β-blockers in advanced cirrhosis: More friend than enemy

Abstract

Nonselective beta-adrenergic blocker (NSBB) therapy for the prevention of initial and recurrent gastrointestinal bleeding in cirrhotic patients with gastroesophageal varices has been used for the past four decades. NSBB therapy is considered the cornerstone of treatment for varices, and has become the standard of care. However, a 2010 study from the group that pioneered β-blocker therapy suggested a detrimental effect of NSBBs in decompensated cirrhosis, especially in patients with refractory ascites. Since then, numerous additional studies have incompletely resolved whether NSBBs are deleterious, although more recent evidence weighs against a harmful effect. The possibility of a “therapeutic window” has also been raised. We aimed to review the literature to analyze the pros and cons of using NSBBs in patients with cirrhosis, not only with respect to bleeding or mortality but also to other potential benefits and risks. β-blockers are highly effective in preventing first bleeding and recurrent bleeding. Furthermore, NSBBs improve congestion/ischemia of the gut mucosa, decrease intestinal permeability, and therefore indirectly alleviate systemic inflammation. β-blockers shorten the electrocardiographic prolonged QTc interval and may also decrease the incidence of hepatocellular carcinoma. On the other hand, the possibility of deleterious effects in cirrhosis has not been completely eliminated. NSBBs may be associated with an increased risk of portal vein thrombosis, although this could be correlational artifact. Overall, we conclude that β-blockers in cirrhosis are much more of a friend than enemy.

Humoral Immunogenicity to SARS-CoV-2 Vaccination in Liver Transplant Recipients: A Systematic Review and Meta-Analysis

“…Nevertheless, notably, OLT patients showed significantly lower immunogenicity than patients with cirrhosis (OR, 0.54; 95% CI, 0.47-0.62). This indicates that the use of immunosuppressive agents in the presence of other associated comorbidities including renal insufficiency (either primary or secondary to underlying liver disease) [37][38][39][40][41], should offset the benefit of OLT, that is, restored hepatic functional reserve and normalised portal pressure in achieving a humoral response to the SARS-CoV-2 vaccination.…”

Real‐world clinical features, health‐care utilization, and economic burden in decompensated cirrhosis patients: A national database

“…Liver cirrhosis (LC), the final stage of chronic liver diseases with progressive liver fibrosis, is known to originate from various etiologies, including chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection, alcoholic liver disease, non‐alcoholic fatty liver disease (NAFLD), autoimmune liver disease, and metabolism‐related genetic disorders 1,2 . Disease progression to LC presents a serious public health burden on the health‐care system, despite considerable advances in therapy and care 3–5 . First, LC itself could substantially increase the risk of morbidity and mortality 1,6 .…”

“…1,2 Disease progression to LC presents a serious public health burden on the health-care system, despite considerable advances in therapy and care. [3][4][5] First, LC itself could substantially increase the risk of morbidity and mortality. 1,6 Second, compared with patients presenting other chronic diseases such as congestive heart failure and chronic obstructive pulmonary disease, those with LC tend to undergo a greater number of hospitalizations, longer lengths of stay (LOSs) at hospitals, more readmissions, and poorer outcomes.…”

Current knowledge about biomarkers of acute kidney injury in liver cirrhosis

“…This induces the upregulation of systemic inflammatory mediators, leading to compromised extrahepatic organ perfusion, including the kidney (28)(29)(30)(31)(32). In patients with bacterial translocation, pathogen-associated molecular patterns, such as endotoxins and bacterial DNA, activates monocytes, which leads to the release of pro-inflammatory cytokines such as tumor necrosis factor-alpha, interleukin 6, and interleukin 1 beta (33,34).…”