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Gout--a disease for the elect.

Gout is a medical condition that features recurrent attacks of inflammatory arthritis, most often involving the metatarsophalangeal joint of the hallux. A gout attack with this localization was formerly known as podagra. Gout can sometimes appear in the ankle, heel, knee, wrist or elbow. The duration of a gout attack may vary between a few days and a few weeks; treatment accelerates the disappearance of symptoms. The evolution of the disease is chronic, with acute attacks alternating -with asymptomatic periods. In time, attacks become more and more frequent and severe, they tend to involve more than one joint and do not remit entirely under treatment. (Rosu&Serban 2011) Although well-known in medicine, gout is only the outward tip of the iceberg represented by hyperuricemia. This is a biochemical syndrome defined by increased blood concentrations of the uric acid, often without clinical expression (the so-called asymptomatic hyperuricemia). Normal values for uricemia (uric acid concentrations in the blood) vary between 3 to 7 mg/dl in men and 3 to 6 mg/dl in premenopausal women; after menopause, differences between the two genders tend to disappear. Prevalences of hyperuricemia vary around the globe between 2 and 13%, even reaching 18-20% in some populations of Oceania, China or Malaysia. Gout incidence increases as concentrations of the uric acid in the blood get higher. In ancient times, gout was considered a disease of the rich social classes, but this trend has been gradually reversed, because of the mass availability of protein-rich fast-food diets and alcoholic beverages, not to forget about the reduced physical activity. (Terkeltaub 2003; Snaith 2004; Rosu&Serban 2011)

Uric acid is the final catabolic product in the metabolism of purines. Two thirds of the total uric acid in the organism derive from the degradation of endogenous purines and only one third--from the catabolism of dietary purines. Uric acid has a limited solubility in blood, which becomes saturated at concentrations of 4 to 6.8 mg/dl. An increased production of uric acid and/ or its reduced excretion is followed by an excess formation of monosodium urate, which is deposited in tissues. Urate solubility is reduced under the existing conditions of lower temperatures in the peripheral joints (32[degrees] Celsius at knee level, 29[degrees] Celsius at ankle level), thus favouring its precipitation in joints and periarticular tissues. The crystals of monosodium urate are responsible for articular inflammation when they are deposited at this level. (Rosu&Serban 2011)

In patients with a long evolution of hyperuricemia and many acute attacks, gout can also be found in a chronic form, having as a main manifestation the gouty tophi (tophus = a friable and porous stone), a tophus being a deposit of small monosodium urate crystals surrounded by inflammatory cells. Tophi are small, superficial, indolor, white-yellowish tumours localized in the subcutaneous tissues (the ear pavilion is a typical, yet rare location; fingers, palms or soles), also in the articular cartilage, synovium, tendons, and renal interstitium. Tophi may increase their dimensions in time, up to those of a small egg, and may become ulcerated, leaving a white, creamy magma to draw off ("urate milk"). Hyperuricemia also induces renal disease, either under the form of urate nephropathy (the interstitial deposition of urate crystals, surrounded by an inflammatory reaction) or under the form of uric acid kidney stones (whose precipitation is favoured by the acid pH of the urine, and inhibited by alkaline foods such as dairy products). (Rosu&Serban 2011)

The human species and the higher primates do not have uricase, the hepatic enzyme which is responsible for converting the uric acid into allantoin. As the other animal species have this enzyme, gout does not appear in their cases (Alvarez-Lario&Macarron-Vicente 2010). The Tyrannosaurus rex, however, is believed to have suffered from gout; the specimen called "Sue," a world-famous fossil in the Chicago Field Museum, went through skeleton modifications highly suggestive for gout.

Hyperuricemia and gout appear on the ground of multiple risk factors: genetic predisposition, male gender, advanced age, dietary factors, reduced physical activity and also prolonged walking, local trauma, infections, prolonged inanition, parenteral feeding and some medications (aspirin, diuretics). In genetically predisposed individuals, the increased consumption of protein-rich foods, the chronic alcohol intake or an acute alcohol abuse can trigger a gout attack. For instance, the Maori population in New Zealand is genetically predisposed to develop hyperuricemia. Nevertheless, gout was rare in this population before the 18th century. The major lifestyle changes induced by the arrival of European colonists determined a pronounced increase of gout incidence in the native populations, today the highest in the world (one in eight Maori men suffers from gout). (Lennane et al 1960; Te Karu et al 2013)

Among alcoholic beverages, the highest risk for triggering gout belongs to spirits and beer, the latter having an increased purine content; wine seems to have a neutral effect. Other dietary factors that can increase the risk of gout are the high consumption of fructose-sweetened beverages, chocolate, cocoa, game meat, viscera, anchois, mackerels, herrings, sardines. On the contrary, lowfat dairy, vitamin C-rich foods and coffee reduce the risk of gout attacks. (Choi et al 2004)

Treatment of gout consists in the early correction of asymptomatic hyperuricemias, the treatment of the acute gout attack, the prevention of new attacks and the prevention of chronic gout. The nonpharmacologic measures consist of putting at rest the inflicted joint during the acute attack and taking dietary choices. The patient should avoid purine-rich foods, alcohol and prolonged fasting, favour the consumption of alkaline foods (fruits, vegetables, dairy products) and have a high liquid intake; protein consumption should be lowered during acute attacks, and normal between crises. The pharmacologic treatment of acute gout attacks may use non-steroidal anti-inflammatory drugs, colchicine or corticoids, while chronic therapy uses inhibitors of the uric acid synthesis (allopurinol or febuxostat), uricosuric drugs that favour the elimination of the uric acid (probenecid, benziodarone or sulfinpyrazone) or uricase derivatives (rasburicase, pegloticase). (Kelsey et al 2007; Rosu&Serban 2011)

Gout in history and culture

Gout arthritis has a long-standing story, being one of the first diseases to be described as a clinical entity. Egyptians identified podagra (the inflammation of the metatarsophalangeal joint of the hallux) in 2640 B.C. (Bhattacharjee 2009) In the 5th century B.C. Hippocrates referred to it as "the unwalkable disease" and related it to an opulent lifestyle, by naming it "the arthritis of the rich," as opposed to rheumatism, which was named "the arthritis of the poor." The Greek physician also left us five aphorisms about this disease: (Pasero&Marson 2004; Nuki&Simkin 2006; Gritzalis et al 2011)

1. Eunuchs do not get podagra.

2. Women do not get podagra until menopause.

3. Men do not get podagra until puberty.

4. Inflammation in podagra lasts up to forty days.

5. The illness exacerbates in spring and autumn.

Aulus Cornelius Celsus (30 A.D.) described the correlation between podagra and excessive alcohol intake; he also described the association between gout and the renal disease. (Copeman 1964)

In the 2nd century A.D. Galen (Claudius Galenus of Pergamon), described the gouty tophi and associated this disease with hedonism and overindulgence; he could not help seeing a hereditary trait in it all. (Copeman 1964; Nuki&Simkin 2006; Gritzalis et al 2011)

The denomination of gout appeared later, in the Middle Ages, when Medicine was being dominated by "the theory of humours" which explained the disease by a disequilibrium in the four humours: blood, yellow bile, black bile and phlegm. In the 13th century, Randolphus of Bocking from Chichester made use for the first time of the term "gout" in order to define podagra, the designation being derived from the Latin word gutta (drop), on the assumption that the excess of one of the four humours might drip off, under particular circumstances, in one joint and trigger the symptoms. (Copeman 1964; Nuki&Simkin 2006)

Henry VIII, when he was not beheading his wives, was fighting with gout attacks. He was a fat man and he was frequently painted holding a slice of meat or a glass of wine in his hand, both of them being risk factors for gout. (Copeman 1964)

Many of the kings of France had gout; it is acknowledged that Louis XIV, his father and his grandfather suffered from gout attacks (Copeman 1964). In the Loire Valley Castles, one may see the stools in front of the thrones where the kings rested their injured legs. In their cases, obesity and dietary excesses, with alcoholic beverages and game meat, were the risk factors for triggering gout.

In 1683, Thomas Sydenham, himself suffering from gout and renal disease, described the symptoms of acute gout arthritis after watching many patients as well as his own illness (Porter&Rousseau 1998; Nuki&Simkin 2006): "The victim goes to bed and sleeps in good health. About 2 o'clock in the morning, he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. This pain is like that of a dislocation, and yet the parts feel as if cold water were poured over them. Then follow chills and shiver and a little fever. The pain which is at first moderate becomes more intense. With its intensity the chills and shivers increase. After a time this comes to a full height, accommodating itself to the bones and ligaments of the tarsus and metatarsus. Now it is a violent stretching and tearing of the ligaments--now it is a gnawing pain and now a pressure and tightening. So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of bedclothes nor the jar of a person walking in the room."

Antonie van Leeuwenhoek, best known for his work on the improvement of the microscope, depicted in 1679 the crystals in the gouty tophi, although their chemical composition was not yet known at that moment. (Porter&Rousseau 1998; Nuki&Simkin 2006)

In the 18th century, gout was thought to have a prophylactic impact on other diseases. Thus, Horace Walpole, son of Prime Minister Robert Walpole (both suffering from gout), describe the distress inflicted by gout in his letters. It is well known that he hated doctors and did not trust them; in one of his letters, he expressed doubts about having to treat his gout: "gout prevents other illnesses and prolongs life [...] could I cure that gout, should not I have a fever, a palsy, or an apoplexy?" (Viseltear 1983; Nuki&Simkin 2006)

William Pitt the Elder also suffered from gout. During one of his frequent leaves of absence in the Parliament, the Stamp Act (1765) was passed, enforcing the American colonists into paying a tax to defray the costs of protecting the Colonies against French attacks. When he got over the gout attack, Pitt returned into the Parliament and got on to abrogate the Act with the famous words "the Americans are the sons, not the bastards of England [...] they cannot be bound to pay taxes without their consent." Unfortunately, during another one of Pitt's leaves of absence in the Parliament (induced by another gout attack), Lord Townshend convinced the Parliament to charge the Colonies a high tax on tea imports, in order to increase England's revenues. This led in 1773 to the Boston Tea Party, which preceded the outbreak of the Independence War. (Graham&Graham 1955; Copeman 1964; Nuki&Simkin 2006)

Benjamin Franklin, the discoverer of electricity and one of the major leaders involved in the American Revolution, the signing of the Declaration of Independance and the amendment of the Constitution, also suffered from gout and was transported in a sedan to the Constitutional Convention. (Graham&Graham 1955; Bruns 1986) Other personalities involved in the American Revolution, such as Thomas Jefferson and the count of Vergeuves (a French nobleman who obtained funds to finance the Revolution), also suffered from gout. It is speculated that the close relationship between the three personalities was finally supported by common sufferance (Copeman 1964; Nuki&Simkin 2006). Benjamin Franklin even wrote in 1780 an essay, "Dialogue between the gout and Mr. Franklin" showing his concern with the disease.

In the 18th and 19th century, William Hogarth, Thomas Rowlandson, James Gillray, William Davison or George Cruikshank, caricatured the gluttonous nobility suffering from gout. (Rodnan 1961)

Ambrose Bierce defined gout in his Devil's Dictionary as "a physician's name for the rheumatism of a rich patient." (Rodnan 1961; Snaith 2004)

As late as 1848, Alfred Baring Garrod realized that the excess of uric acid in blood could well be the cause of gout. His son, Sir Archibald Garrod, further suggested in 1931 that gout should be included in the inborn errors of metabolism. (Porter&Rousseau 1998; Bhattacharjee 2009)

Amongst other personalities to have suffered from gout throughout history, one could mention Leonardo da Vinci, John Milton, Sir Isaac Newton (with gout attacks in both legs), Johann Wolfgang von Goethe and Luciano Pavarotti (with attacks in the left hallux). (Copeman 1964; Nuki&Simkin 2006)

Gout treatment in history

In times of old, treating gout was as primitive as treating the other diseases, the principle being much like a therapy with "flannel and patience" (Graham&Graham 1955). The inflicted joint, most frequently at the hallux, had to be borne up on a stool and "swathed in flannel," and the invalid had to patiently wait for the gout attack to go by, sometimes for one or two weeks.

Although unbalanced diet has been acknowledged as a major factor in the pathogenesis of gout ever since Antiquity, dietary restrictions were ignored for a long time. The high prevalence of gout in 18th century Britain can be explained by the dietary excesses of those times, which are suggestively described in the writings of Daniel Defoe, Samuel Johnson, Lord Hervey, etc. (Graham&Graham 1955; Porter&Rousseau 1998). According to Lord Hervey, there was a Duke of Grafton who ate an ox a day and was taking a course of Bath waters "to enable him to eat two!"

The difference between gout incidence in Asia and Europe shows the role excesses in dietary purines (from meat, seafood and beer) have in its appearance. Traditional Asian diets, based on rice and vegetables, have low purine content; thus, gout is rare among populations in Asia. On the contrary, large amounts of meat and seafood are consumed in Europe and America, and therefore gout is frequent in these areas. (Choi et al 2004)

Colchicine, an alkaloid derived from autumn crocus (Colchicum autumnale) had been used as a hard abstergent for more than 2000 years, since ancient Egypt and Greece. Alexander of Tralles took it for the first time to treat gout in the 6th century A.D. However, its digestive side effects considerably limited its use; as late as 1763, it was "rediscovered" by Baron Von Stoerk. (Graham&Graham 1955; Nuki&Simkin 2006; Bhattacharjee 2009)

The most important historical advance in the treatment of hyperuricemias is perhaps the development of allopurinol, the first xanthine oxidase inhibitor, George Hitchings and Gertrude Elion being responsible for developing it and other six drugs. (Nuki&Simkin 2006)

Gout as a rheumatologic problem is now well-known and easier to manage. Nevertheless, its historical and cultural echo is still there, since so many personalities were influenced in their personal and public choices by the painful attacks of this chronic disease. No one knows how some events would have looked like without the impact of gout on the lives of these personalities and many others around them. The only thing we know for sure is that gout is more than some kind of disease, it is ultimately a fact in human history.

Dialogue between the Gout and Mr. Franklin

DIALOGUE BETWEEN FRANKLIN AND THE GOUT.

Midnight, October 22, 1780.

Franklin. Eh! Oh! Eh! What have I done to merit these cruel sufferings?

Gout. Many things: you have ate and drank too freely, and too much indulged those legs of yours in their indolence.

Franklin. Who is it that accuses me?

Gout. It is I, even I, the Gout.

Franklin What! my enemy in person?

Gout No, not your enemy.

Franklin. I repeat it; my enemy: for you would not only torment my body to death, but ruin my good name: you reproach me as a glutton and a tippler; now all the world that knows me will allow, that I am neither the one nor the other.

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Bogdan Mircea Mihai Grigore T. Popa University of Medicine

Cristina Mihaela Lacatusu Grigore T. Popa University of Medicine

Correspondence concerning this article may be addressed to bogdanmihai2003@yahoo.com or cmlacatusu@yahoo.co.uk.
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Title Annotation:Illness most atrocious
Author:Mihai, Bogdan Mircea; Lacatusu, Cristina Mihaela
Publication:Romanian Journal of Artistic Creativity
Article Type:Report
Geographic Code:1USA
Date:Mar 22, 2015
Words:3123
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