The Role of Intrahepatic Portal Venous Stenosis in the Formation and Progression of Hepatolithiasis

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Abstract
Recently, it has been suspected in animal models that a decrease in portal blood flow plays a role in the formation and progression of hepatolithiasis. To find whether this hypothesis is applicable to humans, we examined histologically the intrahepatic portal venous and arterial systems in normal livers (n = 13), extrahepatic biliary obstruction (n = 18), intrahepatic biliary sludge and microcalculi (n = 18, most of which were associated with biliary obstruction and might represent pathogenesis of an early developmental stage of hepatolithiasis), and fully developed hepatolithiasis composed of calcium bilirubinate stones (n = 30). A scoring method was employed to quantify portal stenosis, portal phlebosclerosis, arterial stenosis, and parenchymal atrophy. We found that these vascular changes were significantly more severe in hepatolithiasis than in biliary sludge and microcalculi, or in extrahepatic biliary obstruction. There were no significant differences in the vascular changes except for arterial stenosis between the latter two. There is a positive correlation between vascular stenosis and parenchymal atrophy. These findings suggest that portal venous stenosis deteriorates during the progression of hepatolithiasis. We could not find direct evidence that portal venous stenosis is an initial lesion followed by the formation of hepatolithiasis. The vascular changes may be caused by an inflammatory extension of cholangitis and may deteriorate, causing parenchymal atrophy during the progression of hepatolithiasis.

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