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Gout
Other namesArthritis uratica, or Podagra when of the foot
Video summary (script). Leading with The Gout (James Gillray, 1799), which depicts the pain of the artist's gout as a demon or dragon.[1][2]
SpecialtyRheumatology
SymptomsJoint pain, swelling, and redness[3]
Usual onsetOlder males,[3] post-menopausal women[4]
CausesUric acid[4]
Risk factorsDiet high in meat or beer, being overweight, genetics[3][5]
Differential diagnosisJoint infection, rheumatoid arthritis, pseudogout, others[6]
PreventionWeight loss, abstinence from drinking alcohol, allopurinol[7]
TreatmentNSAIDs, glucocorticoids, colchicine[4][8]
Frequency1–2% (developed world)[7]

Gout (/ɡt/ GOWT[9]) is a form of inflammatory arthritis characterized by recurrent attacks of pain in a red, tender, hot, and swollen joint,[4][10] caused by the deposition of needle-like crystals of uric acid known as monosodium urate crystals.[11] Pain typically comes on rapidly, reaching maximal intensity in less than 12 hours.[7] The joint at the base of the big toe is affected (Podagra) in about half of cases.[12][13] It may also result in tophi, kidney stones, or 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

side view of a foot showing a red patch of skin over the joint at the base of the big toe
Gout presenting as slight redness in the metatarsophalangeal joint of the big toe

Gout can present in several ways, although the most common is a recurrent attack of acute inflammatory arthritis (a red, tender, hot, swollen joint).[6] The metatarsophalangeal joint at the base of the big toe is affected most often, accounting for half of cases.[12] Other joints, such as the heels, knees, wrists, and fingers, may also be affected.[6] Joint pain usually begins during the night and peaks within 24 hours of onset.[6] This is mainly due to lower body temperature.[3] Other symptoms may rarely occur along with the joint pain, including fatigue and high fever.[12][18]

Long-standing elevated uric acid levels (hyperuricemia) may result in other symptoms, including hard, painless deposits of uric acid crystals called tophi. Extensive tophi may lead to chronic arthritis due to bone erosion.[19] Elevated levels of uric acid may also lead to crystals precipitating in the kidneys, resulting in 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,[22] and include a strong association with the consumption of alcohol, sugar-sweetened beverages,[23] meat, and seafood.[6] Among foods richest in purines yielding high amounts of uric acid are dried anchovies, shrimp, organ meat, dried mushrooms, seaweed, and beer yeast.[24] Chicken and potatoes also appear related.[25] Other triggers include physical trauma and surgery.[7]

Studies in the early 2000s found that other dietary factors are not relevant.[26][27] Specifically, a diet with moderate purine-rich vegetables (e.g., beans, peas, lentils, and spinach) is not associated with gout.[28] Neither is total dietary protein.[27][28] Alcohol consumption is strongly associated with increased risk, with wine presenting somewhat less of a risk than beer or 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 variability in uric acid level.[7] The SLC2A9, SLC22A12, and ABCG2 genes have been found to be commonly associated with gout and variations in them can approximately double the risk.[36][37] Loss-of-function mutations in SLC2A9 and SLC22A12 causes low blood uric acid levels by reducing urate absorption and unopposed urate secretion.[37] 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.[7]

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.[12] Other conditions commonly complicated by gout include lead poisoning, kidney failure, hemolytic anemia, psoriasis, solid organ transplants, and 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

Diuretics have been associated with attacks of gout, but a low dose of hydrochlorothiazide does not seem to increase risk.[40] Other medications that increase the risk include niacin, aspirin (acetylsalicylic acid), ACE inhibitors, 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 purine metabolism,[7] and occurs when its final metabolite, uric acid, crystallizes in the form of monosodium urate, precipitating and forming deposits (tophi) in joints, on tendons, and in the surrounding tissues.[19] Microscopic tophi may be walled off by a ring of proteins, which blocks interaction of the crystals with cells and therefore avoids inflammation.[43] Naked crystals may break out of walled-off tophi due to minor physical damage to the joint, medical or surgical stress, or rapid changes in uric acid levels.[43] When they break through the tophi, they trigger a local immune-mediated inflammatory reaction in macrophages, which is initiated by the NLRP3 inflammasome protein complex.[3][19][43] Activation of the NLRP3 inflammasome recruits the enzyme caspase 1, which converts pro-interleukin 1β into active 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.[18][51] Plain 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 monosodium urate crystals in synovial fluid or a tophus.[6] All synovial fluid samples obtained from undiagnosed inflamed joints by arthrocentesis should be examined for these crystals.[7] Under 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

Hyperuricemia is a classic feature of gout, but nearly half of the time gout occurs without hyperuricemia and most people with raised uric acid levels never develop gout.[12][53] Thus, the diagnostic utility of measuring uric acid levels is limited.[12] Hyperuricemia is defined as a plasma urate level greater than 420 μmol/L (7.0 mg/dL) in males and 360 μmol/L (6.0 mg/dL) in females.[54] Other blood tests commonly performed are white blood cell count, electrolytes, 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 differential diagnosis in gout is septic arthritis.[7][12] This should be considered in those with signs of infection or those who do not improve with treatment.[12] To help with diagnosis, a synovial fluid Gram stain and culture may be performed.[12] Other conditions that can look similar include CPPD (pseudogout), rheumatoid arthritis, psoriatic arthritis, palindromic rheumatism, and reactive arthritis.[3][12] Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma[57] or other neoplasms.[58]

Prevention

Risk of gout attacks can be lowered by complete abstinence from drinking alcoholic beverages, reducing the intake of fructose (e.g. 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.[22][65] Probenecid may be used if undersecretion of uric acid is present (24-hour urine uric acid less than 800 mg).[76] It is, however, not recommended if a person has a history of kidney stones.[76] Probenecid can be used in a combined therapy with allopurinol is more effective than allopurinol monotherapy.[77][78][79]

Pegloticase is an option for the 3% of people who are intolerant to other medications.[80] It is a third line agent.[65] Pegloticase is given as an intravenous infusion every two weeks,[80] and reduces uric acid levels.[81] 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.[82] Potential side effects include kidney stones, anemia and joint pain.[83] In 2016, it was withdrawn from the European market.[84][85]

Lesinurad reduces blood uric acid levels by preventing uric acid absorption in the kidneys.[86] It was approved in the United States for use together with allopurinol, among those who were unable to reach their uric acid level targets.[87] Side effects include kidney problems and kidney stones.[86][88]

Treatment

The initial aim of treatment is to settle the symptoms of an acute attack.[89] Repeated attacks can be prevented by medications that reduce serum uric acid levels.[89] Tentative evidence supports the application of ice for 20 to 30 minutes several times a day to decrease pain.[90] 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.[91] 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.[90] It is unclear whether dietary supplements have an effect in people with gout.[92]

NSAIDs

NSAIDs are the usual first-line treatment for gout. No specific agent is significantly more or less effective than any other.[22] Improvement may be seen within four hours and treatment is recommended for one to two weeks.[7][22] They are not recommended for those with certain other health problems, such as gastrointestinal bleeding, kidney failure, or heart failure.[93] While indometacin has historically been the most commonly used NSAID, an alternative, such as ibuprofen, may be preferred due to its better side effect profile in the absence of superior effectiveness.[40] For those at risk of gastric side effects from NSAIDs, an additional proton pump inhibitor may be given.[94] There is some evidence that COX-2 inhibitors may work as well as nonselective NSAIDs for acute gout attack with fewer side effects.[95][96][97][98]

Colchicine

Colchicine is an alternative for those unable to tolerate NSAIDs.[22] At high doses, side effects (primarily gastrointestinal upset) limit its usage.[99] At lower doses, which are still effective, it is well tolerated.[40][100][97][98] Colchicine may interact with other commonly prescribed drugs, such as atorvastatin and erythromycin, among others.[99]

Glucocorticoids

Glucocorticoids have been found to be as effective as NSAIDs[96][101] and may be used if contraindications exist for NSAIDs.[22][102] 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.[103]

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.[104] They, however, may work less well than usual doses of NSAIDS.[104] The high cost of this class of drugs may also discourage their use for treating gout.[104]

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.[18] Those with gout are at increased risk of hypertension, diabetes mellitus, metabolic syndrome, and kidney and cardiovascular disease and thus are at increased risk of death.[7][105] It is unclear whether medications that lower urate affect cardiovascular disease risks.[106] This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be independent.[105]

Without treatment, episodes of acute gout may develop into chronic gout with destruction of joint surfaces, joint deformity, and painless tophi.[7] These tophi occur in 30% of those who are untreated for five years, often in the helix of the ear, over the olecranon processes, or on the Achilles tendons.[7] With aggressive treatment, they may dissolve. 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]

Epidemiology

Gout affects around 1–2% of people in the Western world at some point in their lifetimes and is becoming more common.[7][22] Some 5.8 million people were affected in 2013.[107] Rates of gout approximately doubled between 1990 and 2010.[19] 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 and 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%.[93]

In the United States, gout is twice as likely in males of African descent than those of European descent.[108] 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.[109] 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.[110]

Taiwan, Hong Kong and Singapore have releatively higher prevalence of gout. A study based on the National Health Insurance Research Database (NHIRD) estimated that 4.92% of Taiwanese residents have gout in 2004. A survey hold by the Hong Kong government found that 5.1% of Hong Kong resident between 45–59 years and 6.1% of those older than 60 years have gout. A study hold in Singapore found that 2,117 in 52,322 people between 45–74 years have gout, roughly equals to 4.1%.[111]

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.[112]

The English term "gout" first occurs in the work of Randolphus of Bocking, around 1200 AD.[113] It derives from the Latin word gutta, meaning "a drop" (of liquid).[112] 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".[114]

Gout has been known since antiquity. Historically, wits have referred to it as "the king of diseases and the disease of kings"[7][115] or as "rich man's disease".[17] The Ebers papyrus and the Edwin Smith papyrus, (c. 1550 BC) each mention arthritis of the first metacarpophalangeal joint as a distinct type of arthritis. These ancient manuscripts cite (now missing) Egyptian texts about gout that are claimed to have been written 1,000 years earlier and ascribed to Imhotep.[116] Greek physician Hippocrates around 400 BC commented on it in his Aphorisms, noting its absence in eunuchs and premenopausal women.[112][117] 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.[118]

Benjamin Welles, an English physician, authored the first medical book on gout, A Treatise of the Gout, or Joint Evil, in 1669.[119] 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.[120]

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 Gonagra; if the hands, Chiragra; if the elbow, Onagra; if the shoulder, Omagra; if the back or loins, Lumbago.[121]

Dutch scientist Antonie van Leeuwenhoek first described the microscopic appearance of urate crystals in 1679.[112] In 1848, English physician Alfred Baring Garrod identified excess uric acid in the blood as the cause of gout.[122]

Other animals

Gout is rare in most other animals due to their ability to produce uricase, which breaks down uric acid.[123] Humans and other great apes do not have this ability; thus, gout is common.[18][123] Other animals with uricase include fish, amphibians and most non-primate mammals.[124] The Tyrannosaurus rex specimen known as "Sue" is believed to have had gout.[125]

Research

A number of new medications are under study for treating gout, including anakinra, canakinumab, and rilonacept.[126] Canakinumab may result in better outcomes than a low dose of a glucocorticoid, but costs five thousand times more.[127] A recombinant uricase enzyme (rasburicase) is available but its use is limited, as it triggers an immune response. Less antigenic versions are in development.[18]

See also

References

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15 Annotations

First Reading

steve h  •  Link

Speaking as a sufferer from gout, I can attest that it can be almost completely debilitating. It's caused, we now know, by the buildup of uric acid crystals in joints, giving an almost unbearable pain. Fortunately, modern medicine can handle it, but at Pepys's time there were only ineffective folk remedies, including eating lots of cherries(not easy to find most times of year in 1660).
Gout has been called "the disease or kings" or "the patricians' malady". It seemed to have a connection with high living. Gout can be aggravated by alcohol, and certain foods (shellfish, beans) can make it worse. But my experience is that there is no easily identifiable cause for most attacks. Gout tends to get progressively worse with time, and can cause deformation of joints, most usually the toes or other [parts of the feet.

Famous gout sufferers: Benjamin Franklin, Dr. Johnson, Kant, Gibbon, Jefferson, and Milton. Milton reportedly told a friend that if he were only free of gout pain, blindness would be tolerable.

A book on the history of gout:
http://www.amazon.com/exec/obidos…

Charlezzzzz  •  Link

Gout has been called

Charlezzzzz  •  Link

"He died, 1686, of gout in the stomach."
I wonder what this "gout" could really have been -- something truly painful, I suppose, since gout in the joints can be amazingly painful. Perhaps it was cancer?

vincent  •  Link

google gout for ones favourite remedy
a )Treatment of Gout
Therefore the following foods which are high in Purines should be restricted or avoided:
Offal foods such as liver, kidneys, tripe, sweetbreads and tongue. Excessive amounts of red meat. Shellfish, fish roe and scallops. Peas. lentils and beans. Alcohol intake should be reduced. Two glasses of beer a day or less is sensible. On special occasions you can drink more. Weight loss may be very important. Medication for high blood pressure may need to be altered.

http://www.rheumatology.org.nz/nz…
It seems to say , the 17C diet was not an ideal eating style.

Ruben  •  Link

John in Austin  •  Link

Sir John Falstaff:

"A pox of this gout! or, a gout of this pox! for the one or the other plays the rogue with my great toe."

King Henry VIII, Part II

netta murray goldsmith  •  Link

If anyone has more suggestions on what 'gout of the stomach' could have been, I would be glad to hear from them.I keep on coming across references to it e.g. in Trollope's Phineas Finn where two minor characters expire because of it. For what it is worth I would not have thought it was cancer as 18th century doctors, let alone 19th century ones could diagnose that

Mary  •  Link

gout of the stomach.

There is an interesting site at www.antiquusmorbus.com/English that suggests explanations of many antique medical terms, including gouts of all descriptions.

in Aqua Scripto  •  Link

Mary your gout ref. could not be summoned; but here be OED oldest ref:
Gout OED: I. 1. A specific constitutional disease occurring in paroxysms, usually hereditary and in male subjects; characterized by painful inflammation of the smaller joints, esp. that of the great toe, and the deposition of sodium urate in the form of chalk-stones; it often spreads to the larger joints and the
internal organs.
The name is derived from the notion of the ‘dropping’ of a morbid material from the blood in and around the joints.
a. OF. goute, goutte (F. goutte) drop, gout: L. gutta drop, in med.L. applied to gout and other diseases attributed to a ‘defluxion’ of humours (see Du Cange).]
c1290 S. Eng. Leg. I. 360/39 bare cam a goute In is kneo, of Anguische gret..So longue, xat is kneo to-swal.
c. falling gout, epilepsy. Obs. [med.L. gutta cadiva or caduca: see Du Cange.]
Stomach Gout may be an Ulcer;

pedro  •  Link

Cure for gout?

JOHN HILL educated as an apothecary, had lived in good style on the malice and fear of the community, he now found resources in its credulity. He brought out certain tinctures and essences of simple plants, sage, valerian, bardana, or water dock, asserting that they were infallible panaceas for all the ills that flesh is heir to. Their sale was rapid and extensive, and whatever virtues they may have possessed, no one can deny that they were peculiarly beneficial to their author, enabling him to have a townhouse in St. James' Street, a country house and garden at Bayswater, and a carriage to ride in from one to the other. The quivers of the epigram writers were once more filled by these medicines, and thus some of their arrows flew:

In spite of the efficacy of his Tincture of Bardana, which Hill warranted as a specific for gout, he died of that disease on the 21st of November 1775. The following is the last fling which the epigrammatists had at him:

'Poor Doctor Hill is dead! Good lack!
Of what disorder? An attack
Of gout. Indeed! I thought that he
Had found a wondrous remedy.
Why, so he had, and when he tried,
He found it true the doctor died!'
(Book of Days)

Mary  •  Link

gout/Antiquus Morbus.

Indeed, the www.antiquusmorbus.com address does seem to have ceased to work, but if you simply Google for 'antique medical terms' you will find that this site appears and can then be searched for specific ailments. Not an elegant way of getting there, but apparently reliable.

Third Reading

San Diego Sarah  •  Link

For about as long as humans have lived in civilisations — complex structures that allow some rule while the others serve, gout has been a recurring affliction. Why? Because it is essentially a life-style disease. Eat too much red meat, drink too much beer and/or wine and you may end up with a gouty joint. But it is not that simple: gout is also from genes as it is a form of arthritis.

Gout is caused by excess uric acid in the blood, leading to swelling, acute pain and redness. Essentially, the uric acid forms miniature crystals that happily converge on the closest joint. Sometimes, gout is chronic, causing permanent damage to the joints. These days, there is medication available that can alleviate the symptoms. Not so back in the days of yore.

The Egyptians were familiar with gout, and in the 5th century BC, Hippocrates called it the “unwalkable disease”.

By then, gout was known as podraga. Romans had it — Seneca commented on that even women could get it, adding a snarky comment that it was no wonder, given just how lecherous these modern women could be. But mostly gout has been a male affliction.

Alexander the Great had gout. As he died in his thirties: how much meat and wine did he consumed on a daily basis?

Charlemagne was another fellow sufferer.

In the medieval period, everyone knew podraga was the result of an imbalance in the humours. If the 4 humours governing health (blood, yellow bile, black bile and phlegm) weren’t balanced, a drop of the excess humour could slither down your veins and settle in your joint, hence the inflammation.

This theory was also the background to the term gout, as Latin for “drop” is “gutta”, and in the late 12th century a Dominican monk named Randolphus of Bocking working for the Bishop of Chichester is credited with shortening the cumbersome “gutta quam podagram vel artiticam vocant” (the drop that causes podraga or arthritis) into “gutta” which became gout.

By 1294 the physicians had discovered a substance that helped gout, namely colchicine, the toxin in autumn crocuses.
(How did they discover that? Did they first try to ingest it -- a bad idea as it is very poisonous. Or was it a case of a desperate physician rushing outside to escape the raging of his angry, hurting patient and stumbling across some autumn crocuses, and thinking “well, at least they’re pretty to look at”, before grabbing a bunch and pulverising them into a salve which -- amazingly -- helped?)

By medieval times, physicians were also convinced it helped to change your diet to minimise the discomfort caused by gout. That advice was not always well-received.

San Diego Sarah  •  Link

CONCLUSION:

Another English king who suffered from gout was Henry VIII. No wonder, as the man ended up almost as broad as he was tall (and he was over 6 ft.).
A contemporary to Henry VIII was Katherine of Aragon's nephew, the Habsburg Emperor Charles. Blood is always thick when we’re talking Habsburgs — so thick that for centuries they preferred to marry close relatives. Charles was a fellow gout sufferer—confirmed by examining his finger in 2006.

Isaac Newton had gout, as did Christopher Columbus, Michelangelo, Leonardo da Vinci and the Swedish king, Gustav II Adolf. Those men rarely bothered with kale and salads or low-fat dairy products.

Those who suffer from gout may find comfort in knowing how many geniuses and powerful people were fellow sufferers. But probably not.

Excerpted from: https://www.annabelfrage.com/2024…

San Diego Sarah  •  Link

How interesting I mentioned HRE Charles V as a gout sufferer, because months later I discovered he treated it by taking China Root:

Chobchini is an Ayurvedic herb, made famous in the treatment of the gout of King Charles V.
Roots are the most commonly used part. Stems are equally beneficial. The rhizome of Chobchini can be used in the form of powder or paste, cooked or raw.
The daily intake should not exceed 10 grams, as more may result in nausea and vomiting. The most important medicinal properties of Chobchini are its ability to fight psoriasis, syphilis and leprosy. It is a preferred herbal treatment for psoriasis.

It is found wild in China and much of Asia, but it was the Chinese who cultivated and exported it to the rest of the world, hense the name.

Pepys drank China Beer, presumably made from the China Root/Chobchini in 1661:
https://www.pepysdiary.com/diary/…

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References

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