Transfer of atopy following bone marrow transplantation

TitleTransfer of atopy following bone marrow transplantation
Publication TypeJournal Article
Year of Publication1997
AuthorsBellou A, Kanny G, Fremont S, Moneret-Vautrin DA
JournalAnn Allergy Asthma Immunol
Volume78
Issue5
Pagination513 - 6
Date PublishedMay
ISSN1081-1206 (Print) 1081-1206 (Linking)
Accession Number9164366
KeywordsBone Marrow Transplantation / *adverse effects, Child, Child, Preschool, Dermatitis, Atopic / diagnosis / *etiology, Food Hypersensitivity / complications / diagnosis, Humans, Male, Radioallergosorbent Test, Skin Tests
Abstract

BACKGROUND: Bone marrow transplantation is an optimal treatment of acute leukemia and aplastic anemia. Allergic manifestations in recipients long after bone marrow transplantation have been reported. A case involving transfer of atopy manifested as food allergy-induced-atopic dermatitis is reported. METHODS: The donor and the patient were investigated by prick tests and RAST to the same food allergens. Single blind, oral challenge to egg documented food allergy in the recipient. RESULTS: A 5-year-old boy without history of atopy developed severe atopic dermatitis after bone marrow transplantation from his HLA-identical sister for acute lymphoblastic leukemia. The patient's course had been marked previously by acute graft versus host disease and cytomegalovirus infection. Immunoallergic evaluation showed an exquisite sensitization to egg, peanut, and soybean. Total IgE was 6400 KIU/L. Concomitantly, the donor showed the same sensitizations. Absolute avoidance resulted in the regression of atopic dermatitis. Subsequently, new sensitization to wheat flour, Dermatophagoides pteronyssinus, birch, and plantain pollens was detected. The donor developed asthma. CONCLUSIONS: This case gives evidence of the transfer of sensitization from donor to recipient. The passive transfer of memory cells within the bone marrow inoculum is a possible mechanism. The current concept of allergy supports down regulation of Th1 cells to the benefit of Th2 cells. Additional deregulation induced by acute graft versus host disease, cytomegalovirus infection, and immunosuppression is possible.

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