Relationship between Histopathology in Cirrhosis of the Liver with or without Hepatocellular Carcinoma and Esophageal Varix Formation

A clinicopathological study using autopsy materials to find out the correlation between histological findings of cirrhosis of the liver (LC) with or without hepatocellular carcinoma (HCC) and morphological evidences of portal hypertension such as esophageal varix formation and splenomegaly. In all 79 cases of LC (accompanied with or without HCC) and HCC (with no LC) out of 1,112 autopsy cases at the Department of Pathology, Institute of Tropical Medicine, Nagasaki University during the period 1967 to 1989 were reviewed. All patients were from Nagasaki City and its suburbs. Histologically, the LC cases were divided into three types; Nagayo\u27s A-type (Nagayo, 1914) which showed wide fibrous septum, Nagayo\u27s B-type which showed thin fibrous septum and macronodular pseudolobule, and micronodular type which showed micronodular pseudolobule with fatty metamorphosis and thin fibrous septum. Five out of six cases (83%) of A-type LC were complicated with esophageal varix and four out of the five cases (80%) showed rupture of varix. Five out of eight cases (63%) of B-type LC were complicated with esophageal varix and two out of the five cases (40%) showed rupture of varix. Two out of five cases (40%) of micronodular type LC were complicated with ruptured esophageal varices and the remaining three cases had no varix. All 16 cases (100%) of A-type LC accompanied with HCC were complicated with esophageal varices. Ten cases (63%) of them showed rupture of varix. On the other hand 23 out of all 31 cases (74%) of B-type LC accompanied with HCC showed esophageal varices. However, only eight (35%) of the varix cases showed rupture of varices. As for HCC without LC, five out of all 13 cases (38%) were complicated with esophageal varices showing no ruptrue. These findings suggest that advanced and thick fibrosis of the liver in the LC cases with architectural distortion of the intrahepatic portal veins and the disturbance of blood flows is one of the most important factors which play an etiological role of portal hypertension followed by esophageal varix formation and splenomegaly. More advanced splenomegaly (mean weight, 470g) and esophageal varix formation may be caused by more severe portal hypertension in A-type LC which shows wide fibrous septa than other types of LC. HCC may play an etiological role of portal hypertension, especially in the cases of occurrence of intrahepatic portal invasion of tumor tissue, but less remarkably than LC cases