Food allergy to hazelnut occurs both with and without concomitant pollen allergy.
We sought to evaluate a panel of hazelnut allergens for diagnosis of hazelnut allergy in Spain, Switzerland, and Denmark.
Fifty-two patients with a positive double-blind, placebo-controlled food challenge result with hazelnuts; 5 patients with a history of anaphylaxis; 62 patients with pollen allergy but hazelnut tolerance; and 63 nonatopic control subjects were included. Serum IgE levels to hazelnut extract, recombinant hazelnut allergens (rCor a 1.04, rCor a 2, rCor a 8, rCor a 11), and native allergens (nCor a 9, nCor a Bd8K, nCor a Bd11K) were analyzed by means of ImmunoCAP.
Among patients with hazelnut allergy, 91% (Switzerland/Spain, 100%; Denmark, 75%) had IgE to hazelnut extract, 75% to rCor a 1.04, 42% to rCor a 2, 28% to rCor a 8, and 2% to rCor a 11. The highest rate of sensitization to Cor a 1.04 was found in the northern regions (Switzerland/Denmark, 100%; Spain, 18%), whereas IgE to the lipid transfer protein rCor a 8 prevailed in Spain (Spain, 71%; Switzerland, 15%; Denmark, 5%). IgE to profilin rCor a 2 was equally distributed (40% to 45%). Among control subjects with pollen allergy, 61% had IgE to hazelnut extract, 69% to rCor a 1.04, 34% to rCor a 2, 10% to rCor a 8, and 6% to rCor a 11.
Component-resolved in vitro analyses revealed substantial differences in IgE profiles of hazelnut allergic and hazelnut tolerant patients across Europe.
Few studies have measured the frequency of atopy with objective measures, and most of these studies have been done in industrialised countries. We analysed serum samples from 859 15-80-year-old Greenlanders who had participated in population-based screening campaigns in 1987 and in 1998. We defined atopy as a positive result in an assay that tests for specific IgE against the eight most common inhalant allergens in one pool (grass, birch, mugwort, dog, cat, horse, Cladosporum herbarum, house dust mite). The frequency of atopy doubled between 1987 (39 [10%] of 392) and 1998 (87 [19%] of 467; risk ratio 1.88 [95% CI 1.31-2.68]). This increase was largest in 15-19-year olds, but also occurred in older people, suggesting that the risk factors responsible for the increase in atopy do not operate only in childhood.
Asymptomatic aeroallergen sensitisation affects approximately 10% of Western adolescents and is an established risk factor for the development of respiratory allergy. The reported incidence is 2-20% annually. Previous studies are based on out-seasonal symptom recollection or selected populations, conferring bias towards higher incidence rates.
The aim was to determine the incidence of onset of symptoms among clinically well-characterised asymptomatic, sensitised subjects compared with controls, and to evaluate the predictive values of common allergological tests.
We performed a prospective, clinical, non-interventional, 2-year follow-up study on subjects (identified by population screening) with seasonal allergic birch or grass pollen rhinitis (n = 52), asymptomatic sensitisation to grass or birch (AS, n = 52) or non-atopic, healthy control subjects (n = 39). Experimental allergen susceptibility was assessed at inclusion and at follow-up by skin prick test, conjunctival challenge, intradermal late-phase reaction and measurement of specific IgE. Participants completed in-seasonal symptom and medication diaries during 2 subsequent seasons.
We observed an annual incidence rate of 5% for the onset of symptoms in the AS group (healthy control group 0%). At baseline, the AS group displayed intermediate experimental allergen susceptibility. Subjects developing symptoms had higher levels of specific IgE and larger late-phase reaction than those persistently asymptomatic. However, the positive predictive values were low (14-27%) in contrast to the negative predictive values (95-100%).
In a well-characterised young population, asymptomatic aeroallergen sensitisation conferred a low risk for onset of symptoms during the 2-year follow-up. Persistent asymptomatic phenotype could be accurately predicted by negative results from simple allergological testing.
Comment In: Int Arch Allergy Immunol. 2011;155(3):189-9021293139
Parasitic helminth infections can protect against allergic airway inflammation in experimental models and have been associated with a reduced risk of atopy and a reduced course of asthma in some observational studies. Although no clinical evidence exists to support the use of helminth therapy for allergic disease, the helminth Trichuris suis has demonstrated efficacy in treatment of inflammatory bowel disease.
To determine efficacy of helminth therapy for allergic rhinitis.
We conducted a double-blind, placebo-controlled, parallel group trial in which 100 subjects age 18 to 65 years with grass pollen-induced allergic rhinitis were randomly assigned to ingest a total of 8 doses with 2500 live T suis ova or placebo with an interval of 21 days. The primary outcome was a change in mean daily total symptom score for runny, itchy, sneezing nose (maximum change, 9.0) or in percentage of well days during the grass pollen season.
Treatment with T suis ova (N = 49) compared with placebo (N = 47) caused transient diarrhea peaking at day 41 in 33% of participants (placebo, 2%), and increased eosinophil counts (P