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Gout is a disease that is often misunderstood. Through the ages, sudden acute joint swelling has been blamed on everything from keeping poor company to the air we breathe. Since it affects the joints, gout is a type of arthritis. In the eighteenth century, it was mostly seen in the noble class whose diet, use of red wine, and distaste for activity produced rampant flare-ups. It is more thoroughly understood as being a product of genetics combining with certain food intake to produce a state where crystals precipitate out of solution. Most persons with gout excrete urea more slowly. Urea is a by-product of purine degradation which is an amino acid found in protein. It seems more likely that a sudden change in the uric acid level, such as starting a new diet regiment or dehydrating naturally or with the aid of alcohol consumption, is more likely to cause a gout attack. More protein metabolism means more degradation and more uric acid is carried dissolved in blood serum. Anyone with basic chemistry knowledge knows that lowering temperature or removing fluid can cause crystallization of a saturated solute. It is of little surprise that gout most often affects the large toe joint and less commonly the knees and elbows. These joints are further from the body center and have lower temperatures. .
When a patient presents with a rapid onset of swelling, redness and pain in the foot joint, gout is suspected. Classically, the diagnosis would be made by aspirating the affected joint with a needle and examining the fluid for gout crystals. It is vital to differentiate the gouty joint from an acutely infected one. Many physicians who are acquainted with their patients' health can make the diagnosis clinically. Aspiration is often reserved for the people who do not respond to initial treatment. Blood work is also done to check for uric acid levels, kidney function and triglyceride levels.
The first goal of treatment is to reduce the pain. Traditional anti-inflammatories like indomethacin still work best. Increasing fluid intake reverses the process and encourages more kidney excretion. Some individuals are prone to repeat attacks. To prevent this, we work with the patient to reduce aggravating influences. The common ones are obesity, hypertension, alcohol overuse, and elevated blood fats. Diets low in purine also help. This means avoiding red meats, lentils, some beans among other foods. Occasionally, patients are placed on allopurinol which inhibits uric acid production. In the old days, gout was treated with extracts derived from a crocus. This alkaloid was called colchicine and pure forms are still used today. Colchicine can inhibit migration of inflammatory cells and can also inhibit mitosis. This latter effect accounts for the side-effects of diarrhea associated with colchicine, since the gastrointestinal tract has a high cell turnover. The main problem in gout sufferers is the slow excretion of uric acid by their kidneys. Uric acid can precipitate in the kidney forming one type of kidney stone. It can also precipitate near joints forming nodules called tophi. This can be aggravated by people using diuretic type medications such as hydrochlorothiazide used to control hypertension. These drugs further inhibit kidney excretion of uric acid. For this reaSson, copious amounts of hydration are recommended to stimulate kidney function.
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