Pathologic and hemodynamic sequelae of unilobar biliary obstruction and associated liver atrophy.

A patient is presented with unilobar biliary obstruction associated with marked liver atrophy and compensatory hypertrophy. Characteristically she was not jaundiced and had no portal hypertension. Quantitative measurements of the degree of hepatocyte hyperplasia showed that over 50% of cells in the hypertrophied lobe were hyperplastic. Surprisingly, a similar percentage of cells in the atrophied lobe were also hyperplastic. No difference was found in the size of hepatocytes between the two lobes or among the hepatocyte subpopulations in the atrophied lobe. The findings in this case suggest (1) lobar atrophy induces a hyperplastic response in more than one half of the cells of the contralateral lobe; (2) the development of atrophy consequent on biliary obstruction is likely the result of destruction of whole cells rather than cytoplasmic loss; (3) the development of a hyperplastic response within the atrophied lobe is a new finding and is consistent with the hormonal theory of hepatic regeneration; and (4) striking compensatory hypertrophy of the liver is associated with normal portal venous pressure.