Mannose‐Binding Lectin–Deficient Donors Increase the Risk of Bacterial Infection and Bacterial Infection–Related Mortality After Liver Transplantation
2018
Mannose-binding lectin (MBL) is synthesized by the liver and binds to microbes. MBL2
gene polymorphismsproduce intermediate/low/null or normal MBL serum levels (
MBL-deficientor MBL-sufficient phenotypes, respectively). We aimed to evaluate the incidence and severity of infection, rejection, and survival within 1 year after liver transplantation (LT) according to donor and recipient MBL2
gene polymorphisms. A repeated-event analysis for infection episodes (negative
binomial regression, Andersen–Gill model) was performed in 240 LTs. Four hundred twenty-eight infectious episodes (310 bacterial, 15 fungal, 65 cytomegalovirus [CMV]-related, and 38 viral non–CMV-related episodes) and 48 rejection episodes were recorded. The main bacterial infections were urinary (n = 82, 26%) and pneumonia (n = 69, 22%). LT recipients of
MBL-deficientlivers had a higher risk of bacterial infection (incidence rate ratio [IRR] 1.48 [95% confidence interval 1.04–2.09], p = 0.028), pneumonia (IRR 2.4 [95% confidence interval 1.33–4.33], p = 0.013), and
septic shock(IRR 5.62 [95% confidence interval 1.92–16.4], p = 0.002) compared with recipients of
MBL-deficientlivers. The 1-year bacterial infection–related mortality was higher in recipients of
MBL-deficientversus MBL-sufficient livers (65.8% vs. 56.1%, respectively; p = 0.0097). The incidence of rejection, viral, or fungal infection was similar in both groups. Recipient MBL2 genotype did not significantly increase the risk of bacterial infection. LT recipients of
MBL-deficientlivers have a higher risk of bacterial infection, pneumonia,
septic shock, and 1-year bacterial infection–related mortality after LT.
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