Abstract

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-5Δ32 (CCR-5Δ32) was strongly associated with the incidence of ITBL in adult liver transplantation. This study re-evaluates the association of CCR-5Δ32 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-5Δ32 mutation. There were no major differences in donor or recipients demographics. No association was found between CCR-5Δ32 mutation and the development of ITBL. We conclude that CCR-5Δ32 is no risk factor for the development of ITBL in our patient cohort.

Highlights

  • The terms “nonanastomotic biliary strictures”, “intrahepatic biliary strictures”, or “ischemic-type biliary lesion” (ITBL) are often used as synonyms for hilar or intrahepatic diffuse bile duct strictures, necrosis, ecstasies, or dilatations [1, 2]

  • This study re-evaluates the association of CCR5Δ32 gene polymorphism and the incidence of Ischemic-type biliary lesion (ITBL). 169 patients were included into this retrospective analysis. 134 patients were homozygous for wild-type chemokine receptors (CCR)-5, 33 patients heterozygous, and 2 patients were homozygous for CCR-5Δ32 mutation

  • We conclude that CCR-5Δ32 is no risk factor for the development of ITBL in our patient cohort

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Summary

Introduction

The terms “nonanastomotic biliary strictures”, “intrahepatic biliary strictures”, or “ischemic-type biliary lesion” (ITBL) are often used as synonyms for hilar or intrahepatic diffuse bile duct strictures, necrosis, ecstasies, or dilatations (see Figure 1) [1, 2]. The reported incidence of ITBL after OLT varies between 1.4% and 20% [3,4,5]. Some centers report even higher incidence [6]. Patient and graft survival after the diagnosis of ITBL are significantly reduced [7]. ITBL is the third most common reason for hepatic retransplantation [8]. This complication encounters for major morbidity and mortality, creates high costs, and aggravates organ shortage [7, 8]

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