Formaldehyde 2% is not a useful means of detecting allergy to formaldehyde releasers- results of the ESSCA network, 2015-2018.

BACKGROUND: Studies suggest that patch testing with formaldehyde releasers (FRs) gives significant additional information to formaldehyde 1% aq. and should be considered for addition to the European baseline series (EBS). It is not known if this is also true for formaldehyde 2% aq. OBJECTIVES: To determine the frequency of sensitization to formaldehyde 2% aq. and co-reactivity with FRs. To establish whether there is justification for including FRs in the EBS. MATERIALS AND METHODS: A 4-year, multi-center retrospective analysis of patients with positive patch test reactions to formaldehyde 2% aq. and five FRs. RESULTS: A maximum of 15 067 patients were tested to formaldehyde 2% aq. and at least one FR. The percentage of isolated reactions to FR, without co-reactivity to, formaldehyde 2% aq. for each FR were: 46.8% for quarternium-15 1% pet.; 67.4% imidazolidinyl urea 2% pet.; 64% diazolidinyl urea 2% pet.; 83.3% 1,3-dimethylol-5, 5-dimethyl hydantoin (DMDM) hydantoin 2% pet. and 96.3% 2-bromo-2-nitropropane-1,3-diol 0.5% pet. This demonstrates that co-reactivity varies between FRs and formaldehyde, from being virtually non-existent in 2-bromo-2-nitropropane-1,3-diol 0.5% pet. (Cohen's kappa: 0, 95% confidence interval [CI] -0.02 to 0.02)], to only weak concordance for quaternium-15 [Cohen's kappa: 0.22, 95%CI 0.16 to 0.28)], where Cohen's kappa value of 1 would indicate full concordance. CONCLUSIONS: Formaldehyde 2% aq. is an inadequate screen for contact allergy to the formaldehyde releasers, which should be considered for inclusion in any series dependant on the frequency of reactions to and relevance of each individual allergen.

Predictors of Food Sensitization in Children and Adults Across Europe.

BACKGROUND: The geographical variation and temporal increase in the prevalence of food sensitization (FS) suggest environmental influences. OBJECTIVE: To investigate how environment, infant diet, and demographic characteristics, are associated with FS in children and adults, focusing on early-life exposures. METHODS: Data on childhood and adult environmental exposures (including, among others, sibship size, day care, pets, farm environment, and smoking), infant diet (including breast-feeding and timing of introduction to infant formula and solids), and demographic characteristics were collected from 2196 school-age children and 2185 adults completing an extensive questionnaire and blood sampling in the cross-sectional pan-European EuroPrevall project. Multivariable logistic regression was applied to determine associations between the predictor variables and sensitization to foods commonly implicated in food allergy (specific IgE ≥0.35 kUA/L). Secondary outcomes were inhalant sensitization and primary (non-cross-reactive) FS. RESULTS: Dog ownership in early childhood was inversely associated with childhood FS (odds ratio, 0.65; 95% CI, 0.48-0.90), as was higher gestational age at delivery (odds ratio, 0.93 [95% CI, 0.87-0.99] per week increase in age). Lower age and male sex were associated with a higher prevalence of adult FS (odds ratio, 0.97 [95% CI, 0.96-0.98] per year increase in age, and 1.39 [95% CI, 1.12-1.71] for male sex). No statistically significant associations were found between other evaluated environmental determinants and childhood or adult FS, nor between infant diet and childhood FS, although early introduction of solids did show a trend toward prevention of FS. CONCLUSIONS: Dog ownership seems to protect against childhood FS, but independent effects of other currently conceived environmental and infant dietary determinants on FS in childhood or adulthood could not be confirmed.

Value of allergy tests for the diagnosis of food allergy.

Eosinophilic esophagitis (EoE) is a chronic T helper 2-type inflammatory disorder. Concurrent allergic diseases have been observed in EoE cases at a high prevalence. The observation that EoE responds to dietary treatment suggests that EoE is an antigen-driven process. However, the pathogenesis by which allergens mediate the eosinophilic disease in the esophagus needs further clarification. In immediate-type food allergy, diagnosis is based on a careful case history followed by a search for food-specific IgE either by skin testing [skin prick test (SPT)] or in vitro (e.g. ImmunoCAP). In children with atopic dermatitis and a food allergy to milk, eggs, peanuts, fish or wheat, the SPT and in vitro determination of specific IgE show excellent sensitivity and negative predictive values, whereas the positive predictive values are low. In pollen-related secondary food allergy, sensitivity and negative predictive values of IgE testing is much lower. Consequently, oral food provocation is the gold standard for the diagnosis of food allergy. Similarly, in EoE patients, SPT, atopy patch test and in vitro determination of IgE to foods do not reliably predict food allergy, and the average positive predictive values of these allergy tests are below 50%. In conclusion, the value of allergy tests to identify triggering foods are limited, and triggering foods have to be identified by an elimination diet and consequent reintroduction of single foods under biopsy control. However, due to the high prevalence of concurrent allergic diseases among EoE patients, an allergy work-up is urgently indicated in each patient with EoE.

Assessment of component-resolved in vitro diagnosis of celeriac allergy.

BACKGROUND: Previous studies have demonstrated insufficient sensitivity of commercially available celeriac extract reagents in the diagnosis of celeriac allergy. OBJECTIVE: We sought to assess the diagnostic performance of specific IgE determination based on recombinant and purified natural celeriac allergens in comparison with an extract-based assay and to investigate interference by IgE to cross-reactive carbohydrate determinants and its biologic activity. METHODS: Twenty-four subjects with a positive double-blind, placebo-controlled food challenge result to celeriac; 20 atopic control subjects with birch pollen allergy who tolerated celeriac; and 20 nonatopic subjects were enrolled. IgE binding was investigated for celeriac allergens (rApi g 1.01, rApi g 4, and nApi g 5), extract reagents (celeriac, birch, mugwort, and timothy grass pollen), birch pollen allergens (rBet v 1 and rBet v 2), and cross-reactive carbohydrate determinants by means of ImmunoCAP analysis. Biologic activity of allergens was determined based on basophil mediator release. RESULTS: Component-resolved ImmunoCAP analysis considerably increased the sensitivity to detect celeriac-specific IgE by 20%. Sensitization to carbohydrate structures was detected in 38% of patients with celeriac allergy, and there was an excellent correlation between sensitization to the glycoprotein Api g 5 and isolated glycan. Positive results among atopic control subjects were mainly caused by protein allergens, whereas the effect of carbohydrate epitopes was marginal. The ability of allergens to induce mediator release decreased in the order Bet v 1 > Api g 1 > Api g 5, confirming the low biologic activity of IgE to carbohydrate epitopes. CONCLUSION: Component-resolved diagnosis allowed an increase in diagnostic sensitivity from 67% to 88% compared with extract-based diagnosis. Sensitization to Api g 5 was attributable to its glycan moieties but did not interfere with diagnostic specificity.

Clinical expression of nickel contact dermatitis primed by diagnostic patch test.

INTRODUCTION: Persistence of allergen and immunocompetent cells at sites of healed contact dermatitis has been reported. Flare-up reactions triggered by patch testing and after systemic provocation with allergen are well-known phenomena. To our knowledge, we report the first flare-up of a previous patch test site following casual cutaneous application of nickel in an individual with hitherto latent nickel sensitization. CASE REPORT: Patch testing in a 23-year-old female patient was performed for dermatitis following application of various gels and adhesive bandages: positive delayed-type hypersensitivity reactions were noted for nickel sulfate and potassium dichromate. The patient had never noticed skin reactions to nickel-containing items before. Three weeks following these patch tests, the patient wore earrings which in the past had been well tolerated. She subsequently developed dermatitis of both earlobes within hours and dermatitis at the site of nickel patch testing within a day. CONCLUSIONS: Nickel exposure for 48 h in a patch test is sufficient to induce overt delayed-type hypersensitivity on re-exposure with a previously tolerated antigen in a previously clinically unresponsive individual. Antigen and/or antigen-specific effector cells at the site of previous positive patch testing can be recruited into a delayed-type hypersensitivity reaction for a prolonged period of time.