Gout

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"Podagra" redirects here. For the moth genus, see
Podagra (moth)
.

Gout
Other namesArthritis uratica, or Podagra when of the
NSAIDs, glucocorticoids, colchicine[4][8]
Frequency1–2% (developed world)[7]

Gout (

kidney damage.[3]

Gout is due to persistently elevated levels of uric acid (urate) in the blood (hyperuricemia).[4][7] This occurs from a combination of diet, other health problems, and genetic factors.[3][4] At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout.[3] Gout occurs more commonly in those who regularly drink beer or sugar-sweetened beverages; eat foods that are high in purines such as liver, shellfish, or anchovies; or are overweight.[3][5] Diagnosis of gout may be confirmed by the presence of crystals in the joint fluid or in a deposit outside the joint.[3] Blood uric acid levels may be normal during an attack.[3]

Treatment with

nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, or colchicine improves symptoms.[3][4][14] Once the acute attack subsides, levels of uric acid can be lowered via lifestyle changes and in those with frequent attacks, allopurinol or probenecid provides long-term prevention.[7] Taking vitamin C and having a diet high in low-fat dairy products may be preventive.[15][16]

Gout affects about 1–2% of adults in the developed world at some point in their lives.[7] It has become more common in recent decades.[3] This is believed to be due to increasing risk factors in the population, such as metabolic syndrome, longer life expectancy, and changes in diet.[7] Older males are most commonly affected.[3] Gout was historically known as "the disease of kings" or "rich man's disease".[7][17] It has been recognized at least since the time of the ancient Egyptians.[7]

Signs and symptoms

big toe

Gout can present in several ways, although the most common is a recurrent attack of acute

fatigue and high fever.[12][18]

Long-standing elevated

kidney stone formation and subsequent acute uric acid nephropathy.[20]

Cause

Arms and hands of a 50-year-old man, showing large tophi of sodium urate affecting the elbow, knuckles, and finger joints.

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.[3] 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%.[7] About 10% of people with hyperuricemia develop gout at some point in their lifetimes.[21] 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.[18]

Lifestyle

Dietary causes account for about 12% of gout,

physical trauma and surgery.[7]

Studies in the early 2000s found that other dietary factors are not relevant.

spirits.[28][29] Eating skim milk powder enriched with glycomacropeptide (GMP) and G600 milk fat extract may reduce pain but may result in diarrhea and nausea.[30]

Physical fitness, healthy weight, low-fat dairy products, and to a lesser extent, coffee and taking vitamin C, appear to decrease the risk of gout;[31][32][33][34] however, taking vitamin C supplements does not appear to have a significant effect in people who already have established gout.[3] Peanuts, brown bread, and fruit also appear protective.[25] This is believed to be partly due to their effect in reducing insulin resistance.[33]

Other than dietary and lifestyle choices, the recurrence of gout attacks is also linked to the weather. High ambient temperature and low relative humidity may increase the risk of a gout attack.[35]

Genetics

Gout is partly genetic, contributing to about 60% of

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.[7]

Medical conditions

Gout frequently occurs

myeloproliferative disorders such as polycythemia.[7][38] A body mass index greater than or equal to 35 increases male risk of gout threefold.[26] Chronic lead exposure and lead-contaminated alcohol are risk factors for gout due to the harmful effect of lead on kidney function.[39]

Medication

angiotensin receptor blockers, beta blockers, ritonavir, and pyrazinamide.[3][19] The immunosuppressive drugs ciclosporin and tacrolimus are also associated with gout,[7] the former more so when used in combination with hydrochlorothiazide.[41] Hyperuricemia may be induced by excessive use of Vitamin D supplements. Levels of serum uric acid have been positively associated with 25(OH) D. The incidence of hyperuricemia increased 9.4% for every 10 nmol/L increase in 25(OH) D (P < 0.001).[42]

Pathophysiology

structure of organic compound: 7,9-dihydro-1H-purine-2,6,8(3H)-trione
Chemical structure of uric acid

Gout is a disorder of

interleukin 1β, one of the key proteins in the inflammatory cascade.[3] An evolutionary loss of urate oxidase (uricase), which breaks down uric acid, in humans and higher primates has made this condition common.[7]

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.[19][44] Other triggers believed to be important in acute episodes of arthritis include cool temperatures, rapid changes in uric acid levels, acidosis, articular hydration and extracellular matrix proteins.[7][45][46] The increased precipitation at low temperatures partly explains why the joints in the feet are most commonly affected.[22] Rapid changes in uric acid may occur due to factors including trauma, surgery, chemotherapy and diuretics.[18] The starting or increasing of urate-lowering medications can lead to an acute attack of gout with febuxostat of a particularly high risk.[47] Calcium channel blockers and losartan are associated with a lower risk of gout compared to other medications for hypertension.[48]

Diagnosis

Synovial fluid examination[49][50]
Type WBC (per mm3) % neutrophils Viscosity Appearance
Normal <200 0 High Transparent
Osteoarthritis <5000 <25 High Clear yellow
Trauma <10,000 <50 Variable Bloody
Inflammatory 2,000–50,000 50–80 Low Cloudy yellow
Septic arthritis >50,000 >75 Low Cloudy yellow
Gonorrhea ~10,000 60 Low Cloudy yellow
Tuberculosis ~20,000 70 Low Cloudy yellow
Inflammatory: Arthritis, gout, rheumatoid arthritis, rheumatic fever

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 if the diagnosis is in doubt.

X-rays are usually normal and are not useful for confirming a diagnosis of early gout.[7] They may show signs of chronic gout such as bone erosion.[47]

Synovial fluid

A definitive diagnosis of gout is based upon the identification of

polarized light microscopy, they have a needle-like morphology and strong negative birefringence. This test is difficult to perform and requires a trained observer.[52] The fluid must be examined relatively soon after aspiration, as temperature and pH affect solubility.[7]

Blood tests

kidney function and erythrocyte sedimentation rate (ESR). However, both the white blood cells and ESR may be elevated due to gout in the absence of infection.[55][56] A white blood cell count as high as 40.0×109/l (40,000/mm3) has been documented.[18]

Differential diagnosis

The most important

basal cell carcinoma[57] or other neoplasms.[58]

  • Light microscopy of a touch preparation of a gout tophus, showing needle-shaped crystals.
    Light microscopy of a touch preparation of a gout tophus, showing needle-shaped crystals.
  • Uric acid crystals in polarized light, showing negative birefringence, with yellow color when aligned parallel to the axis of the red compensator, and blue when aligned perpendicularly to it.[59]
    Uric acid crystals in polarized light, showing negative birefringence, with yellow color when aligned parallel to the axis of the red compensator, and blue when aligned perpendicularly to it.[59]
  • In contrast, CPPD (pseudogout) displays rhombus-shaped crystals with positive birefringence.
    In contrast, CPPD (pseudogout) displays rhombus-shaped crystals with positive birefringence.
  • Gout on X-rays of a left foot in the metatarsal-phalangeal joint of the big toe. Note also the soft tissue swelling at the lateral border of the foot.
    Gout on
    X-rays
    of a left foot in the metatarsal-phalangeal joint of the big toe. Note also the soft tissue swelling at the lateral border of the foot.

Prevention

Risk of gout attacks can be lowered by

high fructose corn syrup)[60] and purine-rich foods of animal origin, such as organ meats and seafood.[5] Eating dairy products, vitamin C-rich foods, coffee, and cherries may help prevent gout attacks, as does losing weight.[5][61] Gout may be secondary to sleep apnea via the release of purines from oxygen-starved cells. Treatment of apnea can lessen the occurrence of attacks.[62]

Medications

As of 2020, allopurinol is generally the recommended preventative treatment if medications are used.[63][64] A number of other medications may occasionally be considered to prevent further episodes of gout, including probenecid, febuxostat, benzbromarone, and colchicine.[14][65][66] Long term medications are not recommended until a person has had two attacks of gout,[22] unless destructive joint changes, tophi, or urate nephropathy exist.[20] It is not until this point that medications are cost-effective.[22] They are not usually started until one to two weeks after an acute flare has resolved, due to theoretical concerns of worsening the attack.[22] They are often used in combination with either an NSAID or colchicine for the first three to six months.[7][14]

While it has been recommended that urate-lowering measures should be increased until serum uric acid levels are below 300–360 µmol/L (5.0–6.0 mg/dl),[63][67] there is little evidence to support this practice over simply putting people on a standard dose of allopurinol.[68] If these medications are in chronic use at the time of an attack, it is recommended that they be continued.[12] Levels that cannot be brought below 6.0 mg/dl while attacks continue indicates refractory gout.[69]

While historically it is not recommended to start allopurinol during an acute attack of gout, this practice appears acceptable.[70] Allopurinol blocks uric acid production, and is the most commonly used agent.[22] Long term therapy is safe and well-tolerated and can be used in people with renal impairment or urate stones, although hypersensitivity occurs in a small number of individuals.[22] The HLA-B*58:01 allele of the human leukocyte antigen B (HLA-B) is strongly associated with severe cutaneous adverse reactions during treatment with allopurinol and is most common among Asian subpopulations, notably those of Korean, Han-Chinese, or Thai descent.[71]

Febuxostat is only recommended in those who cannot tolerate allopurinol.[72] There are concerns about more deaths with febuxostat compared to allopurinol.[73] Febuxostat may also increase the rate of gout flares during early treatment.[74] However, there is tentative evidence that febuxostat may bring down urate levels more than allopurinol.[75]

Probenecid appears to be less effective than allopurinol and is a second line agent.

kidney stones.[76] Pegloticase is an option for the 3% of people who are intolerant to other medications.[77] It is a third line agent.[65] Pegloticase is given as an intravenous infusion every two weeks,[77] and reduces uric acid levels.[78] Pegloticase is useful decreasing tophi but has a high rate of side effects and many people develop resistance to it.[65] Using lesinurad 400 mg plus febuxostat is more beneficial for tophi resolution than lesinural 200 mL with febuxostat, with similar side effects. Lesinural plus allopurinol is not effective for tophi resolution.[79] Potential side effects include kidney stones, anemia and joint pain.[80] In 2016, it was withdrawn from the European market.[81][82]

kidney stones.[83][85]

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.[86] Repeated attacks can be prevented by medications that reduce serum uric acid levels.[86] Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain.[87] Options for acute treatment include nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, and glucocorticoids.[22] While glucocorticoids and NSAIDs work equally well, glucocorticoids may be safer.[88] Options for prevention include allopurinol, febuxostat, and probenecid. Lowering uric acid levels can cure the disease.[7] Treatment of associated health problems is also important.[7] Lifestyle interventions have been poorly studied.[87] It is unclear whether dietary supplements have an effect in people with gout.[89]

NSAIDs

NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other.

COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.[92][93][94][95]

Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs.[22] At high doses, side effects (primarily gastrointestinal upset) limit its usage.[96] At lower doses, which are still effective, it is well tolerated.[40][97][94][95] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.[96]

Glucocorticoids

Glucocorticoids have been found to be as effective as NSAIDs[93][98] and may be used if contraindications exist for NSAIDs.[22][99] They also lead to improvement when injected into the joint.[22] A joint infection must be excluded, however, as glucocorticoids worsen this condition.[22] There were no short-term adverse effects reported.[100]

Others

Interleukin-1 inhibitors, such as canakinumab, showed moderate effectiveness for pain relief and reduction of joint swelling, but have increased risk of adverse events, such as back pain, headache, and increased blood pressure.[101] They, however, may work less well than usual doses of NSAIDS.[101] The high cost of this class of drugs may also discourage their use for treating gout.[101]

Prognosis

Without treatment, an acute attack of gout usually resolves in five to seven days; however, 60% of people have a second attack within one year.

diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus are at increased risk of death.[7][102] It is unclear whether medications that lower urate affect cardiovascular disease risks.[103] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[102]

Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless

Kidney stones also frequently complicate gout, affecting between 10 and 40% of people, and occur due to low urine pH promoting the precipitation of uric acid.[7] Other forms of chronic kidney dysfunction may occur.[7]

  • Gouty tophi presenting as nodules on the finger and helix of the ear
    Gouty tophi presenting as nodules on the finger and helix of the ear
  • Tophus of the knee
    Tophus of the knee
  • Tophii on the toe and ankle
    Tophii on the toe and ankle
  • Gout complicated by ruptured tophi, the exudate of which tested positive for uric acid crystals
    Gout complicated by ruptured tophi, the exudate of which tested positive for uric acid crystals
  • Gout in the big toe of left foot, compared to the healthy right foot
    Gout in the big toe of left foot, compared to the healthy right foot
  • Gout in the joint of the big toe
    Gout in the joint of the big toe
  • Gross pathology of a large tophus
    Gross pathology of a large tophus

Epidemiology

Gout affects around 1–2% of people in the

high blood pressure.[26] Factors that influence rates of gout include age, race, and the season of the year. In men over 30 and women over 50, rates are 2%.[90]

In the United States, gout is twice as likely in males of African descent than those of European descent.[105] Rates are high among Polynesians, but the disease is rare in aboriginal Australians, despite a higher mean uric acid serum concentration in the latter group.[106] It has become common in China, Polynesia, and urban Sub-Saharan Africa.[7] Some studies found that attacks of gout occur more frequently in the spring. This has been attributed to seasonal changes in diet, alcohol consumption, physical activity, and temperature.[107]

History

A man wearing a long, curly wig and a full robe is sitting, looking out. His left arm rests on a small table, with his left hand holding a box. Behind him is a globe.
Antonie van Leeuwenhoek described the microscopic appearance of uric acid crystals in 1679.[108]

The English term "gout" first occurs in the work of Randolphus of Bocking, around 1200 AD.[109] It derives from the Latin word gutta, meaning "a drop" (of liquid).[108] According to the Oxford English Dictionary, this originates from humorism and "the notion of the 'dropping' of a morbid material from the blood in and around the joints".[110]

Gout has been known since antiquity. Historically, wits have referred to it as "the king of diseases and the disease of kings"

premenopausal women.[108][113] Aulus Cornelius Celsus
(30 AD) described the linkage with alcohol, later onset in women and associated kidney problems:

Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera... Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed... some have obtained lifelong security by refraining from wine, mead and venery.[114]

Benjamin Welles, an English physician, authored the first medical book on gout, A Treatise of the Gout, or Joint Evil, in 1669.[115] In 1683, Thomas Sydenham, an English physician, described its occurrence in the early hours of the morning and its predilection for older males:

Gouty patients are, generally, either old men or men who have so worn themselves out in youth as to have brought on a premature old age—of such dissolute habits none being more common than the premature and excessive indulgence in venery and the like exhausting passions. The victim goes to bed and sleeps in good health. About two o'clock in the morning he is awakened by a severe pain in the great toe; more rarely in the heel, ankle, or instep. The pain is like that of a dislocation and yet parts feel as if cold water were poured over them. Then follows chills and shivers and a little fever... The night is passed in torture, sleeplessness, turning the part affected and perpetual change of posture; the tossing about of body being as incessant as the pain of the tortured joint and being worse as the fit comes on.[116]

In the 18th century, Thomas Marryat distinguished different manifestations of gout:

The Gout is a chronical disease most commonly affecting the feet. If it attacks the knees, it is called

Lumbago.[117]

Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[108] In 1848, English physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.[118]

Other animals

Gout is rare in most other animals due to their ability to produce

Tyrannosaurus rex specimen known as "Sue" is believed to have had gout.[121]

Research

A number of new medications are under study for treating gout, including

antigenic versions are in development.[18]

See also

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