Does a combination of opisthorchiasis and ethyl alcohol consumption enhance early cholangiofibrosis, the risk of cholangiocarcinoma?

Combination of Opisthorchis viverrini infection and other factors could drive cholangiocarcinoma (CCA) development in Southeast Asia. However, other CCA factors are obscure. Alcohol consumption is well known in the risk for several cancers, but there is no report in CCA development. Therefore, the present study was to clarify whether drinking alcohol increases the liver pathology of Opisthorchis viverrini (OV) infection which may be the CCA risk. Experimental Syrian hamsters were divided into two groups: (1) infected with OV alone (OV); and (2) infected with OV plus administration of drinking alcohol (OV + ALC) for various lengths of time, i.e., 1, 2, 3, and 6 months. Hamster livers were collected for analysis of histopathological changes through hematoxylin and eosin, Sirius red, and immunohistostaining for proliferating cell nuclear antigen (PCNA) and cytokeratin 19 (CK19). Syrian hamster sera were used for liver function tests. Observed histopathological changes consisted primarily of aggregations of inflammatory cells surrounding the hepatic bile duct, especially at the hilar region, in both OV and OV + ALC groups; however, there was a difference in virulence. The OV + ALC group showed greater severity than the OV group. Moreover, in addition to aggregations of inflammatory cells, new bile duct formation (including hepatic cell death) was observed in subcapsular hepatic tissue. Bile duct proliferation, as determined by positive immunohistochemical staining for CK19 and PCNA, was correlated with the histopathology. Increased fibrosis was observed in subcapsular liver tissue. The present study suggests that alcohol consumption can exacerbate cholangiofibrosis, cholangitis, and lithiasis, which are risk factors for CCA.