[A case of cholangiolocellular carcinoma combined with intrahepatic cholangiocarcinoma diagnosed after 4 years follow-up for hepatic hemangioma].

We report a rare case which had been followed up for hepatic hemangioma and in whom was surgical resection revealed with cholangiolocellular carcinoma (CoCC) combined with intrahepatic cholangiocarcinoma (ICC). A 69-year-old man who was an HBV carrier had been regularly followed up with hepatic hemangioma from November, 2005. Because the arterial phase of dynamic CT scan exhibited an enhanced lesion in the dorsal portion of the hemangioma on November, 2009, the patient was admitted for intensive examination of the liver tumor. After surgical resection of the tumor, histological examination revealed small irregular tubules in the outer part and scattered small duct structures in the inner part of the tumor. In addition, immunohistochemical analysis demonstrated that cytokeratin (CK) 7, CK19 and epithelial membrane antigen (EMA) were all positive in the outer part, and EMA was only negative in the inner part of the tumor. From these findings, this case was diagnosed as CoCC combined with ICC.

Chronic hepatitis C viral infection reduces NK cell frequency and suppresses cytokine secretion: Reversion by anti-viral treatment.

Impaired activity of NK (natural killer) cells has been proposed as a mechanism contributing to viral persistence and chronic infection in hepatitis C (HCV) infection. We aimed to assess the impact of HCV infection on NK cells regarding frequency, subset distribution, and cytotoxic and cytokine secretion functions, as well as IFN-alpha and ribavirin therapeutic effects on NK cells. Significant reduction of total NK frequency and the CD56(dim)16(+) subset was observed in chronic HCV patients. IFN-gamma expression upon stimulation with K562 was severely suppressed but cytotoxicity measured by CD107a expression was maintained. These adverse effects were reversed after treatment with pegylated IFN-alpha and ribavirin; however, these skewed functions were not recovered in treatment-resistant patients. Thus, HCV chronic infection severely affects NK functions, except for cytotoxicity. Altered NK cell frequency and cytokine secretion by HCV infection may contribute to impaired cellular immune response and virus persistence.