ABSTRACT
BACKGROUND: Although hepatectomy has been accepted as a therapeutic option for the primary tumor of hepatocellular carcinoma (HCC), what role the second liver resection will play in the clinical care of patients with intrahepatic recurrence of HCC after the initial resection has not been well evaluated. STUDY DESIGN: In a retrospective review of the 6-year period between January 1991 and December 1996, records were examined of 94 patients who underwent curative liver resection for HCC. Of these, 57 patients had isolated recurrent disease to the liver; 12 of the 57 patients underwent repeat surgical resection and 45 patients received nonsurgical ablative therapy. Clinical data for these patients were reviewed for operative morbidity and mortality, survival, disease-free survival, and pattern of failure. RESULTS: There were no perioperative deaths during repeat liver resections for recurrent HCC. Operative morbidity in the second resection was comparable to the initial resection. The disease-free survival rate after the second hepatectomy was 31% at 2 years, significantly lower than that after initial hepatectomy (62%) (p = 0.009). The overall survival rate after the second hepatectomy was 90% at 2 years, in contrast to 70% after nonsurgical ablative treatment for recurrent HCC (p = 0.253). CONCLUSIONS: Although the second liver resection for recurrent HCC can be performed safely and may improve survival, the disease-free survival rate after such resection therapy is low. This likelihood of further recurrences encourages studies for the selection of patients who may benefit from repeat liver resection.
Subject(s)
Carcinoma, Hepatocellular/surgery , Hepatectomy/methods , Liver Neoplasms/surgery , Neoplasm Recurrence, Local/surgery , Reoperation/methods , Aged , Carcinoma, Hepatocellular/mortality , Carcinoma, Hepatocellular/pathology , Female , Hepatectomy/adverse effects , Hepatectomy/mortality , Humans , Liver Neoplasms/mortality , Liver Neoplasms/pathology , Male , Middle Aged , Morbidity , Neoplasm Recurrence, Local/mortality , Neoplasm Recurrence, Local/pathology , Neoplasm Staging , Patient Selection , Proportional Hazards Models , Reoperation/adverse effects , Reoperation/mortality , Retrospective Studies , Survival Analysis , Treatment OutcomeABSTRACT
BACKGROUND/PURPOSE: The venous drainage from Spiegel's lobe to the terminal portion of the hepatic veins has been described in the literature, but its morphology remains unclear. METHODS: We examined 42 dissected liver specimens and 38 cast specimens. RESULTS: In 8 of the 42 dissected liver specimens and 5 of the 38 cast specimens we found atypical but thick (over 3 mm) caudate veins that drained Spiegel's lobe and emptied into the terminal portion (along the most proximal 5-mm course) of the middle hepatic vein (MHV) or the inferior vena cava (IVC) near the MHV terminal (less than 10 mm from the MHV). We termed these the superior caudate vein. This vein ran upward between the caudate portal branches of the left and hilar bifurcation origins or through the territory of the left origin. The superior caudate vein, consistently coexisted with the typical vein(s). We also found several analogues of the superior caudate vein, such as the cranially shifted opening of the typical caudate vein and relatively thick proximal tributaries of the MHV from Spiegel's lobe. CONCLUSIONS: Although the superior caudate vein, if present, seemed to have a large role in the venous drainage of the lobe, its incidence seemed to be too low for clinical relevance.
Subject(s)
Hepatic Veins/anatomy & histology , Liver/anatomy & histology , Cadaver , Dissection/methods , Humans , Liver/blood supply , Liver CirculationABSTRACT
Interferon gamma (IFN-gamma) plays an important role in host defense mechanism and participates in the progression of chronic liver disease. IFN-gamma exerts its pleiotrophic effects by transcriptional regulation of expression of numerous genes, such as major histocompatibility complex (MHC) class I and Fas, through interaction with IFN-gamma receptor (IFN-gamma-R). Although hepatocytes in normal liver express weak or no IFN-gamma-R, those in acute and chronic liver disease up-regulate its expression. A study using IFN-gamma-R alpha-chain knock-out mice revealed the actions of IFN-gamma on tumor cells as an extrinsic tumor-suppressor mechanism. However, it is unclear whether or how hepatocellular carcinoma (HCC) blocks the signal transduction of IFN-gamma to evade host immune surveillance. We examined the expression of IFN-gamma-R and IFN-gamma-inducible genes in 44 cases with HCC using real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. In noncancerous liver tissues (n = 38), IFN-gamma-R expression on the cell surface was up-regulated in 27 cases. In IFN-gamma-R-negative cases (n = 15), tumor size was larger (P =.032), serum alpha-fetoprotein (AFP) level was higher (P =.001), intrahepatic and extrahepatic metastasis was more common (P =.044 and.013, respectively), and Ki-67 labeling index (LI) was higher (P =.041), compared with IFN-gamma-R-positive cases. Accordingly, the evasion mechanism may play an important role in progression, especially metastasis, in HCC. The significant correlation between the status of IFN-gamma-R and the expression of Fas and MHC implies that the loss of IFN-gamma-R might contribute to the mechanism of escape from host immune rejection in HCC.
