Pharmacologic prevention of variceal bleeding and rebleeding.

Baiges, Anna; Hernández-Gea, Virginia; Bosch, Jaime (2018). Pharmacologic prevention of variceal bleeding and rebleeding. Hepatology international, 12(Suppl 1), pp. 68-80. Springer 10.1007/s12072-017-9833-y

[img] Text
s12072-017-9833-y.pdf - Published Version
Restricted to registered users only
Available under License Publisher holds Copyright.

Download (594kB) | Request a copy

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.

Item Type:

Journal Article (Review Article)

Division/Institute:

04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Hepatology
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Hepatologie
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR) > DBMR Forschung Mu35 > Forschungsgruppe Hepatologie

UniBE Contributor:

Bosch, Jaime

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1936-0541

Publisher:

Springer

Language:

English

Submitter:

Thi Thao Anh Pham

Date Deposited:

15 Feb 2018 12:44

Last Modified:

31 Oct 2019 19:34

Publisher DOI:

10.1007/s12072-017-9833-y

PubMed ID:

29210030

Uncontrolled Keywords:

Pharmacologic prevention Portal hypertension Variceal bleeding

BORIS DOI:

10.7892/boris.109617

URI:

https://boris.unibe.ch/id/eprint/109617

Actions (login required)

Edit item Edit item
Provide Feedback