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A spontaneous regression of hepatocellular carcinoma is an extremely rare phenomenon. A 69-year-old Japanese man with hepatitis C virus-related chronic hepatitis presented with a liver tumor. We diagnosed the tumor to be hepatocellular carcinoma in the course of spontaneous regression, by imaging studies and changes in the tumor markers. Because the possible presence of viable cancer cells could not be ruled out, we recommended surgery. He refused all treatments at first, but finally agreed to undergo surgery about 10 months after presentation. A hepatectomy was performed. Histologically, no viable tumor cells were found. In our case, the vascularity of the tumor according to the imaging findings was followed up during the clinical course. The patient is now doing well and without any evidence of recurrence at 37 months after surgery.

Although curative surgical resection provides the best chance of long-term survival for patients with intrahepatic cholangiocarcinoma, the presence of bile duct invasion decreases postoperative survival rates in patients with mass-forming intrahepatic cholangiocarcinoma. We carried out this study to determine a surgical strategy for patients with bile duct invasion of these tumors. Forty-one patients with mass-forming intrahepatic cholangiocarcinoma were classified as either having bile duct invasion (n= 26) or not having bile duct invasion (n= 15). Clinicopathologic findings, including postoperative outcomes, were compared between these two groups. Perineural invasion, lymphatic invasion, and a positive resection margin were more frequent in patients with ductal invasion. Patients with ductal invasion had lower survival rates than those without ductal invasion. Intraoperative frozen section examination of the bile duct stump to confirm a clear resection margin is required in patients with mass-forming tumors. Resection of the extrahepatic bile duct should be considered when tumor cells are identified at the surgical margin of the resected bile duct.

Erythrocyte deformability is an important factor in the microcirculation. The deformability in patients with chronic liver disease is less than normal. We studied changes in erythrocyte deformability in 32 patients undergoing liver resection for hepatocellular carcinoma with underlying chronic liver disease to investigate whether the measurement of deformability gives information useful for postoperative management. We measured erythrocyte deformability as erythrocyte transit time (ETT) before and after resection, as well as the erythrocyte adenosine triphosphate level, mean corpuscular volume, mean corpuscular hemoglobin concentration, and indices of liver function. The 15-minute indocyanine green retention rate (ICGR15) was measured before resection. Correlations between the change in deformability and these values were evaluated, as was correlation with the scale of the operation and with the occurrence of postoperative complications. Mean ETT was higher in the patients before resection than in healthy volunteers. ETT was correlated with serum high density lipoprotein-cholesterol (p0.05). The incidence of postoperative complications was higher (p = 0.001) in the patients (group A) with ETT increased during the first 3 postoperative days by/=1 SD of the mean of the preoperative value than in patients (group B) with less change. Of the 12 patients whose ICGR15 value was/=20%, all 9 patients in group A had postoperative complications. The increase in ETT (decrease in erythrocyte deformability) is associated with the development of postoperative complications. The measurement of erythrocyte deformability gives information useful for postoperative management, and special monitoring for postoperative complications is necessary in patients with the increase soon after liver resection.

Xanthogranulomatous cholecystitis (XGC) is a rare inflammatory disease of the gallbladder. In severe cases, inflammation extends to adjacent structures, and XGC is sometimes confused with a malignant neoplasm. We recently diagnosed XGC as the preoperative cause of Mirizzi syndrome in a patient based on the clinical course. The patient was admitted because of obstructive jaundice, with gallbladder carcinoma as the suspected cause. The gallbladder was swollen with gallstones and the serum level of carbohydrate antigen 19-9 (CA19-9) was 3070 U/ml at admission. A percutaneous transhepatic cholangiodrainage (PTCD) was done, and the common hepatic duct as well as the right and left hepatic ducts were found to be obstructed. Later, the CA19-9 level and swelling of the gallbladder decreased and the obstruction of the bile ducts disappeared. A cholecystectomy was performed and the intraoperative pathohistological diagnosis of chronic cholecystitis was made from frozen sections. The pathohistological diagnosis of XGC was made from paraffin-embedded sections. Mirizzi syndrome such as that seen in our patient is a rare complication of XGC. XGC occasionally causes extensive inflammation; thus, performing a conventional cholecystectomy can be unsafe. However, in our opinion, a total, not subtotal, cholecystectomy should be done whenever possible because the incidence of gallbladder carcinoma accompanied with XGC is higher than that with ordinary cholecystitis or gallstones.

of hepatic tumors was minimal over 7 years (see Fig. 1), very unlikely as metastatic tumors. Additionally, we failed to find any possible primary site for somatostatinoma, even though extensive searches for the primary sites were performed using upper and lower GI endoscopy, CT scan of the head, neck, and trunk, and 67Ga scintigraphy of the whole body. Therefore, it is reasonable to assume that the tumor originated from the liver. Hepatic tumors observed in patients with VRD, although very rare, include plexiform neurofibromas, angiosarcoma, and malignant schwannoma.2 Primary hepatic somatostatinoma, with or even without VRD, is very rare and has been reported only by Ohwada et al.3 It is known that somatostatin-containing cells are present in the intrahepatic biliary tree.4 Thus, intrahepatic tumors have arisen from these endocrine cells, possible affected by a genetic disorder present in patients with VRD.