Published online May 22, 2021. doi: 10.4291/wjgp.v12.i3.51
Peer-review started: September 23, 2020
First decision: November 16, 2020
Revised: November 30, 2020
Accepted: February 25, 2021
Article in press: February 25, 2021
Published online: May 22, 2021
The overall incidence of cytomegalovirus (CMV) infection is between 50%-60% in liver transplant recipients, with 20%-30% of patients demonstrating a symptomatic infection[1]. The incidence of post-transplant CMV infection depends mainly on the recipient and donor serological profile. The lowest-risk groups include positive serology for both donors and recipients (D+/R+ status) and a negative status for both donors and recipients (D-/R-). Although reactivation of CMV infection is mostly described in the context of overt immunosuppression, reactivation may also occur in critically ill immunocompetent patients[4-7] associated with increased mortality[8,9].
A subgroup of particular interest is patients with chronic liver diseases[10,11]. Whether CMV reactivation in these individuals that are listed for liver transplantation has any impact on post-transplant outcomes has not been determined[12].
To determine the incidence of reactivated CMV prior to liver transplantation.
This was a prospective cohort study that evaluated adult (≥ 18 years of age) patients with chronic liver disease listed to undergo liver transplantation at a referral hospital for organ transplantation in Latin America. Patients were followed for a minimum of 1 year after liver transplantation. During this period, all episodes of CMV reactivation [detected by either quantitative real-time PCR (qRT-PCR) and/or pp65 antigenemia] were documented, as well as events of CMV disease, organ rejection and overall mortality. Screening for CMV reactivation was performed monthly for the first three months after transplantation or whenever the patient presented with clinical symptoms. At the time the enrolled participants were called in for liver transplan
A total of 72 patients were enrolled in the study. Four patients died before transplantation, thus 68 patients were followed up for a median of 44 mo (25%-75% percentile: 20-50 mo). CMV reactivation was demonstrated in 31.9% (23/72) of patients before transplantation. Median plasma CMV DNA concentration in these patients was 1.212 IU/mL (25%-75% percentile: 560-4.197 IU/mL). Following liver transplantation, CMV infection occurred in 16/67 patients (23.8%).
The crude mortality rate was 20/68 (29.4%), median 7.7 mo (perc 25-75: 1-12), and 7/22 (31.8%) in patients with pre-transplant CMV reactivation (P = 0.763). In Kaplan-Meier analyses, pre-transplant CMV reactivation had no impact on mortality following liver transplantation (log rank: 0.92) (Figure 1). Cox regression analysis also identified no statistically significant factor for mortality in this cohort.
The findings of this study suggest that pre-transplant CMV reactivation has no influence on liver transplantation results, and has no impact on post-transplant CMV reactivation or overall mortality.
Based on this study, screening for CMV DNAemia before liver transplantation does not seem justified. A larger sample size, better quality and multicenter studies are required to fully elucidate this issue.