tetano
Editor, Senior Moderator
Genes Dis
. 2020 Nov 18.
doi: 10.1016/j.gendis.2020.11.005. Online ahead of print.
Patients with SARS-CoV-2 and HBV co-infection are at risk of greater liver injury
Yong Lin[SUP] 1 [/SUP], Jun Yuan[SUP] 2 [/SUP], Quanxin Long[SUP] 1 [/SUP], Jieli Hu[SUP] 1 [/SUP], Haijun Deng[SUP] 1 [/SUP], Zhenyu Zhao[SUP] 1 [/SUP], Juan Chen[SUP] 1 [/SUP], Mengji Lu[SUP] 3 [/SUP], Ailong Huang[SUP] 1 [/SUP]
Affiliations
Abstract
To date, it remains unclear if severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) co-infection exacerbates liver injury in patients with chronic hepatitis B virus (HBV) infection. In this study, we present a retrospective study of 133 hospitalized confirmed mild coronavirus disease 2019 (COVID-19) cases, including 116 patients with COVID-19 with negative serum hepatitis B antigen and 17 HBV inactive carriers with COVID-19. We found that there were no significant differences for the discharge rate or duration of hospitalization between the two groups. However, inactive HBV carriers with SARS-CoV-2 co-infection are at a higher risk of abnormal liver function tests. The enhanced liver injury induced by SARS-CoV-2 and HBV co-infection was identified as the hepatocyte type rather than the cholangiocyte type. Moreover, the inflammatory response, including abnormal lactate dehydrogenase, D-dimer and interleukin-6 production, may contribute to this injury following SARS-CoV-2 co-infection. Collectively, SARS-CoV-2 and HBV co-infection exacerbates liver function of the patients with COVID-19.
Keywords: ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; COVID-19; COVID-19, coronavirus disease 2019; GGT, gamma-glutamyltransferase; HBV; HBV, hepatitis B virus; IQR, interquartile range; LDH, lactate dehydrogenase; SARS-CoV-2; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TBIL, total bilirubin; abnormal liver function; inactive HBV carriers; liver injury.
. 2020 Nov 18.
doi: 10.1016/j.gendis.2020.11.005. Online ahead of print.
Patients with SARS-CoV-2 and HBV co-infection are at risk of greater liver injury
Yong Lin[SUP] 1 [/SUP], Jun Yuan[SUP] 2 [/SUP], Quanxin Long[SUP] 1 [/SUP], Jieli Hu[SUP] 1 [/SUP], Haijun Deng[SUP] 1 [/SUP], Zhenyu Zhao[SUP] 1 [/SUP], Juan Chen[SUP] 1 [/SUP], Mengji Lu[SUP] 3 [/SUP], Ailong Huang[SUP] 1 [/SUP]
Affiliations
- PMID: 33225036
- PMCID: PMC7672332
- DOI: 10.1016/j.gendis.2020.11.005
Abstract
To date, it remains unclear if severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) co-infection exacerbates liver injury in patients with chronic hepatitis B virus (HBV) infection. In this study, we present a retrospective study of 133 hospitalized confirmed mild coronavirus disease 2019 (COVID-19) cases, including 116 patients with COVID-19 with negative serum hepatitis B antigen and 17 HBV inactive carriers with COVID-19. We found that there were no significant differences for the discharge rate or duration of hospitalization between the two groups. However, inactive HBV carriers with SARS-CoV-2 co-infection are at a higher risk of abnormal liver function tests. The enhanced liver injury induced by SARS-CoV-2 and HBV co-infection was identified as the hepatocyte type rather than the cholangiocyte type. Moreover, the inflammatory response, including abnormal lactate dehydrogenase, D-dimer and interleukin-6 production, may contribute to this injury following SARS-CoV-2 co-infection. Collectively, SARS-CoV-2 and HBV co-infection exacerbates liver function of the patients with COVID-19.
Keywords: ALP, alkaline phosphatase; ALT, alanine aminotransferase; AST, aspartate aminotransferase; COVID-19; COVID-19, coronavirus disease 2019; GGT, gamma-glutamyltransferase; HBV; HBV, hepatitis B virus; IQR, interquartile range; LDH, lactate dehydrogenase; SARS-CoV-2; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; TBIL, total bilirubin; abnormal liver function; inactive HBV carriers; liver injury.