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Journal of Transplantation
Volume 2009 (2009), Article ID 436515, 6 pages
Clinical Study

Chemokine Receptor-5 32 Mutation is No Risk Factor for Ischemic-Type Biliary Lesion in Liver Transplantation

1Department of General, Visceral and Transplantation Surgery, Charité-University Medicine of Berlin, Campus Virchow Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany
2Department of General and Visceral Surgery, J.W. Goethe University Frankfurt/Main, Theodor Stern Kai 7, 60590 Frankfurt/Main, Germany
3Department of Transplantation Surgery, Johannes Gutenberg University of Mainz, Langenbeckstraße 1, 55131 Mainz, Germany

Received 20 November 2008; Accepted 23 February 2009

Academic Editor: Carlos Esquivel

Copyright © 2009 Christoph Heidenhain et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


It has been shown that certain chemokine receptor polymorphisms may correspond to certain complications after organ transplantation. Ischemic-type biliary lesion (ITBL) encounters for major morbidity and mortality in liver transplant recipients. So far, the exact cause for ITBL remains unclear. Certain risk factors for the development of ITBL like donor age and cold ischemic time are well described. In a previous study, a 32-nucleotide deletion of the chemokine receptor-5 32 (CCR-5 32) was strongly associated with the incidence of ITBL in adult liver transplantation. This study re-evaluates the association of CCR-5 32 gene polymorphism and the incidence of ITBL. 169 patients were included into this retrospective analysis. 134 patients were homozygous for wild-type CCR-5, 33 patients heterozygous, and 2 patients were homozygous for CCR-5 32 mutation. There were no major differences in donor or recipients demographics. No association was found between CCR-5 32 mutation and the development of ITBL. We conclude that CCR-5 32 is no risk factor for the development of ITBL in our patient cohort.