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Pharmacologic prevention of variceal bleeding and rebleeding.
Hepatol Int. 2018 Feb; 12(Suppl 1):68-80.HI

Abstract

BACKGROUND

Variceal bleeding is a major complication of portal hypertension, which is associated with significant mortality. Moreover, patients surviving a variceal bleeding episode have very high risk of rebleeding, which is associated with mortality as high as that of the first bleed. Because of this, prevention of bleeding from gastroesophageal varices has been one of the main therapeutic goals since the advent of the first effective therapies for portal hypertension.

AIM

This review deals with the present day state-of-the-art pharmacological prevention of variceal bleeding in primary and secondary prophylaxis.

RESULTS

Pharmacological therapy aims to decrease portal pressure (PP) by acting on the pathophysiological mechanisms of portal hypertension such as increased hepatic vascular tone and splanchnic vasodilatation. Propranolol and nadolol block the beta-1 in the heart and the peripheral beta-2 adrenergic receptors. Beta-1 blockade of cardiac receptors reduces heart rate and cardiac output and subsequently decreases flow into splanchnic circulation. Beta-2 blockade leads to unopposed alpha-1 adrenergic activity that causes splanchnic vasoconstriction and reduction of portal inflow. Both effects contribute to reduction in PP. Carvedilol is more powerful in reducing hepatic venous pressure gradient (HVPG) than traditional nonselective beta-blockers (NSBBs) and achieves good hemodynamic response in nearly 75 % of cases. Simvastatin and atorvastatin improve endothelial dysfunction mainly by enhancing endothelial nitric oxide synthase (eNOS) expression and phosphorylation and NO production. In addition, statins deactivate hepatic stellate cells and ameliorate hepatic fibrogenesis. These effects cause a decrease in HVPG and improve liver microcirculation and hepatocyte perfusion in patients with cirrhosis. In addition, several promising drugs under development may change the management of portal hypertension in the coming years.

CONCLUSION

This review provides a background on the most important aspects of the treatment of portal hypertension in patients with compensated and decompensated liver cirrhosis. However, despite the great improvement in the prevention of variceal bleeding over the last years, further therapeutic options are needed.

Authors+Show Affiliations

Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS, University of Barcelona, C.Villarroel 170, 08036, Barcelona, Spain.Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS, University of Barcelona, C.Villarroel 170, 08036, Barcelona, Spain. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Barcelona, España.Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clínic-IDIBAPS, University of Barcelona, C.Villarroel 170, 08036, Barcelona, Spain. jbosch@clinic.cat. Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Instituto de Salud Carlos III, Barcelona, España. jbosch@clinic.cat. Swiss Liver Group, Inselspital, Bern University, Bern, Switzerland. jbosch@clinic.cat.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

29210030

Citation

Baiges, Anna, et al. "Pharmacologic Prevention of Variceal Bleeding and Rebleeding." Hepatology International, vol. 12, no. Suppl 1, 2018, pp. 68-80.
Baiges A, Hernández-Gea V, Bosch J. Pharmacologic prevention of variceal bleeding and rebleeding. Hepatol Int. 2018;12(Suppl 1):68-80.
Baiges, A., Hernández-Gea, V., & Bosch, J. (2018). Pharmacologic prevention of variceal bleeding and rebleeding. Hepatology International, 12(Suppl 1), 68-80. https://doi.org/10.1007/s12072-017-9833-y
Baiges A, Hernández-Gea V, Bosch J. Pharmacologic Prevention of Variceal Bleeding and Rebleeding. Hepatol Int. 2018;12(Suppl 1):68-80. PubMed PMID: 29210030.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pharmacologic prevention of variceal bleeding and rebleeding. AU - Baiges,Anna, AU - Hernández-Gea,Virginia, AU - Bosch,Jaime, Y1 - 2017/12/05/ PY - 2017/07/11/received PY - 2017/10/31/accepted PY - 2017/12/7/pubmed PY - 2018/9/18/medline PY - 2017/12/7/entrez KW - Pharmacologic prevention KW - Portal hypertension KW - Variceal bleeding SP - 68 EP - 80 JF - Hepatology international JO - Hepatol Int VL - 12 IS - Suppl 1 N2 - BACKGROUND: Variceal bleeding is a major complication of portal hypertension, which is associated with significant mortality. Moreover, patients surviving a variceal bleeding episode have very high risk of rebleeding, which is associated with mortality as high as that of the first bleed. Because of this, prevention of bleeding from gastroesophageal varices has been one of the main therapeutic goals since the advent of the first effective therapies for portal hypertension. AIM: This review deals with the present day state-of-the-art pharmacological prevention of variceal bleeding in primary and secondary prophylaxis. RESULTS: Pharmacological therapy aims to decrease portal pressure (PP) by acting on the pathophysiological mechanisms of portal hypertension such as increased hepatic vascular tone and splanchnic vasodilatation. Propranolol and nadolol block the beta-1 in the heart and the peripheral beta-2 adrenergic receptors. Beta-1 blockade of cardiac receptors reduces heart rate and cardiac output and subsequently decreases flow into splanchnic circulation. Beta-2 blockade leads to unopposed alpha-1 adrenergic activity that causes splanchnic vasoconstriction and reduction of portal inflow. Both effects contribute to reduction in PP. Carvedilol is more powerful in reducing hepatic venous pressure gradient (HVPG) than traditional nonselective beta-blockers (NSBBs) and achieves good hemodynamic response in nearly 75 % of cases. Simvastatin and atorvastatin improve endothelial dysfunction mainly by enhancing endothelial nitric oxide synthase (eNOS) expression and phosphorylation and NO production. In addition, statins deactivate hepatic stellate cells and ameliorate hepatic fibrogenesis. These effects cause a decrease in HVPG and improve liver microcirculation and hepatocyte perfusion in patients with cirrhosis. In addition, several promising drugs under development may change the management of portal hypertension in the coming years. CONCLUSION: This review provides a background on the most important aspects of the treatment of portal hypertension in patients with compensated and decompensated liver cirrhosis. However, despite the great improvement in the prevention of variceal bleeding over the last years, further therapeutic options are needed. SN - 1936-0541 UR - https://www.unboundmedicine.com/medline/citation/29210030/Pharmacologic_prevention_of_variceal_bleeding_and_rebleeding_ DB - PRIME DP - Unbound Medicine ER -