History and Geography

The ancient Greeks recognized the clinical features of cirrhosis. In about 300 B.C., Erasistratus associated ascites with liver disease. Galen, in the third century A.D., commented on the physical diagnosis, and noted that heavy wine consumption "will increase the damage to the liver when inflammation and scirrhus already existed." His contemporary, Aretaeus the Cappadocian, suggested that cirrhosis may evolve from hepatitis, and carcinoma, from cirrhosis. The clinical descriptions left by the Greeks remained unexcelled until recent times.

In the sixteenth century, Vesalius described rupture of the portal vein in a lawyer with an indurated nodular liver. When pathological anatomy became a discipline in the seventeenth century, sporadic reports of the cirrhotic liver appeared. Among the earliest illustrations of cirrhosis was that by Frederik Ruysch in his atlas of normal and abnormal anatomy (1701-16). In his massive tome on pathology, Giovanni B. Morgagni (1716) introduced the term "tubercle" to denote any nodule of the liver. This covered a variety of lesions, and sowed the confusion between carcinoma and cirrhosis of the liver for decades afterward. Among the English, William Harvey in 1616 reported on two cases of cirrhosis. He antedated John Browne, whose description in 1685 has been regarded by historians as the first in English. Matthew Baillie's accurate description in 1793 established cirrhosis as a nosological entity in pathology. He also noted the strong association between the disease and alcohol intake. During the eighteenth century, a surplus of corn led Parliament to promote distilling and consumption of spirits as a way of stabilizing the price. The excessive consumption of cheap spirits gave rise to an epidemic of cirrhosis, which became popularly known as "gin liver" in England and "brandy liver" in other countries.

Twenty-five years after Baillie, René Laennec, who invented the stethoscope, introduced the name cirrhosis in a brief footnote appended to a case discussion. Subsequently, clinicians on the Continent began to speculate on the morphogenesis of the lesion. In 1829, Gabriel Andral formulated the idea that hypertrophy of the yellow substance of the liver that normally secretes bile accounted for the nodules, whereas atrophy of the red substance containing the vessels represented the depressed areas of cirrhosis. This concept, relating cirrhogenesis to the dual substance of the liver, influenced thinking on this subject for the next two decades. In 1838, Robert Cars-well in England conjectured that cirrhosis depended on the growth of interlobular connective tissue. The speculations acquired a more solid foundation when microscopes with good resolving power became available. Also in the early nineteenth century, Gottlieb Gluge and Dominique Lereboullet saw hepatic fat and argued that this was the basic lesion of cirrhosis, whereas Karl von Rokitansky attributed the "granulations" of cirrhosis to the result of chronic inflammation.

During the mid-nineteenth century, interest in vascular studies gathered momentum after improvements were made in cast corrosion techniques. The vascular alterations in cirrhosis also came under scrutiny during the latter half of that century and the first decades of this century, as researchers from Lionel S. Beale writing in 1857-9, through the work of A. H. Mclndoe in 1928, revealed the vascular damage that occurs with cirrhosis. Some, such as Karl von Liebermeister in 1864 and J. M. Legg in 1872, continued to focus on the interlobular connective tissue as the seat of the cirrhotic process. Others emphasized the regenerative aspects of cirrhosis which represented the end product of many injurious episodes. In 1911, Frank B. Mallory summarized the clinicopathological features in an important paper that introduced the entity of alcoholic hepatitis. He regarded it as a precursor lesion of cirrhosis. Mal-lory's concept was recently revived after a dormancy of 50 years.

While pathologists debated the issue of morphogenesis, speculations on etiology also abounded. Earlier it had been suggested that alcoholic fatty liver was the precursor of cirrhosis. By the second half of the nineteenth century, most physicians accepted this thesis, believing that alcohol intake increased hepatic fat, which in turn was converted into cirrhosis. However, experiments by P. Ruge in 1870 and G. de Rechter in 1892, among others, failed to demonstrate the cirrhogenic effect of alcohol in animals. This result led to the notion that it was not alcohol but some contaminant in the alcohol, such as copper, which damaged the liver, whereas another set of theories stressed that gastric malfunction was the underlying cause in that disturbed gastric function produced or allowed the absorption of hepatotoxins. The hypothesis of nutritional deficiency came to the foreground when experimenters such as J. M. Her-shey and Samuel Soskin in 1931 and D. L. McLean and Charles H. Best in 1934 showed that the fatty liver condition caused by insulin deficiency could be prevented by choline and other lipotropic agents. Other dietary models of cirrhosis soon followed, including lipotroph deficiency, a low-fat diet, and vitamin E deficiency. It remained for Harold P. Hims-worth and L. E. Glynn in 1944 to correlate the two pathways of cirrhogenesis: (1) a diffuse fatty liver developing into a finely nodular cirrhosis seen in the animal model with lipotroph deficiency; and (2) massive hepatic necrosis proceeding to the coarsely nodular liver created experimentally by cystine deficiency. The nutritional theory declined in popularity when careful experiments by Charles S. Lieber and colleagues, among others, showed in 1968 that alcohol was directly hepatotoxic in humans, and cirrhogenic in baboons.

Another technical innovation has advanced our understanding of cirrhosis. Introduced by Paul Ehr-lich in 1884, and popularized by P. Iversen and K. Roholm in 1939, the liver biopsy achieved wide use as a routine method of diagnosis. The accumulated histologic studies clarified the relationship of hepatitis to cirrhosis, and cirrhosis to hepatocellular carcinoma. They also helped to consolidate the various classifications of cirrhosis proposed in the past. The recent standardization of nomenclature (see Table VIII.28.1) was proposed by the Fogarty International Center in 1976 and the World Health Organization in 1977.

Thomas S. N. Chen and Peter S. Y. Chen Bibliography

Chen, Thomas, S., and Peter S. Chen. 1984. Understanding the liver: A history. Westport, Conn. Conn, Harold O., and Colin E. Attenbury. 1987. Cirrhosis. In Diseases of the liver, 6th edition, ed. Leon Schiff and Eugene R. Schiff. Philadelphia. Galambos, John T. Cirrhosis. 1979. Philadelphia. Garagliano, Cederic F., Abraham M. Lilienfeld, and Albert I. Mendeldoff. 1979. Incidence rates of liver cirrhosis and related diseases in Baltimore and selected areas of the United States. Journal of Chronic Disease 32: 543-54.

Herd, Denise. 1985. Migration, cultural transformation and the rise of black liver cirrhosis mortality. British Journal of Addiction 80: 397-410. Jorke, D., and M. Reinhardt. 1982. Contributions to the epidemiology of liver cirrhosis and chronic hepatitis. Deutsche Zeitschrift für Verdauungs-und Stoffwechselkrankheiten 42: 129-37. Millward-Sadler, G. H., E. G. Hahn, and Ralph Wright. 1985. Cirrhosis: An appraisal. In Liver and biliary disease, 2d edition, ed. Ralph Wright et al. Philadelphia.

Tuyns, A. J., and G. Pequignot. 1984. Greater risk of ascitic cirrhosis in females in relation to alcohol consumption. Internationsl Journal of Epidemiology 13: 53-7.

Alcohol No More

Alcohol No More

Do you love a drink from time to time? A lot of us do, often when socializing with acquaintances and loved ones. Drinking may be beneficial or harmful, depending upon your age and health status, and, naturally, how much you drink.

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