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7/31/2019 Gout is a Rheumatoid Form of Arthritis That Causes the Inflammation
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Gout - Topic OverviewWhat is gout?
Gout is a kind ofarthritis. It can cause an attack of sudden burning pain, stiffness, and swelling in a joint,
usually a big toe. These attacks can happen over and over unlessgoutis treated. Over time, they can
harm your joints, tendons, and other tissues. Gout is most common in men.
What causes gout?
Gout is caused by too muchuric acidin theblood. Most of the time, having too much uric acid is not
harmful. Many people with high levels in their blood never get gout. But when uric acid levels in the blood
are too high, the uric acid may form hard crystals in your joints.
Your chances of getting gout are higher if you areoverweight, drink too much alcohol, or eat too much
meat and fish that are high in chemicals called purines. Some medicines, such as water pills (diuretics),
can also bring on gout.
What are the symptoms?
The most common sign of gout is a nighttime attack of swelling, tenderness, redness, and sharp pain in
yourbig toe . You can also get gout attacks in yourfoot, ankle, or knees. The attacks can last a few
days or many weeks before the pain goes away. Another attack may not happen for months or years.
See your doctor even if your pain from gout is gone. The buildup of uric acid that led to your gout attack
can still harm your joints.
How is gout diagnosed?
Your doctor will ask questions about your symptoms and do aphysical exam. Your doctor may also take
a sample of fluid from your joint to look for uric acid crystals. This is the best way to test for gout. Your
doctor may also do a blood test to measure the amount of uric acid in your blood.
How is it treated?
To stop a gout attack, your doctor can give you a shot of corticosteroids, or prescribe a large daily dose of
one or more medicines. The doses will get smaller as your symptoms go away. Relief from a gout attackoften begins within 24 hours if you start treatment right away.
To ease the pain during a gout attack, rest the joint that hurts. Takingibuprofenor anotheranti-
inflammatory medicinecan also help you feel better. But don't takeaspirin. It can make gout worse by
raising the uric acid level in the blood.
To prevent future attacks, your doctor can prescribe a medicine to reduce uric acid buildup in your blood.
If your doctor prescribes medicine to lower your uric acid levels, be sure to take it as directed. Most
people continue to take this medicine for the rest of their lives.
Paying attention to what you eat may help you manage your gout. Eat moderate amounts of a healthy mix
of foods to control yourweightand get the nutrients you need. Avoid regular daily intake of meat,
seafood, and alcohol (especially beer). Drink plenty of water and other fluids.
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Gout is a rheumatoid form of arthritis that causes the inflammation, joint pain and swelling especially in
the toe, knee and ankle, also reducing their mobility. Gout usually appears in midlife and primarily in
males. It can be hereditary or the secondary to some other disease process.
Gout is mainly caused by the clustering of uric acid crystals in the arteries, obstructing normal blood flow
and causing inflammation. Uric acid is a residual product that is excreted from the body through urine
during synthesis of purine a substance that presents in fat meats, fish, some dairy products and
vegetables. The level of uric acid can be found and measured in the blood.
In most cases, the first gout signs appear at the level of the big toe. The skin around the affected regions
turns yellow, appears to be stretched and bruised. The regions affected by gout become very sensitive. It
even causes the sufferers cant tolerate clothing or shoes. Gout attacks in the region of the big toe are
referred to as podagra and they involve inflammation, swelling, pain and a sensation of burning. Podagra
can also occur due to acquired injuries or intense physical effort that involves the lower limbs.
Apart from the region of the toes, recurrent attacks also involve pain and inflammation of the knees,
elbows, shoulders, wrists and fingers. Most types of gout attacks can generate low to moderate fever and
sweating.
And when gout becomes chronic, the damage to the joint is deforming and crippling. Chronic gout attacks
are usually long-lasting and they occur in multiple regions of the body.
The main symptoms of gout are severe pain and swelling in joints. Its the crystallized and lodged of uric
acid in the joints that cause joint pain. The joint gets hot, swollen and tender. In most cases, the pain
attacks seem to amplify at night causing sleeping difficulty to many patients. How long can gout painremain?The pain may remain anywhere from a few minutes to a few hours and in some cases, even days.
As the disease progresses, the duration of gout attacks can exceed 7-10 days.
Other common gout symptoms include fever, discomfort, sourness, malaise, tachycardia, elevations in
skin temperature, itching sensations, body aches, water retention, inflammation and intense pain of the
affected area gout in the knee cause joint pain in the knee whereas gout in the finger or toe cause pain
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in finger or toe. The skin in the affected regions often looks stretched. Gouty arthritis may also cause back
pain since it affects the joints.
There are few therapies available for treating gout. Fortunately gout attacks subside within a period of a
week or so and gout attacks are less frequent. There may be period ranging from months to even years
between two gout attacks.
GoutFrom Wikipedia, the free encyclopedia
"Podagra" redirects here. For the moth genus, seePodagra (moth).
Gout
Classification and external resources
Gout, a 1799 caricature byJames Gillray
ICD-10 M10
ICD-9 274.00274.1274.8274.9
OMIM 138900300323
DiseasesDB 29031
MedlinePlus 000422
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eMedicine emerg/221med/924med/1112oph/506orthoped/124radio/313
MeSH D006073
Gout (also known as podagra when it involves the big toe)[1]is amedical conditionusually characterized by
recurrent attacks of acuteinflammatory arthritisa red, tender, hot,swollen joint. Themetatarsal-phalangeal
jointat the base of thebig toeis the most commonly affected (approximately 50% of cases). However, it may
also present astophi,kidney stones, orurate nephropathy. It is caused by elevated levels ofuric acidin
thebloodwhich crystallize, and the crystals are deposited in joints,tendons, and surroundingtissues.
A clinical diagnosis is confirmed by the visualization of the characteristic crystals in joint fluid. Treatment
withnonsteroidal anti-inflammatory drugs(NSAIDs),steroids, orcolchicineimproves symptoms. Once the acute
attack has subsided, levels of uric acid are usually lowered via lifestyle changes, and in those with frequent
attacks,allopurinolorprobenecidprovide long-term prevention.
Gout has increased in frequency in recent decades, affecting about 1-2% of theWesternpopulation at some
point in their lives. The increase is believed to be due to increasing risk factors in the population, such
asmetabolic syndrome, longerlife expectancyand changes in diet. Gout was historically known as "the
disease of kings" or "rich man's disease".
Contents
[hide]
1 Signs and symptoms
2 Cause
o 2.1 Lifestyle
o 2.2 Genetics
o 2.3 Medical conditions
o 2.4 Medication
3 Pathophysiology
4 Diagnosis
o 4.1 Synovial fluid
o 4.2 Blood tests
o 4.3 Differential diagnosis
5 Prevention
6 Treatment
http://en.wikipedia.org/wiki/EMedicinehttp://www.emedicine.com/emerg/topic221.htmhttp://www.emedicine.com/med/topic924.htmhttp://www.emedicine.com/med/topic924.htmhttp://www.emedicine.com/oph/topic506.htmhttp://www.emedicine.com/oph/topic506.htmhttp://www.emedicine.com/radio/topic313.htmhttp://www.emedicine.com/radio/topic313.htmhttp://www.emedicine.com/radio/topic313.htmhttp://en.wikipedia.org/wiki/Medical_Subject_Headingshttp://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?field=uid&term=D006073http://en.wikipedia.org/wiki/Gout#cite_note-Egg2007-0http://en.wikipedia.org/wiki/Gout#cite_note-Egg2007-0http://en.wikipedia.org/wiki/Gout#cite_note-Egg2007-0http://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Inflammatory_arthritishttp://en.wikipedia.org/wiki/Inflammatory_arthritishttp://en.wikipedia.org/wiki/Joint_effusionhttp://en.wikipedia.org/wiki/Joint_effusionhttp://en.wikipedia.org/wiki/Joint_effusionhttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Halluxhttp://en.wikipedia.org/wiki/Halluxhttp://en.wikipedia.org/wiki/Halluxhttp://en.wikipedia.org/wiki/Tophihttp://en.wikipedia.org/wiki/Tophihttp://en.wikipedia.org/wiki/Tophihttp://en.wikipedia.org/wiki/Kidney_stoneshttp://en.wikipedia.org/wiki/Kidney_stoneshttp://en.wikipedia.org/wiki/Kidney_stoneshttp://en.wikipedia.org/wiki/Urate_nephropathyhttp://en.wikipedia.org/wiki/Urate_nephropathyhttp://en.wikipedia.org/wiki/Urate_nephropathyhttp://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Tendonhttp://en.wikipedia.org/wiki/Tendonhttp://en.wikipedia.org/wiki/Tendonhttp://en.wikipedia.org/wiki/Tissue_(biology)http://en.wikipedia.org/wiki/Tissue_(biology)http://en.wikipedia.org/wiki/Tissue_(biology)http://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Western_worldhttp://en.wikipedia.org/wiki/Western_worldhttp://en.wikipedia.org/wiki/Western_worldhttp://en.wikipedia.org/wiki/Metabolic_syndromehttp://en.wikipedia.org/wiki/Metabolic_syndromehttp://en.wikipedia.org/wiki/Metabolic_syndromehttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Gout#Signs_and_symptomshttp://en.wikipedia.org/wiki/Gout#Signs_and_symptomshttp://en.wikipedia.org/wiki/Gout#Causehttp://en.wikipedia.org/wiki/Gout#Causehttp://en.wikipedia.org/wiki/Gout#Lifestylehttp://en.wikipedia.org/wiki/Gout#Lifestylehttp://en.wikipedia.org/wiki/Gout#Geneticshttp://en.wikipedia.org/wiki/Gout#Geneticshttp://en.wikipedia.org/wiki/Gout#Medical_conditionshttp://en.wikipedia.org/wiki/Gout#Medical_conditionshttp://en.wikipedia.org/wiki/Gout#Medicationhttp://en.wikipedia.org/wiki/Gout#Medicationhttp://en.wikipedia.org/wiki/Gout#Pathophysiologyhttp://en.wikipedia.org/wiki/Gout#Pathophysiologyhttp://en.wikipedia.org/wiki/Gout#Diagnosishttp://en.wikipedia.org/wiki/Gout#Diagnosishttp://en.wikipedia.org/wiki/Gout#Synovial_fluidhttp://en.wikipedia.org/wiki/Gout#Synovial_fluidhttp://en.wikipedia.org/wiki/Gout#Blood_testshttp://en.wikipedia.org/wiki/Gout#Blood_testshttp://en.wikipedia.org/wiki/Gout#Differential_diagnosishttp://en.wikipedia.org/wiki/Gout#Differential_diagnosishttp://en.wikipedia.org/wiki/Gout#Preventionhttp://en.wikipedia.org/wiki/Gout#Preventionhttp://en.wikipedia.org/wiki/Gout#Treatmenthttp://en.wikipedia.org/wiki/Gout#Treatmenthttp://en.wikipedia.org/wiki/Gout#Treatmenthttp://en.wikipedia.org/wiki/Gout#Preventionhttp://en.wikipedia.org/wiki/Gout#Differential_diagnosishttp://en.wikipedia.org/wiki/Gout#Blood_testshttp://en.wikipedia.org/wiki/Gout#Synovial_fluidhttp://en.wikipedia.org/wiki/Gout#Diagnosishttp://en.wikipedia.org/wiki/Gout#Pathophysiologyhttp://en.wikipedia.org/wiki/Gout#Medicationhttp://en.wikipedia.org/wiki/Gout#Medical_conditionshttp://en.wikipedia.org/wiki/Gout#Geneticshttp://en.wikipedia.org/wiki/Gout#Lifestylehttp://en.wikipedia.org/wiki/Gout#Causehttp://en.wikipedia.org/wiki/Gout#Signs_and_symptomshttp://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Life_expectancyhttp://en.wikipedia.org/wiki/Metabolic_syndromehttp://en.wikipedia.org/wiki/Western_worldhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Tissue_(biology)http://en.wikipedia.org/wiki/Tendonhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Urate_nephropathyhttp://en.wikipedia.org/wiki/Kidney_stoneshttp://en.wikipedia.org/wiki/Tophihttp://en.wikipedia.org/wiki/Halluxhttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Metatarsophalangeal_articulationshttp://en.wikipedia.org/wiki/Joint_effusionhttp://en.wikipedia.org/wiki/Inflammatory_arthritishttp://en.wikipedia.org/wiki/Diseasehttp://en.wikipedia.org/wiki/Gout#cite_note-Egg2007-0http://www.nlm.nih.gov/cgi/mesh/2011/MB_cgi?field=uid&term=D006073http://en.wikipedia.org/wiki/Medical_Subject_Headingshttp://www.emedicine.com/radio/topic313.htmhttp://www.emedicine.com/oph/topic506.htmhttp://www.emedicine.com/oph/topic506.htmhttp://www.emedicine.com/med/topic924.htmhttp://www.emedicine.com/med/topic924.htmhttp://www.emedicine.com/emerg/topic221.htmhttp://en.wikipedia.org/wiki/EMedicine7/31/2019 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o 6.1 NSAIDs
o 6.2 Colchicine
o 6.3 Steroids
o
6.4 Pegloticase
o 6.5 Prophylaxis
7 Prognosis
8 Epidemiology
9 History
10 In other animals
11 Research
12 References
13 External links
Signs and symptoms
Gout presenting in themetatarsal-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 thebig 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 24 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,
includingfatigueand a highfever.[1][3]
Long-standing elevateduric acidlevels (hyperuricemia) may result in other symptomatology, including hard,
painless deposits of uric acid crystals known astophi. Extensive tophi may lead to chronicarthritisdue to bone
erosion.[4]
Elevated levels of uric acid may also lead to crystals precipitating in thekidneys, resulting
instoneformation and subsequenturate nephropathy.[5]
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Cause
Hyperuricemiais the underlying cause of gout. This can occur for a number of reasons, including diet, genetic
predisposition, or underexcretion ofurate, 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 than10%.
[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 mol/l (7
and 8.9 mg/dl), the risk is 0.5% per year, while in those with a level greater than 535 mol/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 includephysical traumaand
surgery.[6]
Recent studies have found dietary factors once believed to be associated are, in fact, not, including
the intake ofpurine-rich vegetables (e.g., beans, peas, lentils, and spinach) and total protein.[9][10]
The
consumption ofcoffee,vitamin Canddairy products, as well as physical fitness, appear to decrease the
risk.[11][12][13]
This is believed to be partly due to their effect in reducinginsulin resistance.[13]
Genetics
The occurrence of gout is partly genetic, contributing to about 60% ofvariabilityin uric acid
level.[6]
TwogenescalledSLC2A9andABCG2have been found to commonly be associated with gout, and
variations in them can approximately double the risk.[14]
A few rare genetic disorders, includingfamilial juvenile
hyperuricemic nephropathy,medullary cystic kidney disease,phosphoribosylpyrophosphate
synthetasesuperactivity, andhypoxanthine-guanine phosphoribosyltransferasedeficiency as seen inLesch-
Nyhan syndrome, are complicated by gout.[6]
Medical conditions
Gout frequently occurs in combination with other medical problems.Metabolic syndrome, a combination
ofabdominal obesity,hypertension,insulin resistanceandabnormal lipid levels, occurs in nearly 75% of
cases.[3]
Other conditions commonly complicated by gout include:polycythemia,lead poisoning,renal
failure,hemolytic anemia,psoriasis, andsolid organ transplants.[6][15]
Abody mass indexgreater than or equal
to 35 increases a male's risk of gout threefold.[10]Chronic lead exposure and lead-contaminated alcohol are risk
factors for gout due to the harmful effect of lead on kidney function.[16]
Lesch-Nyhan syndromeis often
associated with gouty arthritis.
Medication
Diureticshave been associated with attacks of gout. However, a low dose ofhydrochlorothiazidedoes not
seem to increase the risk.[17]
Other medicines that have been associated
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ic_acid#Solubility_of_uric_acid_and_its_saltshttp://en.wikipedia.org/wiki/Hyperuricemia7/31/2019 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includeniacinandaspirin(acetylsalicylic acid).[4]
Theimmunosuppressive drugsciclosporinandtacrolimusare
also associated with gout,[6]
the former particularly when used in combination with hydrochlorothiazide.[18]
Pathophysiology
Uric acid
Gout is a disorder ofpurine metabolism,[6]
and occurs when its final metabolite,uric acid, crystallizes in the
form of monosodium urate, precipitating in joints, on tendons, and in the surrounding tissues.[4]
These crystals
then trigger a localimmune-mediatedinflammatoryreaction,[4]
with one of the key proteins in the inflammatory
cascade beinginterleukin 1.[6]
An evolutionary loss ofuricase, which breaks down uric acid, in humans and
higherprimateshas made this condition common.[6]
The triggers for precipitation of uric acid are not well understood. While it may crystallize at normal levels, it is
more likely to do so as levels increase.[4][19]
Other factors believed to be important in triggering an acute
episode of arthritis include cool temperatures, rapid changes in uric acid levels,acidosis,[20][21]
articular
hydration, andextracellular matrixproteins, such asproteoglycans,collagens, andchondroitin sulfate.[6]The
increased precipitation at low temperatures partly explains why the joints in the feet are most commonly
affected.[2]
Rapid changes in uric acid may occur due to a number of factors, including trauma,
surgery,chemotherapy, diuretics, and stopping or startingallopurinol.[1]Calcium channel
blockersandlosartanare associated with a lower risk of gout as compared to other medications
forhypertension.[22]
Diagnosis
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ile:Harns%C3%A4ure_Ketoform.svghttp://en.wikipedia.org/wiki/File:Harns%C3%A4ure_Ketoform.svghttp://en.wikipedia.org/wiki/Gout#cite_note-pmid22240117-21http://en.wikipedia.org/wiki/Hypertensionhttp://en.wikipedia.org/wiki/Losartanhttp://en.wikipedia.org/wiki/Calcium_channel_blockerhttp://en.wikipedia.org/wiki/Calcium_channel_blockerhttp://en.wikipedia.org/wiki/Gout#cite_note-Egg2007-0http://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Chemotherapyhttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Chondroitin_sulfatehttp://en.wikipedia.org/wiki/Collagenshttp://en.wikipedia.org/wiki/Proteoglycanshttp://en.wikipedia.org/wiki/Extracellular_matrixhttp://en.wikipedia.org/wiki/Gout#cite_note-pmid12672211-19http://en.wikipedia.org/wiki/Gout#cite_note-pmid12672211-19http://en.wikipedia.org/wiki/Acidosishttp://en.wikipedia.org/wiki/Gout#cite_note-Nature2009-3http://en.wikipedia.org/wiki/Gout#cite_note-Nature2009-3http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Primatehttp://en.wikipedia.org/wiki/Uricasehttp://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Interleukin_1%CE%B2http://en.wikipedia.org/wiki/Gout#cite_note-Nature2009-3http://en.wikipedia.org/wiki/Inflammationhttp://en.wikipedia.org/wiki/Immunehttp://en.wikipedia.org/wiki/Gout#cite_note-Nature2009-3http://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Purine_metabolismhttp://en.wikipedia.org/wiki/Uric_acidhttp://en.wikipedia.org/wiki/Gout#cite_note-17http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Tacrolimushttp://en.wikipedia.org/wiki/Ciclosporinhttp://en.wikipedia.org/wiki/Immunosuppressive_drughttp://en.wikipedia.org/wiki/Gout#cite_note-Nature2009-3http://en.wikipedia.org/wiki/Aspirinhttp://en.wikipedia.org/wiki/Niacin7/31/2019 Gout is a Rheumatoid Form of Arthritis That Causes the Inflammation
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Gout onX-raysof 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 asynovial fluidsample photographed under a microscope withpolarized 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 podagra. Synovial fluid analysis should be done, however, if the diagnosis is in doubt.[1]
X-rays, while
useful for identifying chronic gout, have little utility in acute attacks.[6]
Synovial fluid
A definitive diagnosis of gout is based upon the identification ofmonosodium urate crystalsinsynovial fluidor
atophus.
[3]
All synovial fluid samples obtained from undiagnosed inflamed joints should be examined for thesecrystals.
[6]Underpolarized lightmicroscopy, they have a needle-like morphology and strong
negativebirefringence. This test is difficult to perform, and often requires a trained observer.[23]
The fluid must
also be examined relatively quickly after aspiration, as temperature and pH affect their solubility.[6]
Blood tests
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Hyperuricemiais a classic feature of gout, but it occurs nearly half of the time without hyperuricemia, and most
people with raised uric acid levels never develop gout.[3][24]
Thus, the diagnostic utility of measuring uric acid
level is limited.[3]
Hyperuricemia is defined as aplasmaurate level greater than 420 mol/l (7.0 mg/dl) in males
and 360 mol/l (6.0 mg/dl) in females.[25]
Other blood tests commonly performed arewhite blood cell
count,electrolytes,renal function, anderythrocyte sedimentation rate(ESR). However, both the white blood
cells and ESR may be elevated due to gout in the absence of infection.[26][27]
A white blood cell count as high as
40.0109/l (40,000/mm
3) has been documented.
[1]
Differential diagnosis
The most importantdifferential diagnosisin gout isseptic arthritis.[3][6]
This should be considered in those with
signs of infection or those who do not improve with treatment.[3]
To help with diagnosis, a synovial fluidGram
stainand culture may be performed.[3]
Other conditions which present similarly
includepseudogoutandrheumatoid arthritis.[3]
Gouty tophi, in particular when not located in a joint, can be
mistaken forbasal cell carcinoma,[28]
or otherneoplasms.[29]
Prevention
Both lifestyle changes and medications can decrease uric acid levels. Dietary and lifestyle choices that are
effective include reducing intake of food such as meat and seafood, consuming adequatevitamin C,
limitingalcoholandfructoseconsumption, and avoidingobesity.[2]
Alow-calorie dietin obese men decreased
uric acid levels by 100 mol/l (1.7 mg/dl).[17]
Vitamin C intake of 1,500 mg per day decreases the risk of gout by
45%.[30]
Coffee, but not tea, consumption is associated with a lower risk of gout.[31]
Gout may be secondary
tosleep apneavia the release ofpurinesfrom oxygen-starved cells. Treatment of apnea can lessen theoccurrence of attacks.[32]
Treatment
The initial aim of treatment is to settle the symptoms of an acute attack.[33]
Repeated attacks can be prevented
by different drugs used to reduce the serum uric acid levels.[33]
Ice applied for 20 to 30 minutes several times a
day decreases pain.[2][34]
Options for acute treatment includenonsteroidal anti-inflammatory
drugs(NSAIDs),colchicineandsteroids,[2]
while options for prevention
includeallopurinol,febuxostatandprobenecid. Lowering uric acid levels can cure the disease.[6]
Treatment
ofcomorbiditiesis also important.[6]
NSAIDs
NSAIDs are the usual first-line treatment for gout, and no specific agent is significantly more or less effective
than any other.[2]
Improvement may be seen within four hours, and treatment is recommended for one to two
weeks.[2][6]
They are not recommended, however, in those with certain other health problems, such
asgastrointestinal bleeding,renal failure, orheart failure.[35]
Whileindomethacinhas historically been the most
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ia.org/wiki/Gout#cite_note-pmid16707532-32http://en.wikipedia.org/wiki/Gout#cite_note-pmid16707532-32http://en.wikipedia.org/wiki/Gout#cite_note-pmid16707532-32http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Comorbidityhttp://en.wikipedia.org/wiki/Comorbidityhttp://en.wikipedia.org/wiki/Comorbidityhttp://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gastrointestinal_bleedinghttp://en.wikipedia.org/wiki/Gastrointestinal_bleedinghttp://en.wikipedia.org/wiki/Gastrointestinal_bleedinghttp://en.wikipedia.org/wiki/Renal_failurehttp://en.wikipedia.org/wiki/Renal_failurehttp://en.wikipedia.org/wiki/Renal_failurehttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Gout#cite_note-JFP09-34http://en.wikipedia.org/wiki/Gout#cite_note-JFP09-34http://en.wikipedia.org/wiki/Gout#cite_note-JFP09-34http://en.wikipedia.org/wiki/Indomethacinhttp://en.wikipedia.org/wiki/Indomethacinhttp://en.wikipedia.org/wiki/Indomethacinhttp://en.wikipedia.org/wiki/Indomethacinhttp://en.wikipedia.org/wiki/Gout#cite_note-JFP09-34http://en.wikipedia.org/wiki/Heart_failurehttp://en.wikipedia.org/wiki/Renal_failurehttp://en.wikipedia.org/wiki/Gastrointestinal_bleedinghttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Comorbidityhttp://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Steroidshttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Nonsteroidal_anti-inflammatory_drugshttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-pmid16707532-32http://en.wikipedia.org/wiki/Gout#cite_note-pmid16707532-32http://en.wikipedia.org/wiki/Gout#cite_note-pmid16171252-31http://en.wikipedia.org/wiki/Purinehttp://en.wikipedia.org/wiki/Sleep_apneahttp://en.wikipedia.org/wiki/Gout#cite_note-30http://en.wikipedia.org/wiki/Gout#cite_note-29http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Low-calorie_diethttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Obesityhttp://en.wikipedia.org/wiki/Fructosehttp://en.wikipedia.org/wiki/Alcoholhttp://en.wikipedia.org/wiki/Vitamin_Chttp://en.wikipedia.org/wiki/Gout#cite_note-28http://en.wikipedia.org/wiki/Neoplasmhttp://en.wikipedia.org/wiki/Gout#cite_note-27http://en.wikipedia.org/wiki/Basal_cell_carcinomahttp://en.wikipedia.org/wiki/Gout#cite_note-PM2010-2http://en.wikipedia.org/wiki/Rheumatoid_arthritishttp://en.wikipedia.org/wiki/Pseudogouthttp://en.wikipedia.org/wiki/Gout#cite_note-PM2010-2http://en.wikipedia.org/wiki/Gram_stainhttp://en.wikipedia.org/wiki/Gram_stainhttp://en.wikipedia.org/wiki/Gout#cite_note-PM2010-2http://en.wikipedia.org/wiki/Gout#cite_note-PM2010-2http://en.wikipedia.org/wiki/Gout#cite_note-PM2010-2htt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commonly used NSAID, an alternative, such asibuprofen, may be preferred due to its better side effect profile
in the absence of superior effectiveness.[17]
For those at risk of gastric side effects from NSAIDs, an
additionalproton pump inhibitormay be given.[36]
Colchicine
Colchicineis an alternative for those unable to tolerate NSAIDs.[2]
Its side effects (primarily gastrointestinal
upset) limit its usage.[37]
Gastrointestinal upset, however, depends on the dose, and the risk can be decreased
by using smaller yet still effective doses.[17]Colchicine may interact with other commonly prescribed drugs,
such asatorvastatinanderythromycin, among others.[37]
Steroids
Glucocorticoidshave been found to be as effective as NSAIDs[38]
and may be used if contraindications exist for
NSAIDs.[2]
They also lead to improvement wheninjected into the joint; ajoint infectionmust be excluded,
however, as steroids worsens this condition.[2]
Pegloticase
Pegloticase(Krystexxa) was approved in the USA to treat gout in 2010.[39]It will be an option for the 3% of
people who are intolerant to other medications.[39]
Pegloticase is administered as an intravenous infusion every
two weeks,[39]
and has been found to reduce uric acid levels in this population.[40]
Prophylaxis
A number of medications are useful for preventing further episodes of gout, includingxanthine oxidase
inhibitor(includingallopurinolandfebuxostat) anduricosurics(includingprobenecidandsulfinpyrazone). They
are not usually commenced until one to two weeks after an acute attack has resolved, due to theoretical
concerns of worsening the attack,[2]
and are often used in combination with either an NSAID or colchicine for
the first three to six months.[6]
They are not recommended until a person has had two attacks of gout,[2]
unless
destructive joint changes, tophi, orurate nephropathyexist,[5]
as medications have not been found to be cost
effective until this point.[2]
Urate-lowering measures should be increased until serum uric acid levels are below
300360 mol/l (5.0-6.0 mg/dl), and are continued indefinitely.[2][6]
If these medications are being used
chronically at the time of an attack, discontinueation is recommended.[3]
If levels cannot be brought below
6.0 mg/dl and there are recurrent attacks, this is deemed treatment failure or refractory gout .[41]
Overall,
probenecid appears to be less effective than allopurinol.[2]
Uricosuricmedications are typically preferred if undersecretion of uric acid, as indicated by a 24-hour collection
of urine results in a uric acid amount of less than 800 mg, is found.[42]
They are, however, not recommended if a
person has a history ofkidney stones.[42]
In a 24-hour urine excretion of more than 800 mg, which indicates
overproduction, axanthine oxidase inhibitoris preferred.[42]
http://en.wikipedia.org/wiki/Ibuprofenhttp://en.wikipedia.org/wiki/Ibuprofenhttp://en.wikipedia.org/wiki/Ibuprofenhttp://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Proton_pump_inhibitorhttp://en.wikipedia.org/wiki/Proton_pump_inhibitorhttp://en.wikipedia.org/wiki/Proton_pump_inhibitorhttp://en.wikipedia.org/wiki/Gout#cite_note-CKS-NLH-35http://en.wikipedia.org/wiki/Gout#cite_note-CKS-NLH-35http://en.wikipedia.org/wiki/Gout#cite_note-CKS-NLH-35http://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Colchicinehttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Gout#cite_note-CFP09-16http://en.wikipedia.org/wiki/Atorvastatinhttp://en.wikipedia.org/wiki/Atorvastatinhttp://en.wikipedia.org/wiki/Atorvastatinhttp://en.wikipedia.org/wiki/Erythromycinhttp://en.wikipedia.org/wiki/Erythromycinhttp://en.wikipedia.org/wiki/Erythromycinhttp://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Gout#cite_note-FDA_Warning-36http://en.wikipedia.org/wiki/Glucocorticoidhttp://en.wikipedia.org/wiki/Glucocorticoidhttp://en.wikipedia.org/wiki/Gout#cite_note-pmid17276548-37http://en.wikipedia.org/wiki/Gout#cite_note-pmid17276548-37http://en.wikipedia.org/wiki/Gout#cite_note-pmid17276548-37http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Joint_injectionhttp://en.wikipedia.org/wiki/Joint_injectionhttp://en.wikipedia.org/wiki/Joint_injectionhttp://en.wikipedia.org/wiki/Septic_arthritishttp://en.wikipedia.org/wiki/Septic_arthritishttp://en.wikipedia.org/wiki/Septic_arthritishttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Pegloticasehttp://en.wikipedia.org/wiki/Pegloticasehttp://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-FDA2010-38http://en.wikipedia.org/wiki/Gout#cite_note-39http://en.wikipedia.org/wiki/Gout#cite_note-39http://en.wikipedia.org/wiki/Gout#cite_note-39http://en.wikipedia.org/wiki/Xanthine_oxidase_inhibitorhttp://en.wikipedia.org/wiki/Xanthine_oxidase_inhibitorhttp://en.wikipedia.org/wiki/Xanthine_oxidase_inhibitorhttp://en.wikipedia.org/wiki/Xanthine_oxidase_inhibitorhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Allopurinolhttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Febuxostathttp://en.wikipedia.org/wiki/Uricosurichttp://en.wikipedia.org/wiki/Uricosurichttp://en.wikipedia.org/wiki/Uricosurichttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Probenecidhttp://en.wikipedia.org/wiki/Sulfinpyrazonehttp://en.wikipedia.org/wiki/Sulfinpyrazonehttp://en.wikipedia.org/wiki/Sulfinpyrazonehttp://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Lancet2010-5http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Acute_uric_acid_nephropathyhttp://en.wikipedia.org/wiki/Acute_uric_acid_nephropathyhttp://en.wikipedia.org/wiki/Acute_uric_acid_nephropathyhttp://en.wikipedia.org/wiki/Gout#cite_note-German09-4http://en.wikipedia.org/wiki/Gout#cite_note-German09-4http://en.wikipedia.org/wiki/Gout#cite_note-German09-4http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wikipedia.org/wiki/Gout#cite_note-Review08-1http://en.wi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Xanthine oxidase inhibitors (including allopurinol andfebuxostat) block uric acid production, and long-term
therapy is safe and well tolerated, and can be used in people with renal impairment or urate stones, although
allopurinol has caused hypersensitivity in a small number of individuals.[2]
In such cases, the alternative drug,
febuxostat, has been recommended.[43]
Prognosis
Without treatment, an acute attack of gout will usually resolve in five to seven days. However, 60% of people
will have a second attack within one year.[1]Those with gout are at increased risk ofhypertension,diabetes
mellitus,metabolic syndrome, and renal andcardiovascular disease, thus are at increased risk of
death.[6][44]
This may be partly due to its association withinsulin resistanceandobesity, but some of the
increased risk appears to be independent.[44]
Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint
deformity, and painless tophi.[6]
These tophi occur in 30% of those who are untreated for five years, often in
thehelixof the ear, over theolecranonprocesses, or on theAchilles tendons.[6]
With aggressive treatment,
they may dissolve.Kidney stonesalso frequently complicate gout, affecting between 10 and 40% of people,
and occur due to low urine pH promoting the precipitation of uric acid.[6]
Other forms ofchronic renal
dysfunctionmay occur.[6]
Nodules of the finger and helix of the ear representing goutytophi
Tophus of the knee
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Tophus of the toe, and over the external malleolus
Gout complicated by ruptured tophi (exudate tested positive for uric acid crystals)
Epidemiology
Gout affects around 12% of the Western population at some point in their lifetimes, and is becoming more
common.[2][6]
Rates of gout have approximately doubled between 1990 and 2010.[4]
This rise is believed to be
due to increasing life expectancy, changes in diet, and an increase in diseases associated with gout, such as
metabolic syndrome andhigh blood pressure.[10]
A number of factors have been found to influence rates of
gout, including age, race, and the season of the year. In men over the age of 30 and women over the age of
50, prevalence is 2%.[35]
In the United States, gout is twice as likely in African American males as it is in European Americans.
[45]
Ratesare high among the peoples of the Pacific Islands and theMoriof New Zealand, but rare in Australian
aborigines, despite a higher mean concentration of serum uric acid in the latter group.[46]
It has become
common in China, Polynesia, and urban sub-Saharan Africa.[6]
Some studies have found attacks of gout occur
more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption,
physical activity, and temperature.[47]
History
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