gout.
Although gout historically has been considered a musculo-skeletal disorder, recent evidence indicates that high levels of uric acid in the blood plays an important role in the development of kidney disease and contributes to cardiovascular morbidity and death.
Uric acid is an end-product of protein breakdown. The molecular structure is carbon, oxygen, hydrogen, and nitrogen.
Although the definition of hyperuricemia (high uric acid in blood) is arbitrary, it is usually defined as a serum uric acid level greater than 7.0 mg/dl in men and greater than 6.0 mg/dl in women.
High uric acid is linked to:
Some pharmaceuticals can lower levels of uric acid AND are shown to decrease the risk of heart attacks. Allopurinol is one example. But as a doctor of cause, let’s look for ways to prevent excess production of uric acid that do NOT involve drugs.
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