Inflammatory and cardiovascular diseases biomarkers in chronic hepatitis C virus infection: A review

Abstract

Hepatitis C virus (HCV) infects 180 million people worldwide and over 4 million people in the United States. HCV infection is a major cause of chronic liver disease and is recognized as a risk factor for clinical cardiovascular disease (CVD). Many studies have shown increased prevalence of cardiac and inflammatory biomarkers in patients with chronic HCV infection (CHC), and though these markers may be used to risk stratify people for cardiac disease in the general population their role in the HCV population is unknown. Patients with CHC have elevated cardiac and inflammatory biomarkers compared to noninfected controls which may play a role in CVD risk stratification. We undertook a systematic review of inflammatory and cardiac biomarkers in people with HCV infection with a focus on the effect of CHC on serum levels of these markers and their utility as predictors of CVD in this population. Medline, EMBASE, and Cochrane databases were searched for relevant articles until June 2019. A total of 2430 results were reviewed with 115 studies included. Our review revealed that HCV infection significantly alters serum levels of markers of inflammation, endothelial function, and cardiac dysfunction prior to HCV treatment, and some of which may change in response to HCV therapy. Current risk stratification tools for development of CVD in the general population may not account for the increased inflammatory markers that appear to be elevated among HCV‐infected patients contributing to increased CVD risk.

Rapid Decline of Serum Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) in Non-Cirrhotic Patients with Chronic Hepatitis C Infection Receiving Direct-Acting Antiviral Therapy

“…Interestingly, a negative association of CRP and PCSK9 existed in HCV-infected patients with cirrhosis before therapy and at 12 weeks posttreatment. CRP is produced by the liver as an acute-phase protein, and impaired IL-6 signaling, lower hepatocyte synthesis and increased inflammation may regulate CRP levels in HCV infection [ 50 ]. Inhibitory monoclonal PCSK9 antibodies did not reduce highly sensitive CRP levels in patients with an increased risk for cardiovascular diseases [ 51 ].…”

Impact of DAA Treatment on Cardiovascular Disease Risk in Chronic HCV Infection: An Update

“…Among various CVDs, HCV mainly promotes atherosclerosis. Of the various proposed underlying pathophysiological mechanisms, the crucial one is that HCV infection-induced hepatic and systemic inflammation ( Zampino et al, 2013 ) results in increased levels of pro-atherogenic chemokines and cytokines (interleukin (IL)-6, tumor necrosis factor (TNF)-α, C-reactive protein (CRP) and fibrinogen) and an imbalance between the anti- and pro-inflammatory cytokines (TNF-α/IL-10, IL6/IL-10) ( Babiker et al, 2020 ; Zampino et al, 2013 ). In addition, a second pathophysiological mechanism is direct invasion of the arterial wall.…”

The Safety of The Directly Acting Antiviral Treatment For Hepatitis C Virus According To The Egyptian National Program Protocol In Patients With Midrange Ejection Fraction

“…Hepatitis C virus (HCV) is a single-stranded ribonucleic acid (RNA) virus. HCV has a worldwide prevalence of 2.5% and infects 180 million people worldwide [ 1 ]. HCV infection in Egyptian people has high health, economic, and social burden.…”

“…Chronic HCV infection has been linked to subclinical and clinical cardiovascular diseases (CVD). The proposed mechanisms include chronic inflammation and immune activation driven by HCV infection as well as direct endothelial invasion and dysfunction, but no mechanism could be confirmed till now [ 1 4 ].…”

“…Chronic HCV infection interferes with glucose and lipid metabolism, resulting in insulin resistance and diabetes mellitus (DM). The potential mechanism is to interfere with insulin signaling pathways related to increased tumor necrosis factor (TNF-α) and higher HCV viral load [ 1 ]. Also, HCV replication within liver cells may impact insulin and lipid metabolism.…”