Gout is a form of inflammatory arthritis characterized by repeated attacks of red, soft, hot, and swollen joints. Pain usually comes quickly in less than twelve hours. Joints in the base of the big toe affected about half the cases. It can also cause tophi, kidney stones, or urate nephropathy.
Gout is caused by elevated levels of uric acid in the blood. This happens because of a combination of diet and genetic factors. At high levels, uric acid crystallizes and crystal deposits in joints, tendons, and surrounding tissues, resulting in attacks of uric acid. Gout is more common in those who regularly eat meat or seafood, drink beer, or be overweight. The diagnosis of gout can be confirmed by the presence of crystals in the joint fluid or tophus. Blood levels of blood uric acid may be normal during an attack.
Treatment with nonsteroidal anti-inflammatory drugs (NSAIDs), steroids, or colchicine improves symptoms. As the acute attack subsides, uric acid levels can be reduced through lifestyle changes and in those who frequently attack, allopurinol or probenecid provide long-term prevention. Consuming vitamin C and eating a diet high in low-fat dairy products may be preventive.
Gout affects about 1 to 2% of the Western population at some point in their lives. This has become more common in recent decades. This is believed to be due to increased risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet. Older men are most commonly affected. Gout is historically known as "king's disease" or "disease of the rich". It has been recognized since at least the time of ancient Egypt.
Video Gout
Signs and symptoms
Gout can be present in many ways, although the most common is the recurrent acute attacks of arthritis (red, soft, hot, and swollen joints). Metatarsal-falangeal joints at the base of the big toe are most commonly affected, accounting for half of cases. Other joints, such as heels, knees, wrists, and fingers, may also be affected. Joint pain usually begins more than 2-4 hours and at night. This is mainly due to lower body temperature. Other symptoms may rarely occur along with joint pain, including fatigue and high fever.
High levels of uric acid (hyperuricemia) can cause other symptoms, including a hard and painless uric acid crystal known as tophi. Broad tooth can cause chronic arthritis due to bone erosion. Increased uric acid levels can also cause crystals to settle in the kidneys, resulting in stone formation and subsequent urate nephropathy.
Maps Gout
Cause
Crystallization of uric acid, often associated with a relatively high level in the blood, is the underlying cause of uric acid. This can occur due to diet, genetic predisposition, or the absence of veins, salts of uric acid. Lack of uric acid by the kidneys is the leading cause of hyperuricemia in about 90% of cases, while overproduction is the cause of less than 10%. About 10% of people with hyperuricemia develop gout at some point in their lives. However, the risks vary depending on the level of hyperuricemia. When the level between 415 and 530? Mol/l (7 and 8.9 mg/dl), the risk is 0.5% per year, whereas in those with levels greater than 535? Mol/l (9 mg/dL), the risk is 4.5% per year.
Lifestyle
Diet causes accounts for about 12% of gout, and includes strong links with alcohol consumption, fructose sweetened drinks, meat and seafood. Among the richest foods in purine that produce high amounts of uric acid are dried anchovies, shrimp, organ meats, dried mushrooms, seaweed, and brewer's yeast. Other triggers include physical trauma and surgery.
Studies in the early 2000s found that other dietary factors were irrelevant. In particular, moderate consumption of purine rich vegetables (eg beans, peas, peanuts, and spinach) is not associated with gout. Not total protein consumption. Alcohol consumption is strongly associated with an increased risk, with wine serving less risk than beer or spirits.
Consumption of coffee, vitamin C, and dairy products, as well as physical fitness, seems to reduce the risk. This is believed to be partly due to its effect in reducing insulin resistance.
Genetics
Gout is partly genetic, contributing about 60% of the variability in uric acid levels. The SLC2A9 , SLC22A12 , and ABCG2 genes have been found to be generally associated with gout and variations in it can be about double the risk. Mutation loss of function in SLC2A9 and SLC22A12 causes hereditary hypericemia by reducing venous absorption and unresolved urate secretion. Rare genetic disorders of familial juvenile hyperuricemic nephropathy, cystic medullary kidney disease, superactivity phosphoribosylpyrophosphate synthetase and hypoxanthine-guanine phosphoribosyltransferase deficiency as seen in Lesch-Nyhan syndrome, complicated by gout.
Medical condition
Gout often occurs in combination with other medical problems. Metabolic syndrome, a combination of abdominal obesity, hypertension, insulin resistance, and abnormal lipid levels, occurs in almost 75% of cases. Other conditions typically complicated by gout include lead poisoning, renal failure, haemolytic anemia, psoriasis, solid organ transplants and myeloproliferative disorders such as polycythemia. Body mass index greater than or equal to 35 increases men's risk three times gout. Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effects of lead on kidney function. Lesch-Nyhan syndrome is often associated with gout arthritis.
Drugs
Diuretics have been linked to uric acid attacks. However, low doses of hydrochlorothiazide do not seem to increase the risk. Other drugs that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, angiotensin receptor blockers (except losartan), beta blockers, ritonavir, and pyrazinamide. Immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout, the first being more used when combined with hydrochlorothiazide.
Pathophysiology
Gout is a disorder of purine metabolism, and occurs when its last metabolite, uric acid, crystallizes in the form of monosodium veins, deposits and forms deposits (tophi) in the joints, in the tendons, and in surrounding tissues. The microscopic tophi may be walled by a protein ring, which blocks the crystal interaction with the cell and therefore avoids inflammation. The naked crystals can rupture from the off-wall tophi due to minor physical damage to joint, medical or surgical joints, or rapid changes in uric acid levels. As they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, initiated by the inflammatory protein complex of NLRP3. Activation of NLRP3 inflammation recruits the caspase 1 enzyme, which converts pro-interleukin 1? into active interleukin 1, one of the key proteins in the inflammatory cascade. The loss of evolution from uric oxidase (uricase), which breaks uric acid, in humans and higher primates has made this condition common.
Triggers for deposition of uric acid are not well understood. Although it may crystallize at a normal level, it is more likely to do so as the rate increases. Other triggers believed to be important in acute episodes of arthritis include cold temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins, such as proteoglycans, collagen, and chondroitin sulfate. Increased rainfall at low temperatures partly explains why joints in the feet are most commonly affected. Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy, diuretics, and stopping or initiating allopurinol. Calcium channel blockers and losartan are associated with lower gout risk compared with other drugs for hypertension.
Diagnosis
Gout can be diagnosed and treated without further investigation in a person with hyperuricemia and classic acute arthritis from the base of the big toe (known as podagra). Analysis of synovial fluid should be done, however, if the diagnosis is in doubt. X-rays, while useful for identifying chronic gout, have little use in acute attacks.
synovial fluid
The exact diagnosis of gout is based on the identification of crystals of monosodium urate in synovial fluid or tophus. All synovial fluid samples obtained from inflamed joints that are undiagnosed by arthrocentesis should be examined for these crystals. Under a polarized light microscope, they have strong needle-like morphology and strong negative birefringence. This test is difficult and requires a trained observer. The fluid should be examined relatively soon after aspiration, as the temperature and pH affect the solubility.
Blood tests
Hyperuricemia is a classic feature of gout, but almost half the time of gout occurs without hyperuricemia and most people with elevated uric acid levels never develop gout. Thus, the diagnostic utility for measuring uric acid levels is limited. Hyperuricemia is defined as plasma veins greater than 420? Mol/l (7.0 mg/dl) in men and 360? Mol/l (6.0 mg/dl) in women. Another common blood test is the number of white blood cells, electrolytes, kidney function and blood sedimentation rate (LED). However, both white blood cells and LEDs may increase due to uric acid in the absence of infection. The number of white blood cells as high as 40.0ÃÆ' â € "10 9 /l (40.000/mm 3 ) has been documented.
Differential diagnosis
The most important differential diagnosis of gout is septic arthritis. This should be considered for those with signs of infection or those who do not improve with treatment. To help with the diagnosis, Gram fluids and synovial fluids can be performed. Other conditions that may look similar include pseudogout, rheumatoid arthritis, psoriatic arthritis, and reactive arthritis. Gouty tophi, especially when it is not located in the joint, can be mistaken as basal cell carcinoma or other neoplasm.
Prevention
Lifestyle changes and treatment can reduce uric acid levels. Effective diet and lifestyle choices include reducing the intake of purine rich foods from animals such as meat and seafood, alcohol, and fructose (especially high fructose corn syrup). Eating dairy products, vitamin C, coffee, and cherries can help prevent gout attacks, as well as lose weight. Gout may be secondary to sleep apnea through the release of purines from oxygen-deficient cells. Apnea treatment can reduce the occurrence of attacks.
Prophylaxis
A number of drugs are useful for preventing further episodes of gout, including allopurinol, febuxostat, and probenecid. Long-term drugs are not recommended until a person has two gout attacks, except for destructive joint changes, tophi, or urate nephropathy. Until now the drugs are not cost-effective. They usually do not start until one to two weeks after the acute flare has been resolved, as theoretical worries worsen the attack. They are often used in combination with NSAIDs or colchicine for the first three to six months.
Urinalization measures should be increased until serum uric acid levels are below 300-360 Ã,Âμmol/l (5.0-6.0 mg/dl) and continue indefinitely. If these drugs are used chronically during an attack, it is recommended that they be continued. Levels that can not be brought below 6.0 mg/dl while attacks continue to show refractory gout.
Although it is historically not recommended to initiate allopurinol during acute attacks of uric acid, this practice appears to be fine. Allopurinol inhibits the production of uric acid, and is the most commonly used agent. Long-term therapy is safe and well-tolerated, and can be used in people with kidney or gastric disorders, although hypersensitivity occurs in a small number of individuals.
Febuxostat is usually recommended only to those who can not tolerate allopurinol. There is concern about further cardiac-associated death with febuxostat compared with allopurinol. Probenecid appears to be less effective than allopurinol and is a second-line agent. Probenecid may be used if uric acid is not available (urine urine 24 hours less than 800 mg). However, it is not recommended if someone has a history of kidney stones. Pegloticase is an option for 3% of people who are intolerant of other drugs. This is a third-line agent. Pegloticase is given as an intravenous infusion every two weeks, and reduces uric acid levels. Pegloticase is useful for reducing tophi but has high side effects and many people develop resistance to it. In 2016 withdrawn from the European market.
Treatment
The initial goal of treatment is to solve the symptoms of acute attacks. Repeated attacks can be prevented by drugs that reduce serum uric acid levels. Temporary evidence supports the application of ice for 20 to 30 minutes several times a day to reduce pain. Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and steroids. While steroids and NSAIDs work well, steroids may be safer. Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure disease. Treatment of related health issues is also important. Lifestyle intervention has been poorly learned. It is unclear whether dietary supplements have an effect on people with gout.
NSAIDs
NSAIDs are the usual first-line treatment for gout. No special agent is significantly more or less effective than others. Improvements can be seen in four hours and treatment is recommended for one to two weeks. They are not recommended, however, in those with other specific health problems, such as gastrointestinal bleeding, kidney failure, or heart failure. While indometacin is historically the most commonly used, alternative, such as ibuprofen, it may be preferred because of its better side-effect profile without superior effectiveness. For those at risk of gastric side effects of NSAIDs, additional proton pump inhibitors may be given. There is some evidence that COX-2 inhibitors can work as well as nonselective NSAIDs for acute uric acid attacks with fewer side effects.
Colchicine
Colchicine is an alternative for those who can not tolerate NSAIDs. At high doses, side effects (especially gastrointestinal disorders) limit their use. At lower doses, which are still effective, it is well tolerated. Colchicine can interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.
Steroids
Glucocorticoids have been found to be as effective as NSAIDs and may be used if there are contraindications to NSAIDs. They also lead to improvement when injected into the joint. However, joint infection should be excluded, as steroids worsen this condition.
More
Interleukin-1 inhibitors, such as canakinumab, exhibit moderate effectiveness to relieve pain and reduce joint swelling, but have an increased risk of side effects, such as back pain, headache, and elevated blood pressure. They, however, can work less well than usual doses of NSAIDS. The high cost of these class medications can also reduce their use to treat gout.
Prognosis
Without treatment, acute gout attacks usually disappear within five to seven days; However, 60% of people suffered a second attack in one year. Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus at an increased risk of death. It is unclear whether drugs that lower uric acid affect the risk of cardiovascular disease. This may be partly due to its association with insulin resistance and obesity, but some increased risks appear to be independent.
Without treatment, acute gout episodes can develop into chronic gout with joint surface destruction, joint deformity, and painless tophi. This tophi occurs in 30% of those not treated for five years, often in the ear helix, above the olecranon process, or on the Achilles tendon. With aggressive treatment, they can dissolve. Kidney stones also often complicate gout, which affects between 10 and 40% of people and occurs because of the low urine pH that encourages the deposition of uric acid. Other forms of chronic renal dysfunction may occur.
- Epidemiology
- Gout on Curlie (based on DMOZ)
- Hui, M; Carr, A; Cameron, S; Davenport, G; Doherty, M; Forrester, H; Jenkins, W; Jordan, KM; Mallen, CD; McDonald, TM; Nuki, G; Pywell, A; Zhang, W; Roddy, E; UK Society for Rheumatology, Audit and Working Group Standards, Group. (May 26, 2017). "The British Society for Rheumatology Guideline for Gout Management". Rheumatology (Oxford, UK) . 56 (7): e1-e20. doi: 10.1093/rheumatology/kex156. PMIDÃ, 28549177.
- Media related to Gout on Wikimedia Commons
- Ã, Chisholm, Hugh, ed. (1911). "Gout". EncyclopÃÆ'Â|dia Britannica . 12 (issue 11). Cambridge University Press. pp.Ã, 289-291.
Gout affects about 1-2% of the Western population at some point in their lifetime and becomes more common. Approximately 5.8 million people are affected by 2013. The gout rate is about twice that between 1990 and 2010. This increase is believed to be due to increased life expectancy, changes in diet and increased uric acid-related diseases, such as metabolic syndrome and high blood pressure. pressure. Factors that affect the gout level, including age, race, and season of the year. In men over 30 years and women over 50 years, the price is 2%.
In the United States, uric acid is twice as likely in men of African descent than in European descent. High prices between the Pacific Islands and M? Ori, but the disease is rare in native Australians, although serum uric acid concentrations are on average higher in the second group. It is common in China, Polynesia, and sub-Saharan African cities. Some studies have found that gout attacks are more common in the spring. It has been linked to seasonal changes in diet, alcohol consumption, physical activity, and temperature.
History
The term "gout" was originally used by Randolphus of Bocking, about 1200 AD. It comes from the Latin gutta , which means "drop" (liquid). According to the Oxford English Dictionary, this comes from humorism and "the idea of ​​'dropping' morbid substances from the blood inside and around the joint."
Gout has been known since antiquity. Historically, it was referred to as "king of disease and disease of the king" or "disease of the rich". The first documentation of the disease came from Egypt in 2,600 BC in the description of the big toe arthritis. Greek physician Hippocrates around 400 BC commented on his Aphorisms, noting his absence in eunuchs and premenopausal women. Aulus Cornelius Celsus (30 AD) describes the association with alcohol, then arises in women and related kidney problems:
Again the thick urine, the sediment from the white, indicates that the pain and illness must be caught in the joint or viscera area... The joint problem in the hands and feet is very frequent and persistent, as is the case with podagra. and cheiragra. They rarely attack eunuchs or boys before a coalition with women, or women unless those who are menstruating have been suppressed... some have gained a lifelong security by refraining from wine, mead and vang.
In 1683, Thomas Sydenham, a British doctor, described the incident in the early hours of the morning and his passion for older men:
Gout patients usually, in general, old men or men who have used it themselves in youth as it has brought on premature old age - from such unscrupulous habits is nothing more common than too early and excessive penchant in life and such tiring. lust. Victims sleep and sleep with good health. Around two o'clock in the morning he was awakened by a tremendous pain in his big toe; more rarely on the heel, ankle, or back foot. The pain is like a dislocation and some feel as if cold water is poured over it. Then follow the chills and chills and a little fever... Evening is passed in torture, sleeplessness, altering the affected part and changing posture continuously; throwing the body like unrelenting as the pain of the tortured joint and getting worse when the fit comes.
Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of crystal veins in 1679. In 1848, British physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.
Other animals
Gout is rare in most other animals because of their ability to produce uricase, which breaks down uric acid. Humans and other great apes do not have this ability, so gout is a common thing. Other animals with uricase include fish, amphibians, and most non-primate mammals. The Tyrannosaurus rex specimen known as "Sue", however, is believed to have suffered from gout.
Research
A number of new drugs are being studied to treat gout, including anakinra, canakinumab, and rilonacept. Canakinumab can produce better results than low-dose steroids, but it costs five thousand times more. Recombinant enzyme uricase (rasburicase) is available; its use, however, is limited, because it triggers an immune response. Less antigenic version is under development.
References
External links
Source of the article : Wikipedia
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