Known as "the disease of kings and the king of diseases", gout has been studied by physicians and has caused suffering in countless humans since at least the days of Hippocrates. Formerly a leading cause of painful and disabling chronic arthritis, gout has been all but conquered by advances in research. Unfortunately, many people with gout continue to suffer because knowledge of effective treatments has been slow to spread to patients and their physicians.
The four phases of gout include elevated uric acid levels without symptoms, acute gouty arthritis, multiple attacks with intervals between attacks, and chronic tophaceous gout, in which nodular masses of uric acid crystals (tophi) are deposited in different soft tissue areas of the body. Patients with asymptomatic hyperuricemia do not require treatment, but efforts should be made to lower their urate levels by encouraging them to make changes in diet or lifestyle.
Uric acid is a product of the chemical breakdown of the purine bases that compose the genetic material, DNA. As cells die and release DNA from their chromosomes, purines are converted into uric acid which is excreted in the urine and, to a lesser extent, the intestinal tract. The level of uric acid dissolved in the bloodstream is directly related to this delicate balance between uric acid production and excretion. The normal level is approximately 2-7mg/dl.
Though an excess of uric acid is known to cause gout, recent studies show that, in proper concentrations in the blood, it has antioxidant properties and helps protect the cells and tissues from irritation and damage caused by singlet oxygens and hydroxyl free radicals. This protection may prevent tissue wear and aging, in addition to other free-radical diseases.
Thus, uric acid has a new image as being an important part of balanced human function and not just a waste product. With its different effects, uric acid is somewhat like cholesterol in its biochemistry: As with cholesterol, it is both made in the body and obtained through the diet; some people are genetically inclined to elevated levels; and, whereas the right amount is essential to important functions, excesses can lead to problems (cholesterol appears to be much more of a concern on this count than uric acid).
Gout in women occurs almost exclusively after menopause. Women develop gout at an older age than men and have twice the prevalence of hypertension, renal insufficiency and exposure to diuretics. The onset of gout before age 30 in men or before menopause in women is unusual and raises concern about an associated inherited enzyme defect or renal disease.
An attack of acute gouty arthritis is caused by the body's inflammatory reaction to intermittent deposition of needle-like uric acid crystals. When these crystals are ingested by white blood cells, the cells release enzymes that evoke inflammation.
The inflammatory process in gout is unrelated to infection. Rather, it is incited by the deposition in the joint of uric acid crystals usually due to an excess of uric acid in the bloodstream. This can be caused by an increase in production by the body, by under-elimination of uric acid by the kidneys or by increased intake of foods containing purines which are metabolized to uric acid in the body. Certain meats, seafood, dried peas and beans are particularly high in purines. Alcoholic beverages may also significantly increase uric acid levels and precipitate gout attacks. Gout is strongly associated with obesity, hypertension, hyperlipidemia, diabetes and dehydration. A familial pattern is observed in 5-15% of cases.
In most cases, an under-excretion of uric acid by the kidneys is responsible. Among the more common predisposing factors are kidney failure from any cause, diuretics, dehydration, hormonal diseases, alcohol consumption and using low doses of aspirin. About 10% of people with hyperuricemia are overproducers of uric acid. For some of these patients, diseases of the blood and bone marrow or inherited enzyme abnormalities can be implicated. Some are associated with metabolic alterations due to obesity, but for most the exact cause is indeterminable.
Attacks are usually marked by intermittent joint pain, swelling, redness and warmth. Other symptoms include:
Since several other kinds of arthritis can mimic a gout attack, and since treatment is specific to gout, proper diagnosis is essential. The definitive diagnosis of gout is dependent on finding uric acid crystals in the joint fluid during an acute attack. However, uric acid levels in the blood alone are often misleading and may be transiently normal or even low. Additionally, uric acid levels are often elevated in individuals without gout. While sudden swelling and pain in a joint, especially the big toe, suggests the diagnosis of gout, many other arthritic conditions and some infections present themselves in a similar manner. Gout is the diagnosis if gout medications resolve the symptoms. Uric acid levels are usually elevated around an attack, and reduced when treated successfully.
Serum uric acid can be elevated due to reduced excretion by the kidneys, and or high intake of dietary purine.
In many instances, people have elevated uric acid levels for hereditary reasons. Diet may also be a factor; eating large amounts of sea salt can cause increased levels of uric acid.
Moderate intake of purine-containing food is not associated with an increased risk of gout. Sources of uric acid to be avoided as far as possible:
Purines are excreted as uric acid. Purines are found in high amounts in animal food products, such as liver and sardines. A moderate amount of purine is also contained in beef, pork, poultry, fish and seafood, asparagus, cauliflower, spinach, mushrooms, green peas, lentils, dried peas, beans, oatmeal, wheat bran and wheat germ.
Examples of high purine sources include: sweetbreads, anchovies, sardines, liver, beef kidneys, brains, meat extracts (e.g. Oxo, Bovril), herring, mackerel, scallops, game meats, and gravy.
Untreated cases may develop chronic gouty arthritis in which multiple joints are involved by a long-term destructive process. Tophi (small nodules consisting of uric acid and inflammatory tissues) may be seen on the ear cartilage and along tendons.
It has been reported that MS (possibly associated with low uric acid) and gout (associated with high uric acid) are mutually exclusive. A study of 20 million Medicare and Medicaid records found no overlap between MS and gout.
In March 2004, an article was published in the New England Journal of Medicine documenting the effect of meat intake on gout risk. Harvard researchers followed almost 50,000 men for 12 years and found that "each additional daily serving of meat was associated with a 21% increase in the risk of gout." In fact, the Atkins Diet has been blamed directly for the rising incidence of this painful disease. [The Observer, 18 January 2004]
Patients with impaired renal function filter and excrete less uric acid and therefore become hyperuricemic. Interestingly, patients with renal failure do not develop gout as frequently as expected, despite their high plasma urate levels. The explanation for this phenomenon may be that they have not incurred sustained hyperuricemia levels long enough to develop gout. Only 1% of renal failure patients develop gout but nearly 30% of patients with adult polycystic kidney disease do.
Hyperuricemia is caused by a variety of means, one of which is abnormal kidney function. In addition, for some individuals gout is a progressive, crippling chronic disease that eventually damages the kidneys.
Beer raises gout risk by 49% per daily serving.
For gout, soft drinks are worse than hard liquor – and nearly as bad as beer – doubling the risk for heavy drinkers. Diet sodas, however, do not affect gout risk. These findings came from a large study of 46,393 male health professionals in Canada who filled in detailed questionnaires about their health and their diet every four years for 12 years. Over that time, 755 of the subjects developed gout.
Elevated uric acid levels, as seen in gout, may be associated with a higher incidence of coronary heart disease amongst alcohol abstainers, but has not been seen to occur in those who were light, moderate or heavy drinkers. [Journal of Clinical Epidemiology,1996;49(6) pp.673-678]
A low-purine diet is commonly used to treat gout. Some people need to follow the diet more closely than others to prevent symptoms.
Intake of diuretics (chiefly coffee and alcohol) should be reduced/avoided as far as possible.
Especially recommended are cherries. Liberal amounts (up to 1 pound per day) of cherries, blueberries, and other anthocyanoside-rich (i.e. red-blue) berries or extracts should be consumed. Consuming fresh or canned cherries has been shown to be very effective in lowering uric acid levels and preventing attacks of gout. Cherries, hawthorn berries, blueberries, and other dark red-blue berries are rich sources of anthocyanidins and proanthocyanidins. These compounds are flavonoid molecules that give these fruits their deep red-blue color, and are remarkable in their ability to prevent collagen destruction.
Preferably no meat should be eaten as it is rich in uric acid forming components. Raw fruit, vegetables, grains, seeds and nuts are highly recommended.
Achieve normal body weight but avoid rapid weight loss diets, which may result in increased uric acid levels in the blood.
Medications such as Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids and allopurinol are commonly used against gout. The NSAID that is most widely used to treat acute gout is indomethacin. NSAIDs may also have significant toxicity, but if used for the short-term, are generally well tolerated.
NSAIDs are the treatment of choice for acute attacks of gout in most patients. NSAIDs should be used sparingly in elderly patients and should be avoided in patients with renal disease and peptic ulcer disease, and in those receiving concurrent systemic anticoagulation. Corticosteroids are a valuable treatment option for patients in whom NSAID therapy is contraindicated. Acute gouty arthritis and chronic gout require different treatment strategies.
Since the 1800s, colchicine has been the standard treatment for acute gout. While colchicine is very effective, it often causes nausea, vomiting and diarrhea. These side-effects are uncommon when this drug is given intravenously, but because of their unpleasant nature, non-steroidal anti-inflammatory drugs (NSAIDs) have become the treatment of choice for most acute attacks of gout.
Therapy directed at normalizing uric acid levels in the blood should be considered for patients who have had multiple gout attacks or have developed tophi or kidney stones. Several drugs that help the kidneys eliminate uric acid are available, such as probenecid, and a drug that blocks production of uric acid by the body, such as allopurinol. The choice between these two types of drugs depends on the amount of uric acid in the urine. With correct treatment, gout should be well controlled in almost all cases.
Among the more common predisposing factors for hyperuricemia are kidney failure from any cause, diuretics, dehydration, hormonal diseases, alcohol consumption and using low doses of aspirin. Aspirin and aspirin-containing products should be avoided during acute attacks because they will further elevate uric acid levels.
Note, however: Molybdenum deficiency may reduce uric acid formation, which was not previously thought to be a problem, but it may be important to supplement molybdenum to maintain uric acid levels in midnormal range for the antioxidant function as well as possible others.
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