Three cases of small hepatocellular carcinoma presenting as obstructive jaundice.

BACKGROUND: Despite improved diagnostic tools, it is often difficult to make a correct diagnosis of small hepatocellular carcinoma (HCC) in patients with obstructive jaundice. CASE OUTLINES: Three cases of small HCC (<2 cm diameter) presenting as obstructive jaundice are reported. All tumours were initially diagnosed as hilar cholangiocarcinoma based on ultrasonography, computed tomography, cholangiography and angiography. Because of insufficient hepatic function, none of the patients underwent hepatic resection. One patient died 8 months after first admission to our hospital, another died of disseminated intravascular coagulation I month after admission, and the third was treated with hepatic arterial infusion chemotherapy and survived >36 months. CONCLUSION: It is important to consider HCC in the diagnosis of obstructive jaundice in patients who are predisposed to HCC because of liver cirrhosis and/or chronic viral hepatitis, and have elevated serum alpha-fetoprotein.

Small bowel perforation caused by metastasis from an extra-abdominal malignancy: report of three cases.

Small bowel perforation is rarely caused by metastasis from an extra-abdominal malignancy. This report describes three cases of small bowel perforation that occurred secondary to a metastatic tumor. The first case involved a 72-year-old man with malignant lymphoma of the larynx that had been treated with chemo- and radiation therapy; the second involved a 70-year-old man with rhabdomyosarcoma of the mediastinum that had been treated with radiation therapy; and the third involved a 41-year-old man with lung carcinoma that had been treated with surgery 10 months prior to perforation. Each patient presented with acute abdominal pain, had X-ray findings of free air in the abdomen, and underwent limited emergency surgery. Wedge resection and closure of the ileum was performed for the first patient and partial bowel resection with the creation of an intestinal stoma was performed for the second and third patients. In each case, the histologic findings of the resected specimens were consistent with the extra-abdominal primary tumors. Although the patients recovered sufficiently to begin eating and moving about, all three died of cancer or cancer-related complications within 45 days of surgery. We conclude that surgeons should be aware of the poor prognosis of such patients and perform only the minimal surgery required.

Appraisal of intra-arterial infusion of prostaglandin E1 in patients undergoing major hepatic resection report of four cases.

In order to reduce risk for postoperative acute liver failure, prostaglandin E1 (PGE1) was administered either from the hepatic artery (HA) or the superior mesenteric artery (SMA) in four high-risk cases undergoing major hepatic resection. Two cases were subjected to HA PGE1 infusion for 3 or 4 days after surgery at a rate of 0.01 microg/kg/min. Both patients had hepatocellular carcinoma (HCC) associated with chronic hepatitis, and ICG R15 was 17.6% and 14.5%, respectively. Right hemihepatectomy and extended right hemihepatectomy were performed. Serum total bilirubin (T. Bil.) peak value was 2.2 mg/100 ml in Case 1 and 2.1 mg/100 ml in Case 2. In Case 1, decreased bile flow was observed immediately after cessation of PGE1. The other two cases were subjected to SMA PGE1 infusion for 5 or 6 days after surgery at the same rate. In Case 3, right hemihepatectomy was performed for HCC on a cirrhotic liver four weeks after right portal vein embolization, in which preoperative ICG R15 was 19.0%. Peak T. Bil level was 3.7 mg/100 ml with uneventful postoperative course. In Case 4 with a huge cholangioma, right trisegmentectomy was performed. Peak serum T. Bil level was 1.7 mg/100 ml in this uneventful postoperative course. In Case 3 and Case 4, portal blood flow, measured by Doppler ultrasonography, was markedly increased by PGE1 infusion. From these results, intra-arterial PGE1 infusion might be useful in prevention of postoperative liver failure after major hepatic resection.

Efficacy of hepatic arterial infusion of prostaglandin E1 in the treatment of postoperative acute liver failure--report of a case.

Prostaglandin E1 (PGE1) has received attention for its protective effects against various types of liver damage. However, it is known that approximately 70% of PGE1 is inactivated during a single passage through the lung. Therefore, direct infusion of PGE1 into the liver bloodstream is preferable to intravenous infusion. A 66-year-old man with hepatocellular carcinoma with liver cirrhosis developed postoperative acute liver failure following posterior segmentectomy under hepatic total vascular exclusion exceeding 1 hour. Because his liver function did not recover in spite of plasma exchange starting on postoperative day 8 and intravenous infusion of PGE1, hepatic arterial continuous infusion of PGE1 at a rate of 0.01 microgram/kg/min was carried out for 7 days from postoperative day 17. Immediately after the start of the arterial infusion, the bile flow significantly increased compared to before the arterial infusion, and the serum total bilirubin level decreased thereafter and finally recovered from the hepatic failure. In addition to its highly efficient drug delivery, the hepatic arterial infusion of PGE1 seems to be more advantageous in oxygen delivery to the liver compared with intravenous infusion. In conclusion, the hepatic arterial infusion of PGE1 may be useful in the treatment of acute liver failure.

Prostaglandin E(1) continuous hepatic arterial infusion in the treatment of postoperative acute liver failure: basic study on hepatic hemodynamics and clinical application.

AIM: In the treatment of severe liver damage, it is of greater advantage to administer prostaglandin E(1) (PGE(1)) directly to the liver compared with systemic intravenous infusion, because of its high inactivation rate in the lungs. In comparison with intraportal infusion, hepatic arterial infusion is more advantageous because of its easier and safer accessibility. This study was designed to prove the superiority of hepatic arterial infusion to intravenous infusion. METHODS: Changes in hepatic hemodynamics and oxygen delivery accompanying PGE(1) infusion using both methods were investigated in pigs. In addition, continuous hepatic arterial infusion was applied in 3 cases of postoperative acute liver failure, for patients in whom other conventional treatments like plasma exchange failed to improve the functioning of the liver. RESULTS: Hepatic arterial flow increased significantly accompanying hepatic arterial infusion of PGE(1) at a rate of 0.1 microg/kg/min compared with intravenous infusion at the same rate in pigs. Such an increase resulted in elevation of total hepatic blood flow and oxygen delivery to the liver. Correspondingly, bile flow significantly increased accompanying hepatic arterial infusion of PGE(1). Continuous hepatic arterial infusion was applied in 3 cases of postoperative acute liver failure. The infusion was continued for 7-9 days at a rate of 0.01 microg/kg/min without any complications through heparin-coated catheters inserted via the femoral artery. Significant increase in bile flow was observed in 2 cases in whom bile was collected, serum total bilirubin began to decrease in all these 3 cases, and the patients recovered from acute liver failure. CONCLUSION: Hepatic arterial infusion of PGE(1) is very useful and effective in the treatment of acute liver failure.

Continuous infusion of prostaglandin E1 via the superior mesenteric artery can prevent hepatic injury in hepatic artery interruption through passive portal oxygenation.

AIMS/BACKGROUND: Hepatic artery interruption (HAI) causes severe ischemic liver damage, especially following hepatopancreatobiliary surgery. In order to inhibit a decrease in oxygen delivery after HAI, continuous infusion of PGE1 via the superior mesenteric artery (SMA) was administered in pigs and changes in hepatic blood flow and oxygen delivery were investigated. Furthermore, its effectiveness in the prevention of liver injury was evaluated by histology and serum enzyme levels. METHODS: Animals were subjected to HAI without PGE1 infusion (control group n=6) and to continuous infusion of PGE1 (0.02 microg/kg/min) into the SMA (PGE1 group n=6). RESULTS AND CONCLUSION: PGE1 infusion via the SMA not only increased the portal blood flow but also elevated the oxygen content of the portal blood. The reduction in oxygen delivery to the liver was 50% in the control group, and only 13% in the PGE1 group. Serum aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels 24 h after HAI in the control group were 3415+/-1283 IU/L and 9839+/-2959 respectively while in the PGE1 group they were 939+/-426 IU/L and 5510+/-1545 IU/L respectively. Histological examination showed massive necrosis in the control group at 72 h but only focal liver cell necrosis in the PGE1 group. Based on this finding and the fact that this treatment can be performed easily and safely, continuous infusion of PGE1 via the SMA may be a useful intervention to prevent severe liver damage after hepatic artery interruption.

Malignant lymphoma of the transverse colon associated with macroglobulinemia.

We present an unusual case of a malignant lymphoma of the transverse colon associated with macroglobulinemia. A 73-yr-old man was incidentally discovered to have high serum gamma-globulin on a regular check-up. Serum immunoquantitation revealed an IgM level of 3490 mg/dl. Kappa-type Bence-Jones protein was positive in the urine. Immunoelectrophoresis identified the abnormal protein as IgM-kappa. After hospitalization an abdominal tumor was detected with barium and CT, identified as a tumor of the transverse colon. Partial resection of the transverse colon was carried out. Histopathologically the tumor were confirmed as small lymphocytic non-Hodgkin lymphoma of B-cell origin, based on the Working Formulation. According to flowcytometric analysis, the tumor cells were positive for IgM-kappa. The lymphoma cells produced monoclonal IgM, giving rise to macroglobulinemia.

Isolation of oval cells from Long-Evans Cinnamon rats and their transformation into hepatocytes in vivo in the rat liver.

Oval cells function as compensatory cells in severe liver injury and are thought to be equivalent to liver stem/progenitor cells. We isolated oval cells from the liver of Long-Evans Cinnamon (LEC) rats by isopyknic centrifugation in a Percoll gradient. The cells were gamma-glutamyl transpeptidase (GGTP)-positive, alpha-fetoprotein-positive, and cytokeratin (CK) 18- and CK 19-positive, but albumin-negative in the cells. When oval cells were transplanted to the liver, they were transformed into hepatocytes. To evaluate albumin biosynthesis, we transplanted oval cells into the liver of Nagase analbuminemic and LEC double mutant rats. The albumin level in the serum of transplanted rats was increased and maintained for up to 10 weeks. These results indicated that the oval cells isolated from LEC rats can differentiate into hepatocytes in vivo.

Detection of influenza virus RNA in peripheral blood mononuclear cells of influenza patients.

Gastroenteritis, arthralgaia and myalgia are frequently associated with influenza virus infections in humans. One explantation for these symptoms may be extrarespiratory transmission of virus by peripheral blood mononuclear cells (PBMC). We tried to detect genomic viral RNA of the nucleoprotein (NP) and H3 subtype hemagglutinin (HA) genes by the method of RT-PCR in PBMC of 18 children aged 1-14 who suffered from an influenza outbreak in the Kansai district of Japan between December 1992 and February 1993. Three of the 18 samples were RT-PCR positive. The NP gene sequence observed in one patient's PBMC was identical to that obtained from his throat swab fluid. The HA gene sequences observed in the two other PBMC differed from those of RT-PCR-amplified DNA from throat swabs by an order of 3-9 nucleotides. We believe these results suggest the presence of a PBMC-associated virus.

Copper incorporation into ceruloplasmin in rat livers.

Ceruloplasmin, a blue copper oxidase found in plasma, is synthesized in hepatocytes as a single polypeptide chain consisting of a 19 amino acid leader peptide plus 1046 amino acids of mature protein (132 kDa). Holoceruloplasmin is secreted into the plasma with 6-7 atoms of copper bound per molecule. In this study we identified apo- and holoceruloplasmin and examined the mechanism of copper incorporation during ceruloplasmin biosynthesis using the Long-Evans Cinnamon (LEC) rat which does not incorporate copper into newly synthesized ceruloplasmin. We followed the conversion from ceruloplasmin precursor (with little or no carbohydrate) to the larger product (after carbohydrate addition), which occurred in the secretory compartments of hepatocytes, by native gel electrophoresis. We found that copper accumulates in the hepatocellular Golgi apparatus of LEC rats due to a disorder in the process of copper incorporation. The data indicate that copper is incorporated into ceruloplasmin late in the course of its transport through the secretory compartments.