EARLY ALLOGRAFT REJECTION IN CHILDREN AFTER LIVER TRANSPLANTATION IS ASSOCIATED WITH PERIPHERAL AND GRAFT EOSINOPHILIA

Abstract

31 Acute allograft rejection in children after liver transplantation has still been a major problem in post transplant care despite improved immunosuppression. In adult patients marked elevation of peripheral eosinophils has been reported during acute rejection after solid organ transplantation. There have been no data reported about the role of eosinophils in children after liver transplantation. We have previously reported an increased expression of TH2-cytokines, especially interleukin-5, the major activator of eosinophils during allograft rejection. We therefore examined prospectively the number of peripheral eosinophils in 28 children after liver transplantation during the first 2-4 weeks post transplant in 1-2 days intervals (18 children transplanted between 1993 and 1994 at the California Pacific Medical Center and 10 children, transplanted between 1995 and 1998 at the University of Munich). The data were grouped according to clinical and histological observations in 4 groups: no rejection, early rejection, ongoing rejection, infection. All rejection episodes were proved by liver histology and results were correlated with the relative number of eosinophils within the periportal infiltrates during rejection. Early rejection was defined as 2 days prior to biopsy proven rejection. Results: 388 consecutive differential blood counts were analyzed during an average period of 21 days after transplant. (Table)TableAcute allograft rejection was associated with peripheral eosinophilia in 87%. Peripheral eosinophil numbers raised prior to GGT and bilirubin in 87% of rejection episodes. 22 of 24 liver biopsies with histological signs of allograft rejection showed a marked increase of eosinophils within the sites of inflammation. After treating rejection episodes with steroids eosinophil numbers decreased in all cases. In conclusion: Peripheral and intragraft eosinophilia might be a sensitive and specific additional marker for acute allograft rejection. Our results support the theory of an alternate pathway of liver allograft rejection including TH2-cytokines (IL-5) and eosinophils which might be not sufficiently suppressed by cyclosporine or tacrolimus.