WASP STING ANAPHYLAXIS

  • 1 January 1983
    • journal article
    • research article
    • Vol. 61  (1) , 132-139
Abstract
Profuse hemostatic defects were demonstrable 14 h after wasp sting anaphylaxis. The patient''s plasma contained an agent or agents that interfered with the action of thrombin, impeding the release of fibrinopeptide A from fibrinogen and the hydrolysis of the synthetic amide H-D-prolyl-L-phenylalanyl-L-arginine-p-nitroanilide. This inhibitor could not be equated with known plasma inhibitors of thrombin nor with heparin. The titers of nearly all other known clotting factors were reduced compared to levels obtained after the patient''s recovery. Of particular interest were profound reductions in the titers of proaccelerin (factor V) and high-MW kininogen. A normal titer of Hageman factor (factor XII) argued against participation of contact-activated mechanisms in the induction of the multiple abnormalities observed. Attempts to demonstrate the release of procoagulant or anticoagulant substances from the patient''s convalescent blood, plasma, serum or leukocytes upon challenge with wasp venom were unsuccessful. The observations confirm and extend information concerning hemostatic abnormalities in anaphylaxis.