Hepato Gastroenterol
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Hepato Gastroenterol · Mar 2003
Case ReportsLaparoscopic splenectomy for variceal bleeding with non-cirrhotic portal vein thrombosis: a case report.
A 57-year-old man was referred to our hospital for treatment of refractory gastric bleeding from gastric varices secondary to portal vein thrombosis. The patient's liver function tests and coagulation profile were normal. The venous phase of the superior mesenteric arteriogram, on the other hand, showed superior mesenteric vein-portal vein occlusion with surrounding hepatopetal variceal collaterals. ⋯ Extrahepatic portal vein thrombosis is the leading cause of variceal hemorrhage in patients with healthy livers. There is a consensus in the literature that splenectomy alone is of minimal value in preventing variceal bleeding in portal vein thrombosis. Splenectomy is, however, indicated in cases in which the patient has hepatopetal collaterals from the mesenteric vein system and whose hemorrhagic gastric varices are related to splenic vein thrombosis as in our case.
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Hepato Gastroenterol · Jan 2003
Case ReportsPylorus-preserving pancreaticoduodenectomy without homologous blood transfusion in a Jehovah's witness with pancreatic cancer: report of a case.
A case of successfully treated pancreatic cancer without homologous blood transfusion in a Jehovah's witness is reported. The patient was a 60-year-old Japanese man and he was diagnosed with pancreatic cancer. Based on the patient's informed consent, human recombinant erythropoietin (12000 IU/day), saccharated ferric oxide (60 mg/day), and 25% human serum albumin (100 mL/day) were administrated for 7 consecutive days prior to the operation. ⋯ He had an uneventful postoperative course, and was discharged on the 31st postoperative day. Although there have been numerous reports on surgery without homologous blood transfusion in Jehovah's witnesses, many of the cases of major surgery have involved cardiovascular procedures. However, major digestive surgery may be feasible in more Jehovah's witnesses if adequate alternative treatments and strict nutritional management are carefully implemented, as in our case.
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Hepato Gastroenterol · Jan 2003
Preoperative estimation of risk in hepatectomy using technetium-99m-galactosyl human serum albumin receptor amount by nonlinear 3-compartment model.
Recently, we developed the method for measurement of the technetium-99m-diethylenetriamine-pentaacetic acid-galactosyl human serum albumin (Tc-GSA) receptor amount (R0) using a nonlinear 3-compartment model. We examined the usefulness of R0 for preoperative estimation of risk in hepatectomy. ⋯ From these results, it can be seen that R0 of remnant liver is a useful parameter to decide indication of hepatectomy and predict postoperative complications.
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Hepato Gastroenterol · Jan 2003
Thrombopoietin levels and peripheral platelet counts following living related donor liver transplantation.
Thrombopoietin is the primary hematopoietic growth factor. Thrombopoietin deficiency may cause thrombocytopenia in advanced liver disease. The aim of our study was to investigate the relevance of thrombopoietin levels to peripheral platelet counts in patients with liver disease who underwent LRDLT (living related donor liver transplantation). ⋯ These findings suggested inadequate thrombopoietin production in advanced stage liver disease which caused thrombocytopenia. Improvement of thrombopoietin production in graft liver function may contribute to increase of peripheral platelet counts.
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Hepato Gastroenterol · Jan 2003
The changes of hepatic sinusoidal microcirculation and effects of nitric oxide synthase inhibitor during sepsis.
Sepsis may cause changes in liver blood flow, which may result in liver injury. Microcirculation in organ undergoes moderate alteration during sepsis or septic shock. The changes in hepatic microcirculation corresponding to liver functions and the effects of nitric oxide synthase inhibitor on the liver during sepsis were studied. ⋯ Our conclusions are that hepatic microcirculation initially increased then decreased and the liver functions deteriorated gradually after sepsis was induced. These changes were aggravated when the nitric oxide synthesis was inhibited.