A complex medical mystery unfolded after a 47-year-old woman received a double lung transplant to treat interstitial lung disease, a condition characterized by inflammation and scarring of the lungs. While recovering in the hospital after surgery, she ate a bowl of cereal and experienced a severe allergic reaction. Over nearly two hours, she suffered generalized flushing, intense itching, shortness of breath, and a dangerous drop in blood pressure.
The reaction puzzled clinicians because the woman had eaten peanuts and peanut products throughout her life without experiencing an allergic reaction. The cereal was not known to contain peanuts, but it was not certified peanut-free, raising the possibility of inadvertent exposure. Over the following weeks, she experienced three additional anaphylaxis-like episodes, including reactions after eating coconut cream pie and an almond candy bar. None of the foods were known to contain peanuts, although they could not be ruled out as possible sources of exposure.
The breakthrough came when doctors reviewed the medical history of her organ donor: a 12-year-old boy with a documented peanut allergy but no history of peanut-induced anaphylaxis. He had not died from his allergy; his death resulted from anoxic brain injury caused by an obstructed ventriculoperitoneal shunt. Doctors began to suspect that peanut-sensitized immune cells had traveled with his lungs and temporarily transferred his allergy to the recipient.
Transplant specialists proposed several possible mechanisms. Donor B lymphocytes capable of producing peanut-specific immunoglobulin E (IgE) may have been transferred with the lungs, or the organs may have carried mast cells or basophils already sensitized with allergen-specific IgE. Exposure to peanut could then prompt these cells to release inflammatory mediators capable of triggering anaphylaxis. Interestingly, blood testing failed to detect peanut-specific IgE in the recipient, lending support to the possibility that previously sensitized mast cells or basophils played a role, although the researchers could not rule out involvement of transferred B cells.
Two months after the transplant, skin-prick testing produced positive reactions to peanut and pine nut, while testing for other tree nuts, including almond, as well as coconut was negative. Doctors continued monitoring her over the following months, and the size of her skin-test reaction to peanut steadily declined. By one year after transplantation, her peanut skin test was negative, supporting the theory that the transferred allergen-sensitized cells were gradually disappearing rather than producing a permanent allergy.
A few months later, doctors conducted a supervised oral peanut challenge. The woman was able to eat peanut without experiencing an allergic reaction, confirming that the acquired sensitivity had resolved. The case provided compelling evidence that an allergy transferred through a transplanted organ can be temporary as donor-derived immune cells within the transplanted tissue gradually diminish.
Although donor-acquired food allergies following solid-organ transplantation are rare, they have been documented following several types of transplantation. Lung and liver recipients appear more frequently in published reports than recipients of some other solid organs, likely because these organs contain substantial populations of immune cells capable of being transferred along with the graft.
The case underscores the importance of considering a donor’s allergy history when a transplant recipient unexpectedly develops allergic reactions. As the researchers concluded, the potential for passive transfer of sensitized cells “should be considered when donor organs are obtained from allergic individuals.” Greater awareness of this rare phenomenon could help clinicians recognize otherwise puzzling post-transplant reactions, appropriately test recipients, and determine whether temporary allergen avoidance and other precautions are warranted while transferred immune cells gradually disappear.
