Summary
In the liver, the development of the chronic interstitial fibrosis which is characteristic of cirrhosis, occurs along, and is limited to the interlobular septa, in which location only, demonstrable lymphatic channels lie. The fibrotic lesion parallels these lymphatic channels accurately. The presence of acute inflammatory changes and lymphatic involvement in acute lesions which rarely demonstrably precede, or are more often associated with cirrhosis, and the fact that the fibrosis is not present elsewhere in the liver than where lymphatic channels are present, seems to make it correct to assume that a chronic lymphangitis is the essential underlying cause of the cirrhosis. Elements of the reticulo-endothelial system are not involved either in the liver or in the spleen. All of the previously assumed causes for the development of this lesion are sometimes consequences of the original causal agent, or frequently only associated agents which mutually aid and abet one another and enhance the total effect to the full development of cirrhosis. The degenerative parenchymal cellular changes are the continuation of some preceding acute parenchymal disease or of some intercurrent associated similar acute episode; or they are secondary effects of the diverse associated causology and of the pathogenetic mechanism. The general inanition causes and/or results bilaterally from interference with cellular function. the peritoneal effusions are evidences of a general nutritional oedema and result from the hypoproteinemia and general protein deficiency which accompanies the general inanition.
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Wilensky, A.O. The pathogenesis and mechanism of cirrhosis of the liver. Jour. D. D. 13, 367–372 (1946). https://doi.org/10.1007/BF03003066
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DOI: https://doi.org/10.1007/BF03003066