Development of colon cancer after liver transplantation for primary sclerosing cholangitis associated with ulcerative colitis

Between February 26, 1981, and July 30, 1987, 36 patients underwent orthotopic liver transplantation for primary sclerosing cholangitis associated with ulcerative colitis. Three of the 36 recipients died within 3 mo because of graft nonfunction or surgical complications. The other 33 (92%) lived for at least 1 yr. Two of the 33 died after 12 and 14 mo, respectively, of recurrent cholangiocarcinoma that was not diagnosed before transplantation. Four other patients died of recurrent liver failure (three cases) or immunoblastic sarcoma (one case) after 14, 21, 36 and 44 mo. Twenty‐seven (75%) of the patients are still alive 23 to 81 mo after transplantation. Two patients have been diagnosed as having colorectal cancer 11 and 21 mo respectively, after transplantation, for an overall incidence of 5.6% (2 of 36) and a corrected incidence of 6.5% (2 of 31) if the three early deaths and two later deaths caused by cholangiocarcinomas are excluded. It is not known whether colorectal malignancies were present but undetected at the time of transplantation or whether they developed afterward. It is clear that patients who undergo liver transplantation for primary sclerosing cholangitis associated with ulcerative colitis should have careful follow‐up of the colon, including colonoscopy and multiple biopsies of the colorectal mucosa. Whether proctocolectomy should be considered prophylactically after liver transplantation is an unresolved issue.(HEPATOLOGY 1990;11:477–480.) Copyright © 1990 American Association for the Study of Liver Disease

Hemodynamic and biochemical changes during normothermic and hypothermic sanguinous perfusion of the porcine hepatic graft

Using an ex vivo liver sanguinous perfusion system, hemodynamic and biochemical changes of the porcine livers were studied, which were preserved cold (4°C) for 24 hr in University of Wisconsin solution and reperfused with normothermic (37°C) (n=8) or hypothermic (32°C) (n=8) blood for 3 hr. Six more livers were reperfused with normothermic blood (37°C) immediately after procurement as controls. The total hepatic blood flow was adjusted to 1 ml/min/g liver weight, in which hepatic artery and portal vein flows were administered at a 1:2 ratio. In livers stored cold for 24 hr in UW solution and perfused normothermically, a statistically higher hepatic artery resistance was exhibited at 30 an 60 min after reperfusion (P<0.05), and there was lower bile output (P<0.05) at 90 and 120 min as compared to the controls. In livers stored cold for 24 hr in UW solution and perfused hypothermically, as compared to ones perfused normothermically, statistically higher hepatic- artery and portal-vein resistances (P<0.05) were observed throughout the perfusion period and 60 min= after reperfusion, respectively. In addition, bile output and oxygen consumption of these livers were statistically lower than those of ones perfused normothermically (P<O.05). In contrast, chemistries of the perfusat of livers perfused hypothermically were comparable to ones perfused normothermically. Histologic examination of the liver perfused hypothermically demonstrated hepatic arterial and/or portal venous congestion and mild-to-moderate hemorrhage in the portal triads. This study suggests that livers preserved for a prolonged period of time demonstrate a high hepatic arterial resistance shortly after revascularization, and that recipient hypothermia after revascularization may be a risk factor for the development of hepatic arterial thrombosis following liver transplantation. © 1990 by Williams & Wilkins

Strategies for Reducing Blood Transfusions in Hepatic Resection

A comparison of 60 blood transfused and 71 nonblood transfused hepatic resection patients was done to evaluate strategies for reducing blood transfusions during hepatic surgery. There were no significant differences between the two groups with regard to preoperative laboratory data, except for prothrombin time and hematocrit value. The mean operative blood loss was 1990 ml and 760 ml in the blood transfused and nonblood transfused groups, respectively. A multivariate analysis suggested that the patient’s body weight, preoperative prothrombin time, and operative blood loss independently predicted the need for intraoperative blood transfusion. Major postoperative complications developed more frequently in the blood transfused group than in the nonblood transfused group (31.7 vs. 11.3%, p<0.005). These results suggest that the difference in operative blood loss between the two groups was related to the prolonged prothrombin time and a susceptibility for blood transfusion was found to exist particularly in patients with a lower hematocrit value as well as a lower body weight. Thus, the improvement of these preoperative laboratory data combined with avoiding the use of the hematocrit value as a determining factor for intraoperative transfusion could correspond to a reduction in operative blood loss, while curtailing the demands on blood bank facilities, and lowering the risk of postoperative complications

Significance of Liver Size in Hepatic Surgery

The purpose of this study was to evaluate the significance of liver volumetry as a parameter for hepatic functional reserve in cirrhotic patients with hepatocellular carcinoma. Liver volume was calculated from preoperative computed tomograms of 44 cirrhotic patients who underwent elective hepatic resections for hepatocellular carcinoma

Calibration of the Isomer Shift for the 35.46 keV Mossbauer Transition of 125Te

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Personal experience with the procurement of 132 liver allografts

A single donor surgeon's experience procuring the livers from 132 donors is described. Thirty-seven grafts (28.9%) had hepatic arterial anomalies, 19 (14.4%) of which required arterial reconstruction prior to transplantation. Of the 121 grafts evaluated for early function, 103 grafts (85.2%) functioned well, whereas 14 grafts (11.6%) functioned poorly and 4 grafts (3.3%) failed to function at all. The variables associated with less than optimal function of the graft consisted of donor age (P<0.05), duration of donor's stay in the intensive care unit (P<0.005), abnormal graft appearance (P<0.05), and such recipient problems as vascular thromboses during or immediately following transplantation (P<0.005). A new preservation fluid, University of Wisconsin solution, allowed safe and longer cold storage of the liver allograft than did Euro-Collins' solution (P<0.0001). A parameter of liver allograft viability, which is simple and predictive of allograft function prior to the actual transplant procedure, is urgently needed. © 1989 Springer-Verlag

Constitutive activation of glycogen synthase kinase-3β correlates with better prognosis and cyclin-dependent kinase inhibitors in human gastric cancer

Background: Aberrant regulation of glycogen synthase kinase-3 beta (GSK-3 beta) has been implicated in several human cancers; however, it has not been reported in the gastric cancer tissues to date. The present study was performed to determine the expression status of active form of GSK-3 beta phosphorylated at Tyr(216) (pGSK-3 beta) and its relationship with other tumor-associated proteins in human gastric cancers. Methods: Immunohistochemistry was performed on tissue array slides containing 281 human gastric carcinoma specimens. In addition, gastric cancer cells were cultured and treated with a GSK-3 beta inhibitor lithium chloride (LiCl) for immunoblot analysis. Results: We found that pGSK-3 beta was expressed in 129 (46%) of 281 cases examined, and was higher in the early-stages of pathologic tumor-node-metastasis (P < 0.001). The expression of pGSK-3 beta inversely correlated with lymphatic invasion (P < 0.001) and lymph node metastasis (P < 0.001) and correlated with a longer patient survival (P < 0.001). In addition, pGSK-3 beta expression positively correlated with that of p16, p21, p27, p53, APC, PTEN, MGMT, SMAD4, or KAl1 (P < 0.05), but not with that of cyclin D1. This was confirmed by immunoblot analysis using SNU-668 gastric cancer cells treated with LiCl. Conclusions: GSK-3 beta activation was frequently observed in early-stage gastric carcinoma and was significantly correlated with better prognosis. Thus, these findings suggest that GSK-3 beta activation is a useful prognostic marker for the early-stage gastric cancer.Hirakawa H, 2009, ONCOL REP, V22, P481, DOI 10.3892/or_00000460Dar AA, 2009, ONCOGENE, V28, P866, DOI 10.1038/onc.2008.434Holmes T, 2008, STEM CELLS, V26, P1288, DOI 10.1634/stemcells.2007-0600Wang Q, 2008, CELL DEATH DIFFER, V15, P908, DOI 10.1038/cdd.2008.2Takahashi-Yanaga F, 2008, CELL SIGNAL, V20, P581, DOI 10.1016/j.cellsig.2007.10.018Pan MH, 2007, J AGR FOOD CHEM, V55, P7777, DOI 10.1021/jf071520hShakoori A, 2007, CANCER SCI, V98, P1388, DOI 10.1111/j.1349-7006.2007.00545.xZheng HC, 2007, ANTICANCER RES, V27, P3561Saegusa M, 2007, J PATHOL, V213, P35, DOI 10.1002/path.2198Ma C, 2007, CANCER RES, V67, P7756, DOI 10.1158/0008-5472.CAN-06-4665Forde JE, 2007, CELL MOL LIFE SCI, V64, P1930, DOI 10.1007/s00018-007-7045-7Li YW, 2007, J BIOL CHEM, V282, P21542, DOI 10.1074/jbc.M701978200Ding QQ, 2007, CANCER RES, V67, P4564, DOI 10.1158/0008-5472.CAN-06-1788Kunnimalaiyaan M, 2007, MOL CANCER THER, V6, P1151, DOI 10.1158/1535-7163.MCT-06-0665Soto-Cerrato V, 2007, MOL CANCER THER, V6, P362, DOI 10.1158/1535-7163.MCT-06-0266Cao Q, 2006, CELL RES, V16, P671, DOI 10.1038/sj.cr.7310078Yang CH, 2006, PRECIS AGRIC, V7, P33, DOI 10.1007/s11119-005-6788-0Crew KD, 2006, WORLD J GASTROENTERO, V12, P354Mai W, 2007, ONCOLOGY-BASEL, V71, P297, DOI 10.1159/000106429Tan J, 2005, CANCER RES, V65, P9012, DOI 10.1158/0008-5472.CAN-05-1226Shakoori A, 2005, BIOCHEM BIOPH RES CO, V334, P1365, DOI 10.1016/j.bbrc.2005.07.041Farago M, 2005, CANCER RES, V65, P5792Ghosh JC, 2005, CLIN CANCER RES, V11, P4580Liao XB, 2003, MOL CANCER THER, V2, P1215Lee HS, 2003, J PATHOL, V200, P39, DOI 10.1002/path.1288Doble BW, 2003, J CELL SCI, V116, P1175, DOI 10.1242/jcs.00384Gotoh J, 2003, CARCINOGENESIS, V24, P435Goto H, 2002, ORAL ONCOL, V38, P549Lee HS, 2001, INT J CANCER, V91, P619D`Amico M, 2000, J BIOL CHEM, V275, P32649, DOI 10.1074/jbc.M000643200Endoh Y, 2000, J PATHOL, V191, P257Wu LY, 1998, J NATL MED ASSOC, V90, P410WOODGETT JR, 1984, BIOCHIM BIOPHYS ACTA, V788, P339