Liver transplantation
The Influence of Late Acute Rejection Episodes on Long-Term Graft Outcome After Liver Transplantation

https://doi.org/10.1016/j.transproceed.2005.04.005Get rights and content

Abstract

Acute cellular rejection represents the most important single risk factor for the occurrence of chronic rejection after organ transplantation. We correlated late acute rejections with the occurrence of chronic graft failure after liver transplantation. We followed 1426 liver transplants for late acute rejection episodes defined as occurring >3 months after OLT. The overall incidence of chronic rejection in our patient population was 3.7%. In summary, we observed a predictive increase of transaminase levels prior to routine biopsies among patients with histologic evidence of late acute rejections. In contrast to other organ systems, late acute rejection episodes were not associated with the occurrence of chronic graft deterioration in liver grafts.

Section snippets

Methods

We followed 1426 liver transplants (OLTx) performed between 1988 and April 2002 for late acute rejection episodes defined as occurring >3 months after OLTx. A total of 1006 follow-up biopsies were grouped into those performed after 6 months, 1, 3, 5, 7, and 10 years, and those with obvious clinical signs for acute rejection. The predictive value of serum parameters was examined in patients prior to routine biopsies. We followed the long-term effects of late acute rejection episodes on chronic

Results

Histologic evidence of acute rejection was found in 52 routine biopsies (5%) among 47 patients (grade 0.5: n = 25 [48%]; grade 1 to 1.5: n = 25 [48%]; grade 2 to 2.5: n = 2 [4%]). Transaminases had significantly (P < .05) increased at 1 month prior to routine biopsies in patients with histologic evidence of rejection (Fig 1, Fig 2). Of patients with histologic evidence of late acute rejection (>3 months post LTx), 79% demonstrated previous early rejection episodes. There was no correlation

Discussion

We observed a predictive increase in transaminase levels prior to routine biopsies in patients with histologic evidence of late acute rejections. In contrast to other organ systems late acute rejection episodes were not associated with the occurrence of chronic graft deterioration in liver grafts.

References (6)

  • S.A. Webber et al.

    J Heart Lung Transplant

    (2003)
  • J. Klempnauer et al.

    Transplant Proc

    (2001)
  • F.V. Veronese et al.

    Clin Transplant

    (2004)
There are more references available in the full text version of this article.

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