Signs and symptoms
Gout presenting
in the metatarsal-phalangeal joint of the big toe: Note the slight redness of
the skin overlying the joint.
Gout can
present in multiple 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
Gout uric
acid levels (hyperuricemia) may result in other symptoms, including
hard, painless deposits of uric acid crystals known as tophi. Extensive
tophi may lead to chronic arthritis due to bone erosion.[11] Elevated
levels of uric acid may also lead to crystals precipitating in the kidneys, resulting
in stone
formation and subsequent urate nephropathy
Cause
The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of 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
Lifestyle
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 found that other dietary factors are not relevant. Specifically, moderate consumption of purine-rich vegetables (e.g., beans, peas, lentils and spinach) are not associated with gout. Neither is total consumption of protein Alcohol consumption is strongly associated with an increased risk, 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.[20]
Genetics
Gout is partly genetic, contributing to about 60% of variability in uric acid level. The SLC2A9, SLC22A12 and ABCG2 genes have been found to be commonly associated with gout and variations in them can approximately double the risk.[22][23] Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion. The rare genetic disorders 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.[5]
Medical conditions
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.[6] Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants and myeloproliferative disorders such as polycythemia.[5][24] A body mass index greater than or equal to 35 increases male 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.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase risk Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers (except losartan), beta blockers, ritonavir, and pyrazinamide.[11][27] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[5] the former more so when used in combination with hydrochlorothiazide.[
Cause
The crystallization of uric acid, often related to relatively high levels in the blood, is the underlying cause of gout. This can occur because of 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
Lifestyle
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 found that other dietary factors are not relevant. Specifically, moderate consumption of purine-rich vegetables (e.g., beans, peas, lentils and spinach) are not associated with gout. Neither is total consumption of protein Alcohol consumption is strongly associated with an increased risk, 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.[20]
Genetics
Gout is partly genetic, contributing to about 60% of variability in uric acid level. The SLC2A9, SLC22A12 and ABCG2 genes have been found to be commonly associated with gout and variations in them can approximately double the risk.[22][23] Loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia by reducing urate absorption and unopposed urate secretion. The rare genetic disorders 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.[5]
Medical conditions
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.[6] Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants and myeloproliferative disorders such as polycythemia.[5][24] A body mass index greater than or equal to 35 increases male 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.
Medication
Diuretics have been associated with attacks of gout. However, a low dose of hydrochlorothiazide does not seem to increase risk Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers (except losartan), beta blockers, ritonavir, and pyrazinamide.[11][27] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[5] the former more so when used in combination with hydrochlorothiazide.[
Diagnosis
Gout on X-rays of a left
foot. The typical location is the big toe joint. Note also the soft tissue
swelling at the lateral border of the foot.
Spiked rods of
uric acid crystals from a synovial fluid sample photographed under a
microscope with polarized light. Formation of uric acid
crystals in the joints is associated with gout.
Gout may be
diagnosed and treated without further investigations in someone with
hyperuricemia and the classic acute arthritis of the base of the great toe
(known as podagra). Synovial fluid analysis should be done, however, if the
diagnosis is in doubt. X-rays, while useful for identifying chronic gout, have little
utility in acute attacks.
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