The identification of the disease-causing insect in venom allergy is often difficult. Here we used a panel of recombinant bee and wasp allergens as well as glycosylated plant allergens for IgE testing in well-defined patient groups. We demonstrate that an allergen panel made up of E coli–expressed nonglycosylated rApi m 1, rApi m 2, and rVes v 5 allowed improvement of an IgE-based diagnosis of bee and wasp allergy.
COBISS.SI-ID: 27138521
We conducted an open study on basophil allergen threshold sensitivity during birch pollen immunotherapy. We showed the decrease in basophil sensitivity after 2 to 5 months of immunotherapy, which was correlated with an improvement in patients' symptoms measured on a visual analogue scale. The serum obtained after immunotherapy induced a significant decrease in allergen threshold sensitivity in donor birch-allergic basophils. This decrease was not observed after IgG depletion from the serum.
COBISS.SI-ID: 27154393
Current guidelines do not adequately address the question of how best to manage patients with a convincing history of insect allergy and negative venom-specific IgE and skin test results. 47 patients out of a total of 1219 (4%), with a clearly positive history of severe sting allergy and negative diagnostic tests, were recruited over a period of 4.5 years. Here we show that in complex cases with inconclusive diagnostic results, the basophil CD63 activation test could be particularly useful and more sensitive than intradermal skin testing.
COBISS.SI-ID: 26253785
Airway angiogenesis may be an important part of structural remodeling in the pathogenesis of asthma. We found significantly increased angiogenin and VEGF concentrations in the induced sputum of both rhinitis and controlled asthma patients. These in vivo results demonstrated increased airway angiogenesis in patients with rhinitis without asthma as well as in corticosteroid-treated and well-controlled asthma patients. We showed that standard therapy does not sufficiently effect lung remodeling, therefore new therapies are needed.
COBISS.SI-ID: 25417689
We hypothesize that alternate regulation of COX-2 may predispose patients to aspirin-induced exacerbations. The main finding of this study was that COX-2 appears to be differentially regulated in aspirin-sensitive patients. What is really new is the observation that aspirin induced COX-2 overexpression might be associated with clinical reaction.
COBISS.SI-ID: 25475545