A Case of Portal Vein Thrombosis by Protein C and S Deficiency Completely Recanalized by Anticoagulation Therapy / 전남의대학술지

Portal vein thrombosis (PVT) is a rare form of venous thrombosis that affects the hepatic portal vein flow, which can lead to portal hypertension. Treatment of PVT includes anticoagulants, thrombolysis, insertion of shunts, bypass surgery, and liver transplantation. Single anticoagulation therapy is not regarded as a curative treatment but can be associated with a reduction in new thrombotic episodes. We experienced a case of acute total occlusion of PVT provoked by protein C and S deficiency syndrome. PVT was completely recanalized with oral anticoagulant therapy following low molecular weight heparin therapy.

A Case of Portal Vein Thrombosis by Protein C and S Deficiency Completely Recanalized by Anticoagulation Therapy / 전남의대학술지

Portal vein thrombosis (PVT) is a rare form of venous thrombosis that affects the hepatic portal vein flow, which can lead to portal hypertension. Treatment of PVT includes anticoagulants, thrombolysis, insertion of shunts, bypass surgery, and liver transplantation. Single anticoagulation therapy is not regarded as a curative treatment but can be associated with a reduction in new thrombotic episodes. We experienced a case of acute total occlusion of PVT provoked by protein C and S deficiency syndrome. PVT was completely recanalized with oral anticoagulant therapy following low molecular weight heparin therapy.

Analysis of portal vein in the colorectal cancer with metastic liver cancer / 中国基层医药

Objective To investigate the characteristic of portal vein with liver mestastic cancer.Methods The clinical data of the diameter,the flow-rate and incidence of tumor thrombus of portal vein in 250 patients with metastasis liver cancer were retrospectively analyzed.Results The diameter of portal vein was (10.4?1.34)mm;The flow-rate of it was (19.7?5.2)cm/s;The incidence of tumor thrombi in metastic liver cancer was 0%,and compared with the incidence of hepatocellular carcinoma,the difference was significant(P

Effects of protein kinase C modulation on hepatic hemodynamics and glucoregulation

This study evaluated the effects of PKC activation using phorbol 12-myristate 13-acetate (PMA) and PKC inhibition using the isoquinoline sulfomide derivative H-7 on hemodynamics and glucoregulation in the isolated perfused rat liver. Livers were isolated from fed male Holtzman rats and perfused with Krebs Ringer bicarbonate solution under a constant flow of 50 ml/min at 35degreeC. Portal vein pressure, glucose and lactate concentrations in the medium and oxygen consumption rates were continuously monitored by a Grass polygraph, YSI glucose and lactate monitors, and a YSI oxygen monitor, respectively. PMA at concentration of 2 to 200 nM increased the portal vein pressure, glucose and lactate production, but decreased oxygen consumption rate in a dose-dependent fashion. H-7 (200 micrometer) attenuated PMA (50 nM)-induced vasoconstriction (15.1+/-1.36 vs 10.56+/-1.17 mmHg), glucose production rate (91.3+/-6.15 vs 71.8+/-2.50 micromoles/g/hr), lactate production rate (72.4+/-6.82 vs 53.6+/-4.82 micromoles/g/hr) and oxygen consumption rate (33.7+/-1.41 vs 27.9+/-1.75 microliter/g/min). The effects of PMA were blocked either by addition of verapamil (9 micrometer) or perfusion with Ca2+-free KRB. These results suggest that the hemodynamic and glucoregulatory changes in the perfused rat liver are mediated by protein kinase C activation and require Ca2+ influx from the extracellular fluid.