2011 - ISBTS 2011 Symposium

Oral Communications 10: Immune & Infectious Monitoring

11.224 - Humoral rejection after intestinal transplantation

Presenter: Florence, Lacaille, Paris, France
Authors: Florence Lacaille1, Laetitia-Marie Petit1, Danielle Canioni2, Nicole Brousse2, Olivier Goulet1

Humoral rejection after intestinal transplantation

Florence Lacaille1, Laetitia-Marie Petit1, Danielle Canioni2, Nicole Brousse2, Olivier Goulet1

1Pediatric Hepatogastroenterology-Nutrition, Hôpital Necker-Enfants malades, Paris, France, Metropolitan; 2Pathology, Hôpital Necker-Enfants malades, Paris, France

Aim: To describe the features of humoral (antibody-mediated) rejection after intestinal transplantation.

Patients: From 1994 on, 88 children received 94 transplantations (Tx). Anti-HLA antibodies were screened only from 2008: 30 children were enlisted, and 20 transplanted. The intestinal biopsies were performed every 2-3 days in the 1st month. Staining with C4d was not systematically performed. When the child had high titers of donor-specific anti-HLA antibodies (DSA), he received methylprednisolon, IV immunoglobulins (IVIg) and plasmapheresis (PP).

Results: Among the 27 enlisted children, 3 had pre-transplant anti-HLA antibodies (2 waiting for retransplantation). A significant titer of DSA was found in 9/20 children after Tx (42%), 4 isolated small bowel Tx (SBTx), 3 combined with the liver (L-SBTx), and 2 multivisceral (MVTx, one with kidneys). In both the first ones (L-SBTx and SBTx),without preformed antibodies, the high DSA were contemporaneous of a severe rejection. One child died, and the graft was removed in the other one. In the 7 others, the biopsies showed an acute rejection in 3, 2 mild, 1 moderate. All children received IVIg, and 5 high dose methylprednisolon. PP was performed in 4. All control intestinal biopsies were normal. Two children died (one retransplanted with preformed DSA and one SBTx) of surgical and infectious complications. With a follow-up of 6 months to 2 years, the 5 other children have a normal graft function.

Discussion: A significant titer of DSA is common early after Tx, and not always responsible for histological damage. The pathological diagnosis of humoral rejection is not easy. The treatment is difficult, with its own complications. An untreated humoral rejection may have been responsible for previous early graft losses. Humoral rejection needs to be better described. Untreated, it may have a severe evolution. It may also contribute to the early mortality after Tx.

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