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Type: Journal article
Title: Donor Mannose - Binding Lectin Deficiency Increases the Likelihood of Clinically Significant Infection after Liver Transplantation
Author: Worthley, D.
Johnson, D.
Eisen, D.
Dean, M.
Heatley, S.
Tung, J.
Scott, J.
Padbury, R.
Harley, H.
Bardy, P.
Angus, P.
Mullighan, C.
Citation: Clinical Infectious Diseases, 2009; 48(4):410-417
Publisher: Univ Chicago Press
Issue Date: 2009
ISSN: 1058-4838
Statement of
Daniel L. Worthley, Douglas F. Johnson, Damon P. Eisen, Melinda M. Dean, Susan L. Heatley, John‐Paul Tung, Justin Scott, Robert T. A. Padbury, Hugh A. Harley, Peter G. Bardy, Peter W. Angus, and Charles G. Mullighan
Abstract: Background. Mannose‐binding lectin (MBL) is an important mediator of innate immunity and is synthesized primarily by the liver. Low MBL levels are common, are due primarily to polymorphisms in the gene encoding MBL (MBL2), and are associated with an increased risk of infection, particularly when immunity is compromised. We report a large, retrospective study that examined the association between MBL status and clinically significant infection following orthotopic liver transplantation. Methods. One hundred two donor‐recipient orthotopic liver transplantation pairs were studied. Five polymorphisms in the promoter and coding regions of MBL2 were examined. MBL levels were measured, using the mannan‐binding and C4‐deposition assays, in serum samples obtained before and after transplantation. Associations between MBL status, as assessed by serum MBL levels and MBL2 genotype, and time to first clinically significant infection (CSI) after transplantation were examined in survival analysis with consideration of competing risks. Results. The median duration of follow‐up after orthotopic liver transplantation was 4 years. Thirty‐six percent of recipients developed CSI after transplantation. The presence of MBL2 coding mutations in the donor was significantly associated with CSI in the recipient; the cumulative incidence function of infection was 55% in recipients of deficient livers, compared with 32% for recipients of wild‐type livers (Ρ = .002). Infection was not associated with recipient MBL2 genotype. Low MBL levels after orthotopic liver transplantation levels (mannan‐binding <1μg/mL or C4 deposition <0.2 C4 U/μL) were also associated with CSI (cumulative incidence function, 52% vs. 20%, Ρ = .003; and cumulative incidence function, 54% vs. 24%, Ρ = .007, respectively). In multivariate analysis, mutation in the MBL2 coding region of the donor (hazard ratio, 2.8; Ρ = .002) and the use of cytomegalovirus prophylaxis (hazard ratio, 2.6; Ρ = .005) were independently associated with CSI. Conclusions. Recipients of MBL‐deficient livers have almost a 3‐fold greater likelihood of developing CSI and may benefit from MBL replacement.
Keywords: Humans
Communicable Diseases
Genetic Predisposition to Disease
Mannose-Binding Lectin
Liver Transplantation
Risk Factors
Retrospective Studies
Polymorphism, Genetic
Open Reading Frames
Middle Aged
Tissue Donors
Promoter Regions, Genetic
Young Adult
DOI: 10.1086/596313
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