BACKGROUND/AIMS: Portal hypertensive symptoms, such as esophageal varices and hypersplenism, are frequently observed in patients with hepatocellular carcinoma (HCC). We investigated whether or not the extent of hepatectomy for HCC has an influence on the deterioration of the portal hypertensive state. METHODOLOGY: Fifty-four patients who underwent curative hepatectomy for HCC at our institute were retrospectively studied. The 54 patients were classified in two groups according to the extent of hepatectomy: Group A patients (n = 38) underwent minor hepatectomy (subsegmentectomy or less) and Group B patients (n = 16) underwent major hepatectomy (segmentectomy or more). On the basis of the endoscopic findings for the esophageal varices and the blood platelet counts, the alterations of portal hypertensive state were evaluated before and after hepatectomy. RESULTS: The number of patients whose esophageal varices deteriorated post-operatively, amounted to 9 (23.7%) in Group A and 1 (6.3%) in Group B (not significant). No significant differences were found in the platelet counts between pre- and post-operative states in each Group (A and B). In all of the 6 patients whose esophageal varices first came about after hepatectomy, the advent of the varices occurred more than 1 year after surgery. CONCLUSIONS: These results suggest that in the patients undergoing hepatectomy for HCC, the clinical deterioration of the portal hypertensive state in not caused by the extent of hepatectomy, but by the advance of the coexisting chronic hepatic diseases or tumor recurrence.
BACKGROUND/AIMS: Portal hypertensive symptoms, such as esophageal varices and hypersplenism, are frequently observed in patients with hepatocellular carcinoma (HCC). We investigated whether or not the extent of hepatectomy for HCC has an influence on the deterioration of the portal hypertensive state. METHODOLOGY: Fifty-four patients who underwent curative hepatectomy for HCC at our institute were retrospectively studied. The 54 patients were classified in two groups according to the extent of hepatectomy: Group A patients (n = 38) underwent minor hepatectomy (subsegmentectomy or less) and Group B patients (n = 16) underwent major hepatectomy (segmentectomy or more). On the basis of the endoscopic findings for the esophageal varices and the blood platelet counts, the alterations of portal hypertensive state were evaluated before and after hepatectomy. RESULTS: The number of patients whose esophageal varices deteriorated post-operatively, amounted to 9 (23.7%) in Group A and 1 (6.3%) in Group B (not significant). No significant differences were found in the platelet counts between pre- and post-operative states in each Group (A and B). In all of the 6 patients whose esophageal varices first came about after hepatectomy, the advent of the varices occurred more than 1 year after surgery. CONCLUSIONS: These results suggest that in the patients undergoing hepatectomy for HCC, the clinical deterioration of the portal hypertensive state in not caused by the extent of hepatectomy, but by the advance of the coexisting chronic hepatic diseases or tumor recurrence.