Book Review

Gout: The patrician malady

N Engl J Med 1999; 340:898March 18, 1999

Article

Gout: The patrician malady
By Roy Porter and G.S. Rousseau. 393 pp., illustrated. New Haven, Conn., Yale University Press, 1998. $35. ISBN: 0-300-07386-0

There are few diseases as easy to recognize as classic gouty podagra (from the Greek word meaning “foot seizure”). A gluttonous, bibulous, upper-class man suddenly notices a severely painful, swollen great toe. The attack passes after several days to several weeks, even without therapy. Hippocrates referred to gout (from the Latin gutta — a drop) as the arthritis of the rich, as opposed to rheumatism, the arthritis of the poor. The list of sufferers throughout history includes important persons of power, prestige, and artistic accomplishment.

Roy Porter and G.S. Rousseau are professors of history and English, respectively. Their talents have combined to produce a scholarly account of the interactions among the disease, the sufferer, and the surrounding culture. This work contains much more detail than the history of gout by W.S.C. Copeman, a noted English rheumatologist, published in 1964 (A Short History of the Gout and the Rheumatic Diseases. Berkeley, Calif.: University of California Press). Interestingly, the dust jackets of both books are adorned with the famous cartoon by James Gillray showing an angry, fire-breathing creature whose teeth and claws dig deeply into the flesh of a swollen, red foot.

High-born sufferers from gout were frequently depicted as comic subjects by the bourgeois artists and writers of the day. The hereditary disease gout became a metaphor for social status (i.e., the hereditary titles, wealth, lands and estates of Britain in the 17th and, especially, 18th centuries). The disease was borne by the gentry as a badge of distinction. Moreover, the acute attacks were thought to rid the body of impurities. If aborted or thwarted, the impurity would be “misplaced” or become “retrocedent,” attacking a vital organ and causing apoplexy (stroke), palsy (paralysis), or even death. It could become “atonic,” causing melancholy, madness, or other neuropsychiatric problems. Charles Darwin's chronic illness was thought to be atonic gout.

As might be anticipated, the book is far stronger from the literary point of view (especially that of the British) than from the standpoint of medical science. The story of “sweet Willy O” provides a fascinating example. It appears that William Cadogan, a Welsh physician practicing in London, became the Dr. Spock of his time after his book on nursing and child care became a bestseller among the general public. A later book entitled A Dissertation on the Gout appeared in 1771 (Philadelphia: William and Thomas Bradford), causing great controversy by its assertion that gout was not inherited, periodic, or incurable. A physiologic puritan, Cadogan maintained that gout was acquired through laziness, gluttony, intemperance, and vexation — that is, the sins of the titled and wealthy. The publication of his book, coinciding as it did with the restlessness and then rebellion of the American colonies, presented a challenge to the established order of things. Cadogan's method of treatment, which consisted of serious physical exercise combined with abstention from rich foods and spirits, was not what the rich and powerful wanted to hear about.

Porter and Rousseau accurately trace the scientific advances influencing the understanding of gout from Antoni van Leeuwenhoek's original description of crystals from a gouty tophus in the mid-17th century. An incredibly clever microscopist, van Leeuwenhoek did not know the composition of these crystals, since uric acid was first discovered in urine by the Swedish chemist Carl Wilhelm Scheele, in 1776, nearly 100 years later.

Despite Sir Alfred Baring Garrod's postulates in the mid-19th century implicating both an elevated level of uric acid in the blood of patients with gout and the deposition of crystals of sodium urate in the affected part, clinicians still asserted as late as 1959 that acute gout had nothing to do with uric acid. Hollander and I used compensated polarized-light microscopy in 1960 to show that the presence of crystals of sodium urate in synovial fluid was specific for the diagnosis of gouty inflammation. Later work by our group fulfilled Koch's postulates. Although these postulates were originally formulated by Robert Koch to implicate a specific microbe as the causal agent of a disease, we used them to implicate crystals of sodium urate as the cause of acute gouty arthritis.

Porter and Rousseau's history of gout omits the important contributions of the Swiss investigators Wilhelm His, Jr., and Max Freudweiler, whose work in 1901 clearly showed that urate crystals caused inflammation. Wilhelm Ebstein's finding of localized death of tissue (necrosis) as a primary event in gout was cited, but the criticism by His was ignored. Ebstein's fixatives for tissue dissolved the crystals, according to the Swiss workers. Although the authors mention the Methuen Treaty with Portugal in 1703, which resulted in the importation into England of large quantities of lead-laden fortified wine (port), inducing the “saturnine” gout, they fail to cite the work of Gene Ball, who showed that the lead content of bottles of port wine from that era was very high. (Ball subsequently drank the wine, which he said was delicious.)

Despite the virtual absence of any details of scientific advances related to gout or the metabolism of uric acid after Garrod's mid-19th-century work, I greatly enjoyed the book. No other disease could provide such reflections on the culture of the time. Porter and Rousseau analyze the interaction between gout and British culture brilliantly.

Daniel J. McCarty, M.D.
Medical College of Wisconsin, Milwaukee, WI 53226