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Guidelines For Gout Success

Gout has a long history and goes back many years. It's amazing how far we've come with treatment for it, because of the discoveries in diet and environment and how they are largely responsible for the outcome. You also have to take into consideration that people are susceptible to it via genetics. You're only going to experience a wicked gout attack if your kidneys no longer can metabolize uric acid like they once did. Take a look at the information we found on the internet below.

Gout is a metabolic problem that was very common throughout history and is mentioned in many historical novels (it is a great excuse for a grouchy personality if needed in a story). The first known description was in Egypt in 2,600 BC, and it was well described by Hippocrates in ancient Greece, about 400 BC. The uric acid crystals which are the cause of gout were first seen in 1679 by Dutch scientist Antonie van Leeuwenhoek.

This painful disease is caused by the buildup of uric acid crystals in a joint, the base of the big toe (called podagra) being involved more than 50% of the time. Other joints may also be affected, such as in the hands, elbows and knees, and other tissues can also be affected. Uric acid crystals can deposit in the skin (gouty tophi), kidneys, tendons and other tissues. High fever can also be associated with this problem. The uric acid build up is caused by decrease in the breakdown of uric acid because of an enzyme deficiency, or increase in production because of dietary factors; in fact genetics and diet are both important factors for most people with clinical gout. It has been known through history as “rich man’s disease” and “the king’s disease” because until the Twentieth Century only the wealthy ate enough of the foods that cause it.

Very simply, when uric acid crystallizes in joints, an immune response occurs and the subsequent inflammation makes for a hot, red joint. Cold seems to be one of the precipitating factors, which might explain why it tends to involve the extremities such as toes and fingers and tends to begin at night. The most common mimic of gout is septic arthritic (and infected joint), which a physician would suspect if the presumed gout does not respond to treatment.

In the Regency Era:

Physicians were aware that gout was caused by over-indulgence in elderly men and it was thought that red meat, rich food, and red wine, especially port wine, caused flares of gout. Treatment of an acute gout attack included keeping the painful foot bandaged and elevated. Bleeding or leeching would be used to decrease the inflammation and laudanum (tincture of opium) would be used for pain. Various other treatments, such as soaking in mineral baths at spas such as those in Bath, England, as well as drinking the mineral water in the Pump Room were held to be helpful. An acute attack of gout will resolve on its own in 5 to 7 days, so every physician has his own regimen that he felt worked, but none of these treatments, except dietary restriction, made a difference in the long term incidence of recurrent arthritis.

In the 21st century:

Modern medical science has learned that the precipitating factors for people predisposed to gout (which is most common in those with metabolic syndrome: abdominal fat, type diabetes, high blood lipids, and high blood pressure). The incidence of gout has doubled in the past twenty years, along with an increase in obesity and metabolic syndrome. It is still more common in older men as well as post-menopausal women.

A patient who comes in with a red, hot joint will be evaluated with a blood test for blood uric acid levels. If the patient clinically fits the diagnosis of gout, and the blood level of uric acid is high, then the diagnosis is made. Unfortunately, half of patients with gout have normal uric acid levels, and other blood tests, such as the white blood cell count and sedimentation rate will be elevated for both gout and septic arthritis. In these cases, a sample of synovial fluid (the fluid inside the joint space) is removed and examined microscopically for uric acid crystals (gout) or for bacteria (septic arthritis).

Treatment for the acute attack of gout is geared towards decreasing inflammation with non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or naproxen, corticosteroids such as prednisone, or colchicine. Pain relievers may be used to help get the patient through the acute attack.

Prevention is the crux of treatment for gout, because a patient who has had an episode has a high risk of having it recur, as well as having the risks of kidney and skin problems. Patients should avoid drugs which can precipitate gout, such as aspirin, hydrochlorothiazide (a diuretic commonly used for hypertension), and long-term immunosuppressive drugs such as cyclosporine and tacrolimus (commonly used to prevent rejection after organ transplant). Diet should avoid meat, fish, fructose, and alcohol.

Long-term drug treatment for those who have recurrent gout attacks include medications which inhibit the enzyme xanthine oxidase and thus decrease uric acid levels, or those which increase the amount of uric acid excreted by the kidneys. The choice of medications depends on how much uric acid the kidneys are removing, determined by a 24-your urine collection. These drugs are generally not started until 2 weeks after the last acute attack because of a risk of worsening the attack. This information was found at

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