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Drug therapy for portal hypertension
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
A major inconvenience of non-selective β- blocker therapy is that over 60% of the patients do not obtain an adequate fall in portal pressure (a fall which adequately protects from rebleeding) despite adequate β-blockade.104 Haemodynamic studies have demonstrated that to significantly reduce the risk of rebleeding, hepatic venous pressure gradient (HVPG) must decrease by more than 20% from baseline or below 12mmHg.104 Thus, there is a wide individual and clinically unpredictable variation in the reduction of portal pressure achieved with β-blockers. This makes it advisable to measure HVPG before and 1–3 months after achieving the final dose of propranolol or nadolol.
Diagnosis and Treatment of Variceal Hemorrhage Due to Cirrhosis
Published in Stephen M. Cohn, Matthew O. Dolich, Kenji Inaba, Acute Care Surgery and Trauma, 2016
Robert M. Esterl, Aaron Lewis, Juan Marcano, Abdul Alarhayem, Gregory A. Abrahamian, K. Vincent Speeg
The HVPG is the preferred method to assess portal venous pressure and the most reliable predictor of variceal development [1]. This technique involves advancing a balloon catheter into the hepatic vein to measure the wedge hepatic vein pressure (WHVP) (balloon inflated) and the free hepatic vein pressure (FHVP) (balloon deflated). The HVPG is WHVP–FHVP. Normal HVPG is 3–5 mmHg, and in PH, the HVPG is >12 mmHg. The HVPG is elevated in sinusoidal causes of PH, but is normal in presinusoidal causes of PH [1].
Peripheral versus central venous blood sampling does not influence the assessment of platelet activation in cirrhosis
Published in Platelets, 2022
Ksenia Brusilovskaya, Benedikt Simbrunner, Silvia Lee, Beate Eichelberger, David Bauer, Kerstin Zinober, Philipp Schwabl, Mattias Mandorfer, Simon Panzer, Thomas Reiberger, Thomas Gremmel
Measurement of the hepatic venous pressure gradient (HVPG) is the gold-standard technique to determine portal venous pressure and the severity of portal hypertension in patients with liver cirrhosis [22]. During HVPG measurement or transjugular intrahepatic portosystemic stent shunt (TIPS) placement [22,23], central venous blood samples can easily be collected in order to avoid the need for blood sampling from the cubital vein [24]. However, little is known about the effects of central vs. peripheral blood sampling on platelet activation in cirrhosis. One may speculate that differences in shear stress, which may be greater in peripheral blood withdrawal [18,25,26], on the one hand, and platelet activation due to HVPG measurement or TIPS placement, which may be more present in the central veins, on the other hand, could influence the results obtained by flow cytometry [26,27]. Finally, local platelet activation in the portal and hepatic veins in cirrhosis might be differently reflected in central and peripheral venous blood samples. In order to investigate if central and peripheral venous blood sampling can be used interchangeably for the assessment of platelet activation in ACLD, we compared platelet activation as assessed by whole blood flow cytometry between central and peripheral venous blood samples from patients with cirrhosis.
Hepatic blood volume is decreased in patients with cirrhosis and does not decrease further after a meal like in healthy persons
Published in Scandinavian Journal of Gastroenterology, 2021
One of the limitations of the study is that the hepatic venous pressure gradient was not measured during the second PET study because the subjects were placed in the PET/CT-camera. Reliable postprandial measurements of HVPG could not be obtained because the subject had to be moved out of the scanner which interfered with the measurements and sometimes caused displacement of the hepatic venous catheter into the vena cava. A postprandial increase in HVPG of up to 33% and a decrease in hepatic vascular resistance of 31% in patients with cirrhosis has been demonstrated by others [9]. The present results are in accordance with those observations since an increased blood flow would increase the vascular pressure. A compensatory decrease in vascular resistance would allow blood to be mobilized from the liver and seek to counteract the increased pressure. This is further supported by the vascular resistance across the liver primarily being post-sinusoidal [17]. The present findings in conjunction with other studies could thus indicate that normal hemodynamic changes caused by a meal could induce a risk for patients with cirrhosis and portal hypertension as the liver’s ability to adjust is ameliorated and the meal itself may increase the portal pressure. This could potentially increase the risk of gastric and esophageal varices and thus bleeding.
Review of galectin-3 inhibitors in the treatment of nonalcoholic steatohepatitis
Published in Expert Review of Clinical Pharmacology, 2021
Atef Al Attar, Ani Antaramian, Mazen Noureddin
These phase I results were encouraging and prompted for a phase IIb trial to test GR-MD-02 (Belapectin) safety and efficacy in patients with NASH cirrhosis and portal hypertension (hepatic venous pressure gradient [HVPG] ≥6 mmHg). In a double-blind manner, patients received biweekly infusions of GR-MD-02 2 mg/kg (n = 54), 8 mg/kg (n = 54), or placebo (n = 54) for 52 weeks. The primary endpoint was a change in HVPG at the end of the 52-week period and the secondary endpoints were changes in liver histology and development of liver-related outcomes. In all treatment groups, there were neither significant HVPG changes nor were there any effects on fibrosis, NAFLD activity score, or liver-related outcomes. A sub-analysis revealed that in a separate group of patients without esophageal varices, 2 mg/kg of GR-MD-02 reduced HVPG and prevented the development of new varices [51]. Overall, although the primary endpoint was not significant, the drug and dosage were well-tolerated and produced no safety concerns.