Advances in therapeutic options for portal hypertension

Abstract

Portal hypertension represents one of the major clinical consequences of chronic liver disease, having a deep impact on patients’ prognosis and survival. Its pathophysiology defines a pathological increase in the intrahepatic vascular resistance as the primary factor in its development, being subsequently aggravated by a paradoxical increase in portal blood inflow. Although extensive preclinical and clinical research in the field has been developed in recent decades, no effective treatment targeting its primary mechanism has been defined. The present review critically summarizes the current knowledge in portal hypertension therapeutics, focusing on those strategies driven by the disease pathophysiology and underlying cellular mechanisms.

Portal Hemodynamics In Hyponatremic Egyptian Cirrhotic Patients

“…Also, the difference in MELD score, MELD-Na score, portal vein CI and Hepatic A. RI between patients with complication (SBP, HRS and bleeding OV) and those without was statistically insignificant in both groups. This could provide new insights on unusual targetable molecular pathways and metabolites that may affect the outcome in such patients [20]. In addition, our study revealed high statistically significant difference in MELD score, MELD-Na score between patients complicated with hepatic encephalopathy and those without in both groups and high statistically significant difference in PV congestive index and hepatic A RI in hyponatremic group only.…”

Changes in Hepatic Venous Pressure Gradient Predict Hepatic Decompensation in Patients Who Achieved Sustained Virologic Response to Interferon‐Free Therapy

“…Because resources are limited, only a minority of the emerging treatment approaches are tested in phase 3 clinical trials assessing direct endpoints, which greatly inhibits scientific progress in the field of PH. (21) Thus, we aimed to assess the impact of pretreatment HVPG, changes in HVPG, and posttreatment values on the development of hepatic decompensation in patients with PH who achieved SVR to IFN-free therapy. Moreover, we investigated the use of transient elastography (TE) and von Willebrand factor (VWF) for monitoring the evolution of PH and the impact of HCV cure on markers of bacterial translocation and inflammation.…”

“…This is particularly problematic in patients with cACLD, in whom the incidence of hepatic decompensation is comparatively low, resulting in tremendously larger trials and longer study periods, if clinical endpoints (e.g., hepatic decompensation) are assessed. Because resources are limited, only a minority of the emerging treatment approaches are tested in phase 3 clinical trials assessing direct endpoints, which greatly inhibits scientific progress in the field of PH …”

Emricasan Ameliorates Portal Hypertension and Liver Fibrosis in Cirrhotic Rats Through a Hepatocyte‐Mediated Paracrine Mechanism

“…Improvement of ACLD might be accomplished with the cessation of injury or by drug‐induced amelioration of hepatic cells . Unfortunately, current options to improve ACLD and its main clinical complications are limited, and although statins have shown beneficial effects on portal hypertension and survival, the risk reduction afforded by these and other agents is limited, indicating that new therapeutic strategies are warranted.…”