RESUMO
AimThe present study discussed the humoral immune response and antibody dynamics after primary and booster immunity of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines among patients with chronic liver disease (CLD) in the real world. Thus, it provided data to develop SARS-CoV-2 vaccination strategy. MethodsPatients with confirmed CLD and completed primary or booster immunity of SARS-CoV-2 vaccines were enrolled. Serological specimens were collected after primary or booster immunity of SARS-CoV-2 vaccines to detect novel coronavirus neutralizing antibody (nCoV NTAb) and novel coronavirus spike receptor-binding domain antibody (nCoV S-RBD). Thus, we could evaluate the humoral immune response and antibody dynamics after primary and booster immunity of SARS-CoV-2 vaccines among patients with CLD. Simultaneously, baseline demographics, liver disease-related situations, comorbidity-related situations, SARS-CoV-2 vaccination information, and laboratory examination-related indicators of patients were collected. ResultsA total of 315 patients received SARS-CoV-2 vaccines, including 223 patients who completed the primary immunity of SARS-CoV-2 vaccines, 114 patients who completed booster immunity of SARS-CoV-2 vaccines, and 22 patients who underwent the antibody detection of SARS-CoV-2 vaccines after both primary and booster immunities. The positive rate of nCoV NTAb was 59.64% in Primary and 87.72% in Booster (P<0.001). The median level of nCoV NTAb was 11.53 AU/mL in Primary and 31.98 AU/mL in Booster (P<0.001). The positive rate of nCoV S-RBD was 69.06% in Primary and 91.23% in Booster (P<0.001). The median level of nCoV S-RBD was 21.60AU/mL in Primary and 112.65 AU/mL in Booster (P<0.001). After booster immunity of SARS-CoV-2 vaccines in 22 patients, the positive rate of nCoV NTAb increased from 59.09% to 86.36%, and that of nCoV S-RBD increased from 68.18% to 90.91%. The median level of nCoV NTAb increased from 11.24 AU /mL to 59.14 AU /mL after booster immunity. The median level of nCoV S-RBD increased from 27.28 AU/mL to 219.10 AU/mL. Compared to the antibody level of primary immunity, the median level of nCoV NTAb and nCoV S-RBD in 22 patients was increased by 5.26 and 8.03 times, respectively. Among 22 patients, 9 were negative for nCoV NTAb after primary immunity, while 6 were transformed positive after booster immunity, and the positive conversion rate of nCoV NTAb was 66.7%. On the other hand, 7 patients were negative for nCoV S-RBD after primary immunity, while 5 were transformed positive after booster immunity, and the positive conversion rate of nCoV S-RBD was 71.4%. ConclusionPatients with CLD show improved humoral immune response after completing primary and booster immunity of SARS-CoV-2 vaccines, while booster immunity further improves the positive rate and antibody level of patients with CLD. Finally, the positive conversion rate among patients with primary immunity failure also can be improved after booster immunity.
RESUMO
Objective To investigate the effects of prophylactic antiviral therapy for HBV DNA negative HBV-relat-ed hepatocellular carcinoma (HCC) patients undergoing hepatic arterial chemoembolization (TACE). Methods Fifty-four consecutive patients with HBV-related HCC and received TACE were enrolled in this study. Thirty patients received pre-emptive antiviral drugs before TACE were defined as the treatment group. Twenty-four patients, who did not use antiviral drugs until HBV reactivation after TACE, were included in control group. The incidence of HBV reactivation, duration from HBV DNA positive point to the last time of TACE, the occurrence of abnormal alanine aminotransferase (ALT) caused by HBV reactivation, the peak of aspartate aminotransferase (AST) and the number of liver failure caused by HBV reactivation were observed after TACE in two groups. Results The incidence of HBV reactivation, the occurrence of abnormal ALT, the occurrence of abnormal ALT caused by HBV reactivation, the peak ALT and peak AST were significantly lower in treatment group than those of control group (P ＜ 0.05). No liver failure caused by HBV reactivation was found in treatment group. There were four patients with liver failure caused by HBV reactivation in control group. There was no significant difference in cumulative survival rate between two groups (P=0.071). Conclusion It is suggested that preemptive antiviral therapy can prevent the reactivation of hepatitis B virus, prevent the deterioration of liver function,and decrease the occurrence of liv-er failure caused by HBV reactivation in patients receiving TACE.
