A historical review of the Gout

Gout is a historical disease. The first gouty or affected by gout of which we have some reference is Hieron (478-467 B.C.) tyrant of Syracuse. Also of Asa (944-904 B.C.) the King of Judah, of whom it is said that he suffered from a chronic disease in the joints of the feet, although it is not certain that it was what we know today as gout.

Regarding Hieron, Plutarch went so far as to affirm that “he was simultaneously afflicted with kidney stones”, which may prove the existence of one of the most frequent complications of gout, colic in the kidney.

Throughout time, gout has been called the king of diseases and the disease of kings, due to the frequency with which it has affected aristocratic personalities such as Charles V, Philip II, Isaac Newton…

In the 5th century BC, Hippocrates described this disease as podagra, cheinagra or gonagra, depending on how it affected the metatarsophalangeal joint of the first toe, the wrist or the knee.

Hippocrates’ concepts about gout appear in a series of aphorisms attributed to him concerning this disease: Such aphorisms are:

  • Eunuchs do not become gouty nor do they become bald.
  • The child does not get gout before he has had sexual intercourse.
  • The woman does not become gouty until after the period has disappeared.
  • Gouty affections become active in spring and autumn.

Hippocrates’ concept is that gout does not affect eunuchs, children and women until menopause. His authority became such that in the following centuries his opinion was accepted even without discussion; however, later authors such as Galen or Seneca, with euphemisms and more or less concealed explanations, recognize that the aphorisms do not constitute a constant law.

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The appearance of the term gout

During the 13th century, the term GOUT was introduced from Latin, which implied a belief that a foreign cause – such as a poison – that distilled little by little, i.e. drop by drop into the joint, was mainly responsible for the development of the disease.

The modern clinical history of gout begins with Thomas Sydenhan, who described the clinical picture in an unsurpassed manner (probably on the authority of more than three decades of personal suffering from the disease). It is impossible not to resist transcribing this description:

The immortal Seneca mentioned the familiar nature of the disease. However, the more modern history of gout begins in 1776 when Scheele discovered uric acid as a component of a kidney stone.

Wollaston in 1797 and Pearson in 1798 proved the presence of urate in tophi. More than 50 years later, Garrod (1854) performed his historical experiments demonstrating the presence of a greater amount of uric acid in the blood of those affected by the disease. Subsequently, the enzyme deficiency responsible for the different types of hereditary gout was found.

Nevertheless, perhaps the most important milestones, due to their therapeutic implications, are the introduction in the mid-20th century of the first uricosuric agent (which promotes renal elimination of uric acid) and the introduction of the inhibitor of xanthine oxidase, i.e. the enzyme responsible for the creation of uric acid, allopurinol, which has made it possible to control the disease.

Gout, then, is a metabolic disease (similar to diabetes and cholesterol) that affects the joints and causes arthritis. The biochemical characteristic is the presence of an elevated level of urate in the blood together with a deposit of these crystals in the tissues, by precipitation of these crystals.

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The deposition of these crystals in the joint tissue can cause an inflammatory reaction and lead to arthritis. Urate crystals can also end up in the kidney, leading to urate neuropathy.