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Traditional view of the Gout
Gout (also known as Metabolic Arthritis when it involves the joint at the base of the big toe) is usually characterized by recurrent attacks of inflammatory arthritis—a red, tender, hot, and swollen joint. Pain typically comes on rapidly in less than twelve hours. The joint at the base of the big toe is affected in about half of cases. It may also result in tophi, kidney stones, or urate nephropathy.
The cause is a combination of diet and genetic factors. It occurs more commonly in those who eat a lot of meat, drink a lot of beer, or are overweight. The underlying mechanisms involves elevated levels of uric acid in the blood. When the uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, an attack of gout occurs. Diagnosis may be confirmed by seeing the characteristic crystals in joint fluid or tophus. Blood uric acid levels may be normal during an attack.
Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. Once the acute attack subsides, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks, allopurinol or probenecid provides long-term prevention. Taking vitamin C and eating a diet high in low fat dairy products may be preventative.
Signs and symptoms
Gout affects about 1 to 2% of the Western population at some point in their lives. It has become more common in recent decades which is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet. Older males are most commonly affected. Gout was historically known as "the disease of kings" or "rich man's disease". It has been recognized at least since the time of the ancient Egyptians.
Gout can present in a number of ways, although the most usual is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint). The metatarsal-phalangeal joint at the base of the big toe is affected most often, accounting for half of cases. Other joints, such as the heels, knees, wrists, and fingers, may also be affected. Joint pain usually begins over 2–4 hours and during the night. This is mainly due to lower body temperature. Other symptoms may rarely occur along with the joint pain, including fatigue and a high fever.
Long-standing elevated uric acid levels (hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritis due to bone erosion. Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stone formation and subsequent urate nephropathy.
The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur for a number of reasons, including diet, genetic predisposition, or underexcretion of urate, the salts of uric acid. Underexcretion of uric acid by the kidney is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lifetimes. The risk, however, varies depending on the degree of hyperuricemia. When levels are between 415 and 530 μmol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 μmol/l (9 mg/dL), the risk is 4.5% per year.
Dietary causes account for about 12% of gout, and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood. Other triggers include physical trauma and surgery.
Studies in the early 2000s have found that other dietary factors once believed associated are, in fact, not. Specifically, moderate consumption of purine-rich vegetables (e.g. beans, peas, lentils, and spinach) are not associated with the development of gout. Neither is total consumption of protein. Alcohol consumption is a factor, with wine presenting somewhat less of a risk than beer and spirits.
The consumption of coffee, vitamin C, and dairy products, as well as physical fitness, appear to decrease the risk. This is believed to be partly due to their effect in reducing insulin resistance.
The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level. Three genes called SLC2A9, SLC22A12, and ABCG2 have been found to be commonly associated with gout, and variations in them can approximately double the risk. Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion. A few rare genetic disorders, including familial juvenile hyperuricemic nephropathy, medullary cystic kidney disease, phosphoribosylpyrophosphate synthetase superactivity, and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, are complicated by gout.
Gout frequently occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in nearly 75% of cases. Other conditions commonly complicated by gout include: polycythemia, lead poisoning, kidney failure, hemolytic anemia, psoriasis, and solid organ transplants. A body mass index greater than or equal to 35 increases a male's risk of gout threefold. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function. Lesch-Nyhan syndrome is often associated with gouty arthritis.
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