Beta blockers in portal hypertension. Are they really a good option?

López-Méndez, Eric; Uribe, Misael

doi:10.1016/s1665-2681(19)32023-x

Cited by 10 publications

(6 citation statements)

References 37 publications

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“…Despite their proven clinical effectiveness, traditional NSBBs such as propranolol and nadolol are contraindicated or poorly tolerated in up to 15%-20% of patients and up to 60% of patients do not achieve any therapeutically useful fall in HVPG with these NSBBs[ 105 , 124 , 125 ]. NSBBs produce a number of cardiac and non-cardiac adverse effects, such as headaches, fatigue, asthma and shortness of breath, which led to the discontinuation of treatment in about 15% of the patients in clinical trials[ 126 , 127 ].…”

Section: Therapies Targeting Splanchnic Vasodilatationmentioning

confidence: 99%

Cirrhotic portal hypertension: From pathophysiology to novel therapeutics

Gunarathne¹,

Rajapaksha²,

Shackel³

et al. 2020

WJG

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Portal hypertension and bleeding from gastroesophageal varices is the major cause of morbidity and mortality in patients with cirrhosis. Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state. The latter is characterized by a high cardiac output, increased total blood volume and splanchnic vasodilatation, resulting in increased mesenteric blood flow. Pharmacological manipulation of cirrhotic portal hypertension targets both the splanchnic and hepatic vascular beds. Drugs such as angiotensin converting enzyme inhibitors and angiotensin II type receptor 1 blockers, which target the components of the classical renin angiotensin system (RAS), are expected to reduce intrahepatic vascular tone by reducing extracellular matrix deposition and vasoactivity of contractile cells and thereby improve portal hypertension. However, these drugs have been shown to produce significant off-target effects such as systemic hypotension and renal failure. Therefore, the current pharmacological mainstay in clinical practice to prevent variceal bleeding and improving patient survival by reducing portal pressure is non-selective -blockers (NSBBs). These NSBBs work by reducing cardiac output and splanchnic vasodilatation but most patients do not achieve an optimal therapeutic response and a significant proportion of patients are unable to tolerate these drugs. Although statins, used alone or in combination with NSBBs, have been shown to improve portal pressure and overall mortality in cirrhotic patients, further randomized clinical trials are warranted involving larger patient populations with clear clinical end points. On the other hand, recent findings from studies that have investigated the potential use of the blockers of the components of the alternate RAS provided compelling evidence that could lead to the development of drugs targeting the splanchnic vascular bed to inhibit splanchnic vasodilatation in portal hypertension. This review outlines the mechanisms related to the pathogenesis of portal hypertension and attempts to provide an update on currently available therapeutic approaches in the management of portal hypertension with special emphasis on how the alternate RAS could be manipulated in our search for development of safe, specific and effective novel therapies to treat portal hypertension in cirrhosis.

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Section: Therapies Targeting Splanchnic Vasodilatationmentioning

confidence: 99%

Cirrhotic portal hypertension: From pathophysiology to novel therapeutics

Gunarathne¹,

Rajapaksha²,

Shackel³

et al. 2020

WJG

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“…The patient was treated with propranolol—a non‐selective beta blocker to minimize the risk of bleeding from esophageal varices. Non‐selective beta blockers are commonly used to manage esophageal varices in patients with cirrhosis and act by (1) blocking β1 receptors and reducing the cardiac output and (2) by blocking β2 receptors, producing splanchnic vasoconstriction and reducing portal flow 10 . The Food and Drug Administration of the United State classified propranolol as category C because its potential benefits may outweigh the fetal risks of growth retardation, bradycardia, and neonatal hypoglycemia 11 …”

Section: Discussionmentioning

confidence: 99%

A case report of a pregnant woman with compensated liver cirrhosis and pancytopenia

S. S

Bako

Yaqoub

et al. 2023

Clinical Case Reports

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Liver cirrhosis may worsen during pregnancy resulting in adverse maternal and fetal outcomes. Proper antenatal evaluation, staging, and variceal screening will facilitate the management. Elective endoscopic variceal ligation (EVL) during the second trimester can prevent unexpected variceal bleeding. A multidisciplinary approach including the planning of delivery and shared decision-making is recommended for favorable pregnancy outcomes.

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“…Subgroup analysis of these two studies showed that users of CCB were 1.9‐fold (95% CI 1.44–2.62) more likely to develop GIB compared with users of beta‐blockers, while this association was nonsignificant in subgroups with unspecified comparators. Since, beta‐blockers can reduce cardiac output by blocking β1 receptors and induce splanchnic vasoconstriction by blocking β2 receptors, this may be a biologically plausible mechanism for the protective effects of GIB. Indeed, beta‐blockers have been shown to prevent variceal GIB .…”

Section: Discussionmentioning

confidence: 99%