Ranković I, Milivojević V, Pavlović Marković A, Bezmarević M. Interplay between chronic hepatitis B and atherosclerosis: Innovative perspectives and theories. World J Gastroenterol 2022; 28(4): 497-499 [PMID: PMC8790556 DOI: 10.3748/wjg.v28.i4.497]
Corresponding Author of This Article
Mihailo Bezmarević, MD, MSc, Doctor, Senior Researcher, Surgical Oncologist, Department of Hepatobiliary and Pancreatic Surgery, Clinic for General Surgery, Military Medical Academy, University of Defense, Crnotravska 17, Belgrade 11000, Serbia. bezmarevicm@gmail.com
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Letter to the Editor
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jan 28, 2022; 28(4): 497-499 Published online Jan 28, 2022. doi: 10.3748/wjg.v28.i4.497
Interplay between chronic hepatitis B and atherosclerosis: Innovative perspectives and theories
Ivan Ranković, Vladimir Milivojević, Aleksandra Pavlović Marković, Mihailo Bezmarević
Ivan Ranković, Clinic for Gastroenterology and Hepatology, University Clinical Center of Serbia, Belgrade 11000, Serbia
Vladimir Milivojević, Aleksandra Pavlović Marković, Clinic for Gastroenterology and Hepatology, University Clinical Center of Serbia, School of Medicine, University of Belgrade, Belgrade 11000, Serbia
Mihailo Bezmarević, Department of Hepatobiliary and Pancreatic Surgery, Clinic for General Surgery, Military Medical Academy, University of Defense, Belgrade 11000, Serbia
Author contributions: Ranković I and Bezmarević M designed the research and analyzed the data; Ranković I and Milivojević V performed the research; Ranković I drafted the letter; Pavlović Marković A revised the letter.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Mihailo Bezmarević, MD, MSc, Doctor, Senior Researcher, Surgical Oncologist, Department of Hepatobiliary and Pancreatic Surgery, Clinic for General Surgery, Military Medical Academy, University of Defense, Crnotravska 17, Belgrade 11000, Serbia. bezmarevicm@gmail.com
Received: September 20, 2021 Peer-review started: September 20, 2021 First decision: November 7, 2021 Revised: November 17, 2021 Accepted: January 14, 2022 Article in press: January 14, 2022 Published online: January 28, 2022 Processing time: 123 Days and 21.8 Hours
Abstract
Elaboration of carotid atherosclerosis in the setting of hepatitis B virus (HBV) infection should emphasize the significance of extrahepatic manifestations of the infection pathogenesis. Diverse processes comprise the pathoevolution of HBV infection, rendering it a multi-systemic disease in its essence. Our work not only exemplified atherosclerosis as an often-underestimated contributor to the severity of HBV infection but has also highlighted the bidirectional relationship between the two. Therefore, it is suggested that HBV-induced inflammation is one of the root causes of atherosclerosis, which in turn has a consequent effect on the severity of the chronic infection disease state, creating a vicious cycle. Additionally, we coupled prior data with the current concepts of HBV infection to postulate intriguing perspectives and theories.
Core Tip: Hepatitis B virus (HBV) infection is a multifaceted disease, with significant cardiovascular morbidity. Our innovative approach to this pathophysiologic relationship harbors several key ideas. First, HBV infection may carry a specific atherosclerosis distribution pattern, with predilection for carotid arteries. Second, we propose wider use of more sensitive inflammatory markers, such as high-sensitivity C-reactive protein and homocysteine. Third, macrophage phenotype function should be investigated, utilizing its potential role as an atherosclerosis biomarker in HBV infection and therapeutic target. Last but not least, we reason that statins should be exploited more in current practice, due to their favorable pleotropic effects.
