Basophil histamine release remains unaffected by clinical desensitization to penicillin.

A penicillin-allergic patient who required therapy with beta-lactam antibiotics was desensitized with increasing parenteral doses of benzylpenicillin. After desensitization, the patient tolerated, without signs of allergic reaction, intravenous piperacillin. Immunologic studies were undertaken to investigate humoral and cellular changes accompanying desensitization. Serum penicilloyl IgG and IgE antibodies did not change significantly during induction of clinical tolerance to the drug. The patient's previously positive immediate skin reaction to penicilloyl polylysine (PPL) converted to negative. Nonspecific releasability of skin mast cells as tested with polymyxin B skin test was unchanged. In contrast, in vitro blood basophil activation, both by specific antigen (penicilloyl-human albumin) and a nonspecific IgE-dependent stimulus (anti-IgE) remained strong after the desensitization procedure and during weeks of high-dose piperacillin therapy. A monovalent penicilloyl hapten inhibited penicilloyl-albumin-induced basophil histamine release, whereas the patient's own serum taken while the patient was receiving treatment did not. Moreover, the patient's treatment serum, while the patient was receiving piperacillin, was able to trigger histamine release from passively sensitized basophils of a donor not allergic to penicillin, suggesting the presence of a sufficient amount of complete multivalent antigen to initiate release and/or desensitization. The presence of high concentrations of penicilloated serum proteins in the patient's treatment serum was confirmed by immunoassay. Basophil histamine release could, nevertheless, be elicited from the patient's whole blood sample taken while the patient was receiving piperacillin treatment by adding penicilloyl-human albumin in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)