A 22-year-old man with a history of allergic reactions to peanuts was admitted to our hospital in a coma. After inadvertently ingesting satay sauce, which contains peanuts, during a Chinese meal, he had become unwell and had had a cardiorespiratory arrest that resulted in cerebral anoxia, coma, and brain death. A high level of peanut-specific IgE was detected in his serum by a radioallergosorbent test (Pharmacia Diagnostics, Uppsala, Sweden). Multiple organs were subsequently procured. The donor's HLA phenotype was A1,24;B8,44;DRB1*03,13.

On November 21, 1989, the donor's liver and right kidney were given in transplantation to a 35-year-old man, and the left kidney and pancreas were given to a 27-year-old woman. The man (HLA phenotype, A2,19;B12,-;DRB1*07,13) had end-stage renal failure due to subacute glomerulonephritis and had begun hemodialysis in 1970. He received a first cadaveric kidney transplant in May 1981. Because of chronic rejection, his renal function slowly deteriorated. He also had chronic active hepatitis due to hepatitis C virus, and cirrhosis was diagnosed in 1987. The woman (HLA phenotype, A1,24;B8,44;DRB1*03,04) had chronic renal failure due to type I diabetes mellitus and had begun hemodialysis in February 1988. Both transplant recipients received immunosuppressive induction therapy with muromonab-CD3 (OKT3) and corticosteroids, azathioprine, and cyclosporine. Neither had ever had any allergy to peanuts. They had not been told the cause of the donor's death. Both had an uneventful postoperative course.

Figure 1. Figure 1. Results of Tests for Peanut IgE Antibodies, Basophil Degranulation Tests, Tests of Peripheral-Blood Cells for Microchimerism, and Assays for Anti-Peanut T-Cell Proliferation in the Recipients of Organ Transplants from a Donor Allergic to Peanuts.

Three months after transplantation, the recipient of the liver–kidney transplant reported a skin rash and laryngeal dyspnea after eating peanuts. Allergy to peanuts was diagnosed on the basis of the clinical findings; the absence of specific IgE antibodies before transplantation, their presence at the time the symptoms appeared, and their decline thereafter; and a positive basophil degranulation test (Figure 1).

The woman who received the pancreas–kidney transplant confirmed that since her transplantation she had not had any symptoms similar to these after eating peanuts. After giving informed consent, she ingested peanuts under close medical supervision, but no symptoms were noted. She had no peanut-specific IgE antibodies in her serum, and a basophil degranulation test was negative.

Tests for systemic donor–recipient microchimerism were performed in the two recipients. DNA was extracted from peripheral-blood cells and from skin in the forearm by a phenol–chloroform procedure; it was precipitated in ethanol and resuspended in distilled water. The identity of the HLA-DRB1 alleles was determined with allele-specific amplification by the polymerase chain reaction with sequence-specific primers, as previously described.10 A positive internal control specific for a non-HLA locus was present during each amplification so that we could assess the quality of the reaction. This sensitive technique allows donor:recipient DNA ratios of 1:4000 to be detected. Microchimerism was not found in the blood but was found in the skin of the recipient of the liver–kidney transplant, as shown by the presence of both the donor's DRB1*03,13 allele and the recipient's DRB1*07,13 allele. No microchimerism was detected in either blood or skin from the kidney–pancreas recipient.

In vitro proliferation assays were performed in an attempt to identify peanut-specific T cells in the recipient of the liver–kidney transplant. Peripheral-blood lymphocytes were isolated by Ficoll–Hypaque density-gradient centrifugation. They were cultured in 96-well plates at a final concentration of 1 million per milliliter in RPMI 1640 medium supplemented with 10 percent normal AB-positive serum, in the presence of 10 or 20 μg of crude peanut extract per milliliter (the gift of Dr. W. Burks, Little Rock, Ark.), or 10 μg of purified protein derivative (Pasteur-Mérieux Institut, Paris) per milliliter as a positive control. After six to eight days, 1 μCi of tritium-labeled thymidine was added. The cultures were continued for 18 hours, after which radioactivity incorporated into DNA was counted. Although a substantial proliferative response to purified protein derivative was observed, there was no peanut-specific proliferation above the negative control value.

The patient with the allergy was of course advised to avoid peanuts permanently, and specific IgE antibodies rapidly disappeared from his serum. Seven years later, his liver and kidney were functioning well.