Abstract

BackgroundApelin is the endogenous ligand of the angiotensin-like receptor. The expression of apelin–APJ (apelin receptor) signaling is associated with the development of portal hypertension (PH) and contributes toward the formation of Porto systemic collaterals and splanchnic neovascularization in PH.AimsWe aimed to study the relationship between apelin and portal hemodynamics in cirrhotic patients.Patients and methodsThus study included 60 cirrhotic patients from Menoufia University Hospitals (Egypt) and 20 healthy volunteers as a control group. Participants underwent a physical examination and laboratory investigations [complete blood count, urea, creatinine, alanine transaminase, aspartate transaminase (AST), serum albumin, bilirubin, international normalized ratio, hepatitis C virus antibody, hepatitis B virus antigen, hepatitis C virus PCR, alpha feto protein (AFP), and serum level of apelin]. Abdominal ultrasonographic studies of portal vein diameter, splenic size, and portal hemodynamics were carried out for all participants. Child–Pugh score, model for end-stage liver disease score, and AST/platelet (PLT) index were calculated for all participants.ResultsSerum apelin was highly significantly elevated in cirrhotics than in controls, with a P value of 0.001. Serum apelin was significantly correlated to some laboratory parameters in cirrhotics such as PLT count, alanine transaminase, AST, γ-glutamyl transferase, and bilirubin, with P value less than 0.05. There was a positive correlation between serum apelin level and the degree of liver fibrosis estimated by the AST/PLT index. Serum apelin was significantly correlated to portal vein diameter and portal flow velocity, with a P value less than 0.05, and highly significantly correlated to splenomegaly, with a P value of 0.001. The optimal cut-off point of serum apelin for the prediction of PH in cirrhotics is 2550 ng/dl, with a sensitivity of 89%, a specificity of 65%, and an accuracy of 81%.ConclusionSerum apelin is elevated in patients with cirrhosis and PH, and a positive correlation is found between serum apelin and the degree of hepatic fibrosis. Measurement of serum apelin represents a rapid, noninvasive method for the prediction of PH in cirrhotics and can assess the degree of hepatic fibrosis.

Highlights

  • Portal hypertension (PH) is a hemodynamic outcome of liver cirrhosis in western countries

  • This study aimed to determine whether there is a relation between serum apelin and portal hemodynamics in liver cirrhosis

  • Tiani et al [5] reported that the administration of apelin receptor blocker (F13A) effectively decreased splanchnic neovascularization and the formation of Porto systemic collateral vessels as well as the expression of proangiogenic factors vascular endothelial growth factor, PLT-derived growth factor, and angiopoietin-2. These findings strongly suggested a possibility of the apelin antagonist (F13A) as a new therapeutic target in terms of both fibrosis and portal hypertension (PH)

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Summary

Introduction

Portal hypertension (PH) is a hemodynamic outcome of liver cirrhosis in western countries. It causes severe alterations responsible for the onset of complications of cirrhosis. Apelin is a peptide isolated from bovine stomach extracts acts as an endogenous ligand for previously orphaned G protein-coupled receptors (APJ receptor). Apelin is the endogenous ligand of the angiotensin-like receptor. The expression of apelin–APJ (apelin receptor) signaling is associated with the development of portal hypertension (PH) and contributes toward the formation of Porto systemic collaterals and splanchnic neovascularization in PH. Aims We aimed to study the relationship between apelin and portal hemodynamics in cirrhotic patients. Child–Pugh score, model for end-stage liver disease score, and AST/platelet (PLT) index were calculated for all participants

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