View clinical trials related to Portal Hypertension.
Filter by:The purpose of the present clinical trial is to study the effect of somatostatin in the regulation of velocity and blood flow of the hepatic circulation in patients undergoing liver resection. The patients will be randomized in two groups: the study group will receive somatostatin and the control group will receive the placebo. In both groups, patients will undergo hepatectomy and directly postoperatively they will receive either somatostatin or placebo, depending on their randomization. The primary endpoint will be the increase or decrease of the velocity and the flow of the hepatic circulation estimated by ultrasonography compared to the same parameters when measured preoperatively.
Portal hypertension is a common complication of chronic liver diseases and is responsible for most clinical consequences of cirrhosis. measurement of the hepatic venous pressure gradient(HVPG) is the gold standard for evaluating the presence and severity of portal hypertension, this technique is considered invasive and is not routinely performed in all centers. Wisteria floribunda agglutinin-positive human Mac-2 binding protein (WFA+-M2BP) is a secreted N-glycoprotein, which has been reported as a novel marker in assessing liver fibrosis.However, the correlation of WFA+-M2BP with HVPG is unclear.The aim of this study was to explore the relationship between WFA+-M2BP and HVPG.
Terlipressin is the mainstay drug for the treatment of acute variceal bleeding in liver cirrhosis. According to the drug instructions, intravenous bolus infusion is the standard approach of terlipressin. It remains unclear about whether or not continuous infusion of terlipressin should be considered.
To prospectively evaluate the efficacy of real-time 3D CT-image guidance and CO2 portography during transjugular intrahepatic portosystemic shunt (TIPS) creation.
The purpose of this study is to determine whether simvastatin is effective in the prevention of progression of porta hypertension in compensated cirrhosis patients.
In the genesis and maintenance of PH associated with liver cirrhosis are two mechanisms that act synergistically. The first is an increase in hepatic vascular resistance, due in part to the disruption of liver structure inherent cirrhosis, and increased hepatic vascular tone is caused by the contraction of perivascular smooth muscle cells, myofibroblasts and hepatic stellate cells, which represents about 30% of global intrahepatic resistance and is believed to be due to the production Defective nitric oxide (NO). The second mechanism, which maintains and exacerbates HTP, is an increase of splanchnic blood flow caused by increased NO and other vasodilators at this level In this regard, we believe that in patients with compensated liver cirrhosis, with portal pressure gradient> 10 mmHg, both acute responders betablockers test as non-responders, the association of antifibrotic drugs and / or vasodilators, chronic liver selective May be beneficial in the control of portal hypertension