Delayed hypersensitivity reaction following a sea urchin sting.
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42 patients with confirmed hypersensitivity to honey bee (HBV) and/or yellow jacket (YJV) were treated with the respective venoms (7 with HBV, 5 with VJV and 30 with both venoms). Treatment tolerance, skin tests (ST), specific IgE- and specific IgG-antibodies were monitored before, after 3, 6, 12, 24 and 36 months. 21 patients had a rush and 21 a conventional treatment schedule. Maintenance dose was 100 micrograms. Adverse effects occurred as large local (8 patients), slight systemic (12 patients) and moderate to severe systemic reactions (4 patients). Of 24 re-exposed patients 17 had no reaction at all, six a markedly decreased and one an unchanged reaction. After 3 years of treatment ST became negative in nine of 31 patients on HBV and in seven of 26 patients on YJV. RAST became negative in three of 30 patients on HBV and 17 of 29 patients on YJV treatment. Both ST and RAST became negative in five HBV- and 10 YJV-treated patients. Loss of venom hypersensitivity according to diagnostic tests may correspond to actual desensitization and enable discontinuation of immunotherapy.
The study comprised 28 patients from the centre of Spain (Madrid and surroundings) who had suffered systemic reactions when stung by vespids. Specific IgE antibodies to Vespula spp. and Polistes spp. venoms were measured by RAST. All patients had positive RAST to Vespula venom and half of them also had positive RAST to Polistes venom. A patient can be sensitive to both venoms due to either a clinical sensitization to both venoms, or common antigenic determinants. To differentiate these states we used a RAST inhibition assay. We could inhibit Polistes RAST with either Polistes or Vespula venom to a similar degree. Inhibition of Vespula RAST was possible with Vespula venom, but only to a limited degree with Polistes venom. Direct RAST and RAST inhibition studies indicate that in our geographic region sensitization to Vespula venom is more common than to Polistes venom and Polistes might have cross-reactivity in our patients.
Serum anti-IgE autoantibodies (aaIgE) were investigated by dot immunobinding assay in bee-allergic patients in comparison with nonallergic beekeepers, healthy blood donors, and atopic subjects. Elevated serum levels of aaIgE--either free or combined with IgE--were found in both bee-allergic patients and atopic subjects as compared with beekeepers and healthy donors. With regard to a possible significance of aaIgE for the protective mechanism induced by specific allergen immunotherapy, we estimated aaIgE in bee-allergic patients before, during, and after bee-venom immunotherapy (BVIT) in relation to the outcome of a provocation test with a living bee (PT). During the first year of BVIT, there was no significant change in either free or combined aaIgE, but aaIgE decreased during protracted BVIT over 3-7 years. By using two monoclonal anti-IgE antibodies with different epitope specificity (Le27 and BSW17), we were able to detect two kinds of IgE/aaIgE immune complexes. Our data show that during and after BVIT the levels of one kind of IgE-aaIgE immune complex (the non-BSW17 type) tended to decrease in PT-negative patients but stayed elevated in PT-positive patients. The levels of the other kind of immune complex (the non-Le27 type) were similar in treatment failures and successfully treated patients. These data suggest that there are various kinds of aaIgE with different in vivo functions related to their epitope specificity. Some of them (non-BSW17 type) might be associated with BVIT failure.
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