Open AccessClinical relevance of the de novo production of anti‐ HLA antibodies following intestinal and multivisceral transplantation
Author(s) -
Gerlach Undine A.,
Lachmann Nils,
Sawitzki Birgit,
Arsenic Ruza,
Neuhaus Peter,
Schoenemann Constanze,
Pascher Andreas
Publication year - 2014
Publication title -
transplant international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.998
H-Index - 82
eISSN - 1432-2277
pISSN - 0934-0874
DOI - 10.1111/tri.12250
Subject(s) - medicine , plasmapheresis , rituximab , immunology , transplantation , bortezomib , antibody , human leukocyte antigen , clinical significance , eculizumab , gastroenterology , antigen , multiple myeloma , complement system
Summary Despite a negative pretransplant cross‐match, intestinal transplant recipients can mount humoral immune responses soon after transplantation. Moreover, the development of donor‐specific anti‐ HLA antibodies ( DSA s) is associated with severe graft injury. Between June 2000 and August 2011, 30 patients (median age 37.6 ± 9.8 years) received isolated intestinal transplantations ( ITX , n = 18) or multivisceral transplantations ( MVTX s, n = 12) at our center. We screened for human leukocyte antigen ( HLA ) antibodies pre‐ and post‐transplant. If patients produced DSA s, treatment with plasmapheresis and intravenous immunoglobulin ( IVIG ) was initiated. In the event of DSA persistence and/or treatment‐refractory rejection, rituximab and/or bortezomib were added. Ten patients developed DSA s and simultaneously showed significant signs of rejection. These patients received plasmapheresis and IVIG . Eight patients additionally received rituximab, and two patients were treated with bortezomib. DSA values decreased upon antirejection therapy in 8 of the 10 patients. The development of DSA s following ITX is often associated with acute rejection. We observed that the number of mismatched antigens and epitopes correlates with the probability of developing de novo DSA s. Early diagnosis and therapy, including B‐cell depletion and plasma cell inhibition, are crucial to preventing further graft injury.