Managing portal hypertension in patients with liver cirrhosis

Abstract

Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.

Keywords: chronic liver disease; liver cirrhosis; portal hypertension.

Figure 1.. Two main pathways in the development of liver disease.

A. The liver (L) is primarily affected (mainly by chronic infection with hepatotropic viruses). This leads to liver cirrhosis and portal hypertension causing leakiness of the intestine (I) and dysbiosis, affecting the brain ( B), and altering the splanchnic and systemic circulation, including the heart (H) and the kidneys (K). Prevention and therapy is interruption and/or suppression of viremia. B. Increasingly, nutrition has become the main culprit in liver disease. Here, inflammatory and metabolic stimuli from the gut affect the liver, visceral fat (VF), and cardiovascular system, including the heart and the kidneys, but also, concomitantly and early on in the process, the brain, which may support a vicious cycle of craving more food and liquids. Prevention and therapy is modification of food and liquid intake. Only in the later stages of liver disease do the complications of liver cirrhosis and portal hypertension determine pathogenesis, diagnosis, and therapy similar to A).

Figure 2.. Stages of chronic liver disease and portal hypertension.

The figure depicts the diagnostic and therapeutic procedures during the pathogenesis and aggravation of portal hypertension for patients with suspected fibrosis/cirrhosis of the liver ( A), compensated cirrhosis ( B), and decompensated cirrhosis ( C). Asc, ascites; EV, esophageal varices; FXR, farnesoid X receptor; HCC, hepatocellular carcinoma; HVPG, hepatic venous pressure gradient; IB, intestinal barrier; IH, intrahepatic; IHR, intrahepatic resistance; M, microbiome; MRI, magnet resonance imaging; NSBB, non-selective beta-blocker; SVB, splanchnic vascular bed; US, ultrasound.