Get access
Clinical & Experimental Allergy

Serial immunological investigations in a patient who had a life-threatening reaction to intravenous protamine

Authors

  • M. E. WEISS,

    1. Johns Hopkins University School of Medicine, Division of Clinical Immunology at the Johns Hopkins Asthma and Allergy Center, Baltimore, U.S.A.
    Search for more papers by this author
  • F. CHATHAM,

    1. Franklin Square Hospital. Department of Internal Medicine, Baltimore, U.S.A.
    Search for more papers by this author
  • ANNE KAGEY-SOBOTKA,

    1. Johns Hopkins University School of Medicine, Division of Clinical Immunology at the Johns Hopkins Asthma and Allergy Center, Baltimore, U.S.A.
    Search for more papers by this author
  • N. F. ADKINSON JR

    Corresponding author
    1. Johns Hopkins University School of Medicine, Division of Clinical Immunology at the Johns Hopkins Asthma and Allergy Center, Baltimore, U.S.A.
      Dr N. Franklin Adkinson Jr. Johns Hopkins University School of Medicine, The Johns Hopkins Asthma and Allergy Center. 301 Bayview Boulevard. Baltimore, MD 21224, u.s.a.
    Search for more papers by this author

Dr N. Franklin Adkinson Jr. Johns Hopkins University School of Medicine, The Johns Hopkins Asthma and Allergy Center. 301 Bayview Boulevard. Baltimore, MD 21224, u.s.a.

Summary

Reactions to intravenous protamine include rash, urticaria, bronchospasm, hypotension. and/or pulmonary artery pressure elevation. We have previously shown that in diabetic patients receiving daily protamine insulin injeetions, the presence of anti-protamine IgE or IgG antibodies are significant risk factors for acute, life-threatening reactions when protamine is given intravenously. To study protamine reactions further, we measured serum anti-protamine IgE and IgG antibody levels, in-vitro basophil histamine release and intracutaneous skin testing to protamine serially in an NPH-insulin dependent diabetic who had a severe, protracted anaphlactic reaction to protamine. At the time of his protamine reaction, his serum contained 8·5 ng/ml of anti-protamine IgE and 1·3 μg/ml of anti-protamine IgG antibody. One month following the reaction both anti-protamine IgE and IgG increased to 16 ng/ml (twofold rise) and 90·5 μg/ml (70-fold rise), respectively. With time, both anti-protamine IgE and IgG antibody declined. Serial intradermal skin tests using protamine sulphate did not discriminate between the protamine reactor and nine normal control subjects who had no prior exposure nor any demonstrable serum IgE antibody to protamine. In-vitro basophil histamine release to protamine sulphate was inconclusive in discriminating between the protamine reactor and normal control subjects. We postulate that protamine may be an incomplete or univalent antigen that must first combine with a tissue macromolecule or possibly heparin to become a complete multivalent antigen capable of eliciting IgE antibody-dependent mediator release.

Get access to the full text of this article

Ancillary