Abstract
ObjectiveThe study aimed to evaluate the prevalence and predictor factors for compensated advanced chronic liver disease (c-ACLD) in patients with hepatitis Delta virus (HDV) infection.MethodsThis cross-sectional study included consecutive HDV-infected patients defined by positive anti-HDV. Patients with hepatitis C coinfection, liver transplantation or presence of conditions that limit liver (LSM) or spleen stiffness measurement (SSM) were excluded. Blood tests, abdominal ultrasound, SSM and LSM by transient elastography (FibroScan®) were performed at the same day. Alcohol consumption was quantified using the AUDIT score and c-ACLD was defined by LSM ≥ 15 kPa performed by an experimented operator blinded for clinical and laboratory data.Results101 patients were eligible and few patients were excluded due to negative anti-HDV (n = 7), hepatitis C coinfection (n = 2), liver transplantation (n = 10) and limitation for LSM or SSM (n = 5). Therefore, 77 patients [61% male, age = 43 (IQR,36–52) years] were included. The prevalence of c-ACLD was 57% (n = 44/77). Patients with c-ACLD had a higher rate of detectable HBV viral load (p = 0.039), higher levels of transaminases, GGT, alkaline phosphatases, total bilirubin and INR (p<0.001 for all), as well as lower platelet count and albumin levels (p>0.001 for both) compared to those without c-ACLD. Patients with c-ACLD had higher SSM [65.2 (IQR,33.8–75.0) vs 21.8 (16.5–32.0) kPa; p<0.001] and higher splenic volume [475 (IQR,311–746) vs 154 (112–283) cm3; p<0.001] compared to those without. Detectable HBV viral load (>10 UI/ml), alkaline phosphatase (per IU/L) and GGT levels (per IU/L) were independently associated with c-ACLD in all multivariate models. Splenic volume [per cm3,OR = 1.01 (95%CI,1.01–1.02);p = 0.002], SSM [per kPa, OR = 1.04 (1.01–1.07);p = 0.012] and splenomegaly [yes vs no,OR = 28.45 (4.42–182.95);p<0.001] were independently associated with c-ACLD.ConclusionsThe prevalence of c-ACLD was high in patients with chronic HDV infection in western Amazon basin. HBV viral load, liver enzymes and splenic features can be used to predict severe liver disease in HDV-infected patients.
Highlights
Patients with compensated advanced chronic liver disease (c-ACLD) had a higher rate of detectable hepatitis B viral (HBV) viral load (p = 0.039), higher levels of transaminases, GGT, alkaline phosphatases, total bilirubin and international normalized ratio (INR) (p0.001 for both) compared to those without c-ACLD
Hepatitis Delta virus (HDV) requires the hepatitis B surface antigen (HBsAg) for replication and this coinfection has been associated with severe liver disease [1]
HDV has been associated with an accelerated course of fibrosis progression and increased risk of hepatocellular compared to other types of viral hepatitis [5]
Summary
Hepatitis Delta virus (HDV) requires the hepatitis B surface antigen (HBsAg) for replication and this coinfection has been associated with severe liver disease [1]. HDV infection is endemic in Mediterranean countries, the Middle East, Central Africa, and northern parts of South America, such as the western Amazon basin. Its incidence has been increasing in nothern and central Europe mainly due to immigration from endemic regions [3]. Studies have been showing that chronic HDV infection leads to more severe liver disease than chronic hepatitis B monoinfection [4]. HDV has been associated with an accelerated course of fibrosis progression and increased risk of hepatocellular compared to other types of viral hepatitis [5]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.