Materials on Gout (from wiki)

Gout(also known aspodagrawhen it involves the big toe) [ 1 ]is a medical conditionusually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint. The metatarsal-phalangeal jointat the base of the big toeis the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acidin the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues. Clinical diagnosis may be confirmed by seeing the characteristic crystals in joint fluid. Treatment with nonsteroidal anti-inflammatory drugs(NSAIDs), steroids, or colchicineimproves symptoms. Once the acute attack subsides, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent attacks, allopurinolor probenecidprovide long-term prevention. Gout has become more common in recent decades, affecting about 1–2% of the Westernpopulation at some point in their lives. The increase is believed due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancyand changes in diet. Gout was historically known as "the disease of kings" or "rich man's disease." Signs and symptoms Gout presenting in the metatarsal-phalangeal jointof the big toe: Note the slight redness of the skin overlying the joint. 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). [ 2 ]The metatarsal-phalangeal joint at the base of the big toeis affected most often, accounting for half of cases. [ 3 ]Other joints, such as the heels, knees, wrists and fingers, may also be affected. [ 3 ]Joint pain usually begins over 2–4 hours and during the night. [ 3 ]The reason for onset at night is due to the lower body temperature then. [ 1 ]Other symptoms may rarely occur along with the joint pain, including fatigueand a high fever. [ 1 ] [ 3 ] Long-standing elevated uric acidlevels ( hyperuricemia) may result in other symptomatology, including hard, painless deposits of uric acid crystals known as tophi. Extensive tophi may lead to chronic arthritisdue to bone erosion. [ 4 ]Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in stoneformation and subsequent urate nephropathy. [ 5 ] Cause High levels of uric acidin the blood ( hyperuricemia) 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. [ 2 ]Renal underexcretion of uric acid is the primary cause of hyperuricemia in about 90% of cases, while overproduction is the cause in less than 10%. [ 6 ]About 10% of people with hyperuricemia develop gout at some point in their lifetimes. [ 7 ]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. [ 1 ] Lifestyle Dietary causes account for about 12% of gout, [ 2 ]and include a strong association with the consumption of alcohol, fructose-sweetened drinks, meat, and seafood. [ 4 ] [ 8 ]Other triggers include physical traumaand surgery. [ 6 ]Recent studies have found that other dietary factors once believed associated are, in fact, not, including the intake of purine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein. [9] [10]With respect to risks related to alcohol, beer and spirits appear to have a greater risk than wine. [11] The consumption of coffee, vitamin Cand dairy products, as well as physical fitness, appear to decrease the risk. [12] [13] [14] This is believed partly due to their effect in reducing insulin resistance. [14] Genetics The occurrence of gout is partly genetic, contributing to about 60% of variability in uric acid level. [6] Three genes called SLC2A9, SLC22A12 and ABCG2 have been found commonly to be associated with gout, and variations in them can approximately double the risk. [ 15 ] [ 16 ] Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion. [16]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. [6]