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Tumor Necrosis Factor Alpha Inhibitors as Immunomodulatory Antirejection Agents after Intestinal Transplantation
Author(s) -
Gerlach U. A.,
Koch M.,
Müller H.P.,
VeltzkeSchlieker W.,
Neuhaus P.,
Pascher A.
Publication year - 2011
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1111/j.1600-6143.2011.03497.x
Subject(s) - infliximab , medicine , ulcerative colitis , transplantation , gastroenterology , refractory (planetary science) , tumor necrosis factor alpha , surgery , immunology , physics , disease , astrobiology
We reported the successful administration of infliximab for late‐onset OKT3‐resistant rejection in two patients, who presented persistent ulcerative inflammation of the ileal graft after intestinal transplantation (ITX). Based on this experience, the present study demonstrated our long‐term experience with infliximab for different types of rejection‐related and inflammatory allograft alterations. Infliximab administration (5 mg/kg body weight (BW)) was initiated at a mean of 18.2 ± 14.1 months after transplantation. The number of administrations per patient averaged 8.4 ± 6.7. Repeat dosing was timed according to clinical signs and graft histology in addition to serum‐levels of tumor necrosis factor alpha (TNFα), lipopolysaccharide binding protein (LBP) and C‐reactive protein (CRP). Infliximab was successful in the following patients: patients with late‐onset OKT3‐ and steroid‐refractory rejection who presented persistent ulcerative alterations of the ileal graft (n = 5), patients with ulcerative ileitis/anastomositis, who did not show typical histological rejection signs (n = 2), and one patient with early‐onset OKT3‐resistant rejection. Infliximab was not successful in one patient with early‐onset OKT3‐resistant rejection that was accompanied by treatment‐refractory humoral rejection. In conclusion, infliximab can expand therapeutic options for late‐onset OKT3‐ and steroid‐refractory rejection and chronic inflammatory graft alterations in intestinal allograft recipients.