Peanut allergy is one of the leading food-related allergies with significant morbidity and mortality. Immunoglobulin E (IgE)-mediated type 1 hypersensitivity to peanut is a leading cause of anaphylaxis. Anaphylaxis is a mast cell dependent process mediated by IgE. Mast cells sensitized by peanut-specific IgE can initiate the anaphylaxis cascade resulting in multisystem involvement, including cardiovas cular, respiratory, gastrointestinal, neurologic, and dermatological manifestations. Transfer of IgE-mediated hypersensitivity to peanuts following transplantation is rare and has only once been previously described following lung transplant.(1) The mechanism for allergy transfer following transplantation is postulated to result from transfer of IgE-producing donor B cells or from passive transfer of sensitized mast cells. While serum IgE has a short half-life of days, mast cell bound IgE may persist for up to 6 months and cause allergic symptoms or anaphylaxis upon allergen exposure.
A 47-year-old female underwent bilateral lung transplantation for non-specific interstitial pneumonitis (NSIP) and received donor lungs from a twelve-year-old patient with a known allergy to peanuts. The recipient was not known to have a history of tree nut or peanut allergy, but had a history of generalized urticaria following ingestion of shellfish. Post-transplant, the patient experienced four anaphylaxis-like reactions (flushing, itching, hypotension) after consuming cereal, coconut cream pie (on two occasions), and chocolate. No single episode involved clear peanut or tree nut consumption; however, consumed products were not certified as peanut free. Searching for a causal agent, initial skin prick test (SPT) to coconut and subsequent oral coconut challenge were negative. Skin prick tests to tree nuts were negative; however, peanut SPT was 4+ positive (8×7mm). Interestingly, radioallergosorbent test (RAST) for peanut-specific IgE was negative at <0.35kU/L. The patient was counseled to avoid peanut exposure and carry an epinephrine auto-injector (EpiPen®). The positive result of peanut SPT testing steadily declined over serial assessments and reverted to negative one year post-transplant. The patient declined oral peanut challenge following the negative peanut SPT.
Transfer of food allergy post-transplantation is theorized to occur via transfer of donor B cells producing peanut-specific IgE into the circulation of the recipient. An alternate mechanism proposes passive transfer of IgE-sensitized mast cells within the transplanted tissue that then migrate into recipient tissues. A negative RAST assay in our patient suggests the absence of ongoing peanut-specific IgE production. Positive peanut-specific SPT supports the tissue presence of mast cells sensitized by peanut-specific IgE. The gradual decline in the magnitude of the peanut SPT and its return to negative over the course of one year supports the gradual depletion of donor sensitized mast cells in recipient tissue and supports the passive transfer of sensitized mast cells from donor tissue during transplantation.
Passive transfer of allergen-sensitized mast cells following organ transplantation can result in donor anaphylaxis and death. Lack of an anaphylaxis history in a donor may not exclude the possibility of the recipient experiencing an anaphylactic episode. However, detailed donor allergy histories and recipient avoidance of known donor-sensitive allergens can reduce the morbidity and mortality associated with post-transplantation anaphylaxis. Post-transplantation skin prick testing of recipients may be appropriate in the setting of donors with severe allergy to predict those at greater risk of anaphylactic episodes.
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