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Background: The aim of this study was to analyze the influence of total serum IgE and other potential risk factors on severity of systemic allergic Hymenoptera sting reactions. Methods: In a retrospective analysis of one thousand and two patients referred for insect allergy over 5 years, 865 reported systemic allergic sting reactions, most often by honey bees and wasps. In 758, total IgE, venom-specific IgE, and baseline tryptase levels were available and analyzed together with atopy state, age, and sex in relation to severity of sting reactions according to H. L. Mueller. Results: In a binary logistic regression model considering, besides IgE, also other risk factors for severity, an influence of total and specific IgE on severity of systemic allergic sting reactions could not be shown, while high severity of systemic allergic sting reactions was significantly more often reported in patients with a baseline tryptase of ≥11.4 μg/l (P Language: en

Diagnostic tests in patients with Hymenoptera venom allergy are frequently positive to venoms of both honey bee and wasp (Vespula). Component-resolved analysis with recombinant species-specific major allergens (rSSMA) may help to distinguish true double sensitization from crossreactivity.Included were 121 patients with systemic allergic reactions to Hymenoptera stings, 76 with double positivity of serum-specific IgE (sIgE) to both venoms, 45 with single positivity to bee or wasp venom, and 32 controls without history of systemic reactions to Hymenoptera stings and no sIgE to whole venoms. In venom-allergic patients and controls, sIgE to rSSMA Api m 1 of bee venom and to Ves v 1 and Ves v 5 of wasp venom were tested by ImmunoCAP.Only 47% of 76 patients with double positivity to whole venoms reacted also to rSSMA of both species. Specificity of sIgE to the 3 rSSMA was very high, with no sIgE to rSSMA of the other species in single-positive venom-allergic patients and only one control with low sIgE to Ves v 1. All wasp-allergic single-positive patients had sIgE to Ves v 5 and/or Ves v 1, and 78.3% of single-positive bee venom-allergic patients had sIgE to Api m 1.Specificity of sIgE to rSSMA of both species is excellent. Sensitivity of sIgE to rSSMA was optimal for wasp venom. Sensitivity of bee venom Api m 1 could be increased by adding rSSMA of other important bee venom allergens.

BACKGROUND: Exhaled nitric oxide (FENO) is a marker for allergic airway inflammation. We wondered whether in patients with intermittent allergic rhinitis only (i) natural pollen exposure and (ii) artificial pollen exposure by repeated nasal allergen provocations may lead to an elevation of FENO. METHODS: In two prospective studies, we compared the FENO of nonatopic controls with the FENO of nonasthmatic individuals with mild intermittent rhinitis to tree and/or grass pollen. Study I: 13 atopic individuals and seven controls had measurements of FENO, blood eosinophils and eosinophilic cationic protein (ECP) before, during and after pollen season. Study II: 16 atopic individuals and 12 controls had nasal allergen provocations on four following days out of pollen season, with daily measurements of FENO before, 2 and 6 h after provocation, and determination of blood eosinophils, ECP and FEV1 at baseline, on days 5 and 10-12. RESULTS: Natural pollen exposure (study I) caused a significant elevation of FENO in allergic individuals. Nasal allergen provocations (study II) did not elicit a statistically significant rise neither of FENO nor of blood eosinophils between baseline and day 5. However, a subgroup of four individuals with a rise of blood eosinophils during nasal allergen provocations showed also a rise of FENO. CONCLUSIONS: We suppose that in allergic rhinitis a concomitant reaction of the bronchial system is dependent on a strong local inflammation leading to a generalized immune stimulation.

Drug allergy is a common problem in daily practice (1,2). However, the lack of understanding of its physio-pathology, the lack of animal models, the wide varietyof clinical features, and the abundance of potentialelicitors, make it a difficult and somewhat neglectedfield in medical research. Nevertheless, allergologistsoften see certain clinical features that may represent adrug allergy, and will want to know which drug mightbe responsible for a presumed drug allergy. Yet thereare only limited possibilities to determine this, for aslong as the pathomechanisms of different types of drugallergy are not clarified, since diagnostic proceduresrelate to the type of immune mechanism.The most frequent drug reactions are different formsof exanthems. Some appear rapidly after drug intake,e.g. immediate-type reactions like urticaria and angieo-dema. Others appear hours or days after drug intake;they are the so-called delayed-type reactions, compris-ing a broad spectrum of clinical and distinct histo-pathological features. They manifest themselves asmaculopapular, bullous and even pustular exanthema.In recent years immunohistological studies of skinlesions, as well as the generation and analysis of drug-specific T-cell lines (TCL) and T-cell clones (TCC) fromallergic patients, suggested that drug-specific T cellsplay a major role in these drug-induced skin reactions(3–5). These studies have revealed that distinct func-tions of T cells can be associated with different clinicalpictures of drug allergies (6–15). This review presentsthese developments and their impact on the under-standing of three distinct drug-induced side-effects,namely maculopapular exanthema (MPE; which repre-sents the most commonly encountered cutaneousadverse drug reaction), bullous, and pustular skinreactions.

Twenty-seven patients with allergy to house-dust mite and the clinical symptoms of perennial rhinitis and/or mild asthma were treated with specific immunotherapy (SIT) with standardized extracts of house-dust mite for 3 years. The success of therapy was evaluated in yearly intervals by 1) subjective rhinitis and asthma scores. 2) allergen-specific skin and conjunctival tests. 3) nonspecific bronchial hyperreactivity to methacholine. 4) medication scores of rhinitis and asthma. SIT induced a significant improvement of all parameters already after 1 year, with further improvement in the follow-up measurements at 2 and 3 years. We found a constant improvement of the rhinitis and asthma symptom scores, a reduced reactivity in the skin prick and conjunctival provocation tests, and a constantly increasing reduction of bronchial hyperreactivity to methacholine. Concomitantly, the use of medication (topical corticosteroids, beta2-mimetics, and antihistamines) was reduced. Our data support the concept that SIT with standardized extracts of house-dust mite results in an improvement of allergen-specific parameters in patients with perennial rhinitis and intermittent asthma. This beneficial effect of SIT on allergen-specific immune parameters seems to induce also a diminution of nonspecific bronchial hyperreactivity and enables reduction of symptomatic treatment.

Thirty-three patients with histologically verified urticaria pigmentosa were studied for coexisting atopic disease by means of history, skin prick testing with five common inhalants and serological investigation for total IgE and specific IgE antibodies to five common inhalants. The prevalence of atopy in urticaria pigmentosa was similar to that observed in the normal Swiss population, both on the basis of history (7/33 = 21%) and of positive skin prick tests to common inhalants (12/33 = 36%). However, total serum IgE levels were significantly lower (geometric mean value 16.8 kU/l) than in a control group of 52 Swiss blood donors of comparable age and sex distribution (geometric mean value 43.0 kU/l, t = 2.93, P less than 0.005). Specific IgE antibodies to common inhalants were also observed less frequently in urticaria pigmentosa patients than in controls, although this difference was not statistically significant. Low total and specific IgE values in patients with urticaria pigmentosa may be explained by increased absorption of circulating IgE to abundant tissue mast cells.