BACKGROUND:The consumption of plant-based food has lately largely increased, raising concerns about allergic reactions from ingredients which are currently not subject to mandatory labelling. METHODS:We analysed the frequency and severity of allergic reactions to non-mandatory labelled allergenic foods (pea, lentil, bean, chickpea, fenugreek, pine nut, sunflower-, poppy-, pumpkin seed, buckwheat) from two large European cohorts: The Anaphylaxis Registry (NORA) and EuroPrevall outpatient clinic study. Severity was assessed using the Food Allergy Severity Score (FASS) and compared with reactions to mandatory labelled allergenic foods. RESULTS:Among 589 reactions from both cohorts, sunflower seed was the most frequent trigger (n = 126). In NORA, pine nut (1.0% of food-induced allergic reactions) was most common followed by pea and buckwheat (0.7% each); in EuroPrevall, sunflower seed (1.2%), poppy seed (0.6%) and lentil (0.6%) predominated. After adjusting for age and sex, the severity of reactions to mandatory labelled seeds and legumes (excluding peanut) were not different (nFASS median: 4.39 vs. 4.43 and 4.56 vs. 4.49). Whereas, cereal-induced reactions (6.47) were significantly more severe than buckwheat (4.77). In Nora, the number of reactions to fenugreek and pumpkin seed were 7.4- and 3.7-fold higher in 2015-2022 versus 2007-2014. CONCLUSION:Non-mandatory labelled allergenic foods were identified to cause severe allergic reactions in two large European cohorts. The frequent involvement of sunflower seed, pine nut, pea and lentil, but also rising numbers of reactions to fenugreek and pumpkin seed, indicates their potential risk. These allergenic foods warrant close monitoring and consideration in future allergen labelling revisions.

Jian et al1Jian L. Yi W. Zhang N. Wen W. Krysko O. Song W.J. et al.Perspective: COVID-19, implications of nasal diseases and consequences for their management.J Allergy Clin Immunol. 2020; 146: 67-69Abstract Full Text Full Text PDF PubMed Scopus (24) Google Scholar in a recent article refer to the immune reaction of the upper respiratory tract (URT) in patients infected by severe acute respiratory syndrome coronavirus (SARS-CoV)-2 (coronavirus disease 2019 [COVID-19] pandemic). The authors wonder about the consequences of inhaled corticosteroids (ICSs) on immune reaction. We share the queries of Jian et al, from a practical point of view. Since late February 2020, when the COVID-19 outbreak exploded in Greece, emergency departments (EDs) of major hospitals were enrolled in triaging patients with suspicious clinical presentation. Medical staff was called to perform nasopharyngeal and oropharyngeal swabbing, irrespective of specialization, and forwarding the samples for a PCR. Training was offered through educational videos.2Marty F.M. Chen K. Verrill K. How to obtain a nasopharyngeal swab specimen.N Engl J Med. 2020; 382: e76Crossref PubMed Scopus (171) Google Scholar The authors of this letter are going to maintain such a triage during the summer months when a wave of tourists from countries with different prevalence of COVID-19 is going to visit Greece. Pitfalls in performing nasopharyngeal or oropharyngeal swabbing are not negligible. Learning from the experience of previous medical personnel engaged in ED, we focus on an intriguing problem we are going to cope with. Given the pneumonologic character of the hospital and the seasonal allergies, 15% to 25% of patients admitted to the ED are expected to suffer exacerbations of chronic obstructive pulmonary disease, asthma, rhinitis, and rhinosinusitis. Most of them are under chronic or seasonal therapies with ICSs, oral or intranasal. With the URT sprayed by ICSs, we are wondering about the diagnostic accuracy of specimens collected. Asking patients to blow their nose, or postponing the procedure is not feasible, as far as we ignore the washout period needed for an ICS, especially in chronic administration. ICSs are likely to modify the replication of commensal and pathogenic virome in the nasopharynx, oropharynx, and saliva.3Ramakrishnan V.F. Holt J. Nelson L.F. Ir D. Robertson C.E. Frank D.N. Determinants of the nasal microbiome: pilot study of effects of intranasal medication use.Allergy Rhinol. 2018; 9: 1-10Crossref Google Scholar Medical literature regarding the effects of ICSs on pathogenic virome of the URT is scarce. We try to extrapolate data from previous coronavirus epidemics, namely, SARS-CoV, Middle East respiratory syndrome (MERS), and HCoV-229E. ICSs are expected to enhance pathogenic viral replications in the URT, predisposing to subsequent bacterial infection.4Singanayagam A, Johnston SL. Long-term impact of inhaled corticosteroid use in asthma and chronic obstructive pulmonary disease (COPD): review of mechanisms that underlie risks [published online ahead of print 2020]. J Allergy Clin Immunol. https://doi.org/10.1016/j.jaci.2019.12.907.Google Scholar This is likely for inhaled cortisone, prednisolone, dexamethasone, and fluticasone. Contrarily, mometasone inhibits the replication of SARS-CoV and HCoV-229E.5Matsuyama S. Kawase M. Nao N. Shirato K. Ujike M. Kamitani W. et al.The inhaled corticosteroid ciclesonide blocks coronavirus RNA replication by targeting viral NSP15.bioRxiv. 2020; Google Scholar Similarly, budesonide degrades the virulence of HCoV-229E.6Yamaya M. Nishimura H. Deng X. Sugawara M. Watanabe O. Nomura K. et al.Inhibitory effects of glucopyrronium, formoterol, and budesonide in coronavirus HCoV-229E replication and cytokine production by primary cultures of human nasal and tracheal epithelial cells.Respir Investig. 2020; 58: 155-168Crossref PubMed Scopus (193) Google Scholar Recently, the ICS ciclesonide was found to suppress the replication of SARS-CoV-2, by directly attacking the NSP15 viral endoribonuclease, demonstrating an antiviral function.7Jean S, Ko M, Lee J, Choi I, Byun SY, Park S, et al. Identification of antiviral drug candidates against SARS-CoV-2 from FDA-approved drugs [published online ahead of print 2020]. Antimicrob Agents Chemother. https://doi.org/10.1128/AAC.00819-20.Google Scholar Therapies with ICSs modulate the innate defensive mechanisms of the URT, interfering with cytokines, while at the same time perturbate the abundance and replication of commensal and pathogenic viruses.3Ramakrishnan V.F. Holt J. Nelson L.F. Ir D. Robertson C.E. Frank D.N. Determinants of the nasal microbiome: pilot study of effects of intranasal medication use.Allergy Rhinol. 2018; 9: 1-10Crossref Google Scholar,7Jean S, Ko M, Lee J, Choi I, Byun SY, Park S, et al. Identification of antiviral drug candidates against SARS-CoV-2 from FDA-approved drugs [published online ahead of print 2020]. Antimicrob Agents Chemother. https://doi.org/10.1128/AAC.00819-20.Google Scholar Depending on the chemical composition of ICSs, the impact on the virome of the URT is unpredictable. With this in mind, swabbing the URT of coronavirus-infected patients under an ICS regimen renders the quality of the viral load collected questionable. Taking alternative specimens from pleural effusions, stools, or even blood is of dubious diagnostic value. With all this scepticism in our minds, we are preparing ourselves to cope with the intricacies of triaging in a COVID-19 era, performing with responsibility the swabbing techniques, ensuring specimens of high diagnostic accuracy. Perspective: COVID-19, implications of nasal diseases and consequences for their managementJournal of Allergy and Clinical ImmunologyVol. 146Issue 1PreviewThe severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) has caused a global health emergency. With increasing numbers of infected people and deaths worldwide reported daily since the beginning of the year, we have to urgently focus on a new pandemic caused by the SARS-CoV-2, a betacoronavirus related to SARS-CoV. We have to urgently learn more about this virus, its ways of transmission to spread infection so fast all over the world, the pathomechanisms involved in human infection and intracellular entry, the consecutive spreading within the body, and finally the factors that determine the difference between a mild or even asymptomatic infection in one and a deadly disease in another patient. Full-Text PDF

BACKGROUND: Walnut allergy is common across the globe, but data on the involvement of individual walnut components are scarce. OBJECTIVES: To identify geographical differences in walnut component sensitization across Europe, explore cosensitization and cross-reactivity, and assess associations of clinical and serological determinants with severity of walnut allergy. METHODS: As part of the EuroPrevall outpatient surveys in 12 European cities, standardized clinical evaluation was conducted in 531 individuals reporting symptoms to walnut, with sensitization to all known walnut components assessed in 202 subjects. Multivariable Lasso regression was applied to investigate predictors for walnut allergy severity. RESULTS: Birch-pollenerelated walnut sensitization (Jug r 5) dominated in Northern and Central Europe and lipid transfer protein sensitization (Jug r 3) in Southern Europe. Profilin sensitization (Jug r 7) was prominent throughout Europe. Sensitization to storage proteins (Jug r 1, 2, 4, and 6) was detected in up to 10% of subjects. The walnut components that showed strong correlations with pollen and other foods differed between centers. The combination of determinants best predicting walnut allergy severity were symptoms upon skin contact with walnut, atopic dermatitis (ever), family history of atopic disease, mugwort pollen allergy, sensitization to cat or dog, positive skin prick test result to walnut, and IgE to Jug r 1, 5, 7, or carbohydrate determinants (area under the curve [ 0.81; 95% CI, 0.73-0.89). CONCLUSIONS: Walnut-allergic subjects across Europe show clear geographical differences in walnut component sensitization and cosensitization patterns. A predictive model combining results from component-based serology testing with results from extract-based testing and information on clinical background allows for good discrimination between mild to moderate and severe walnut allergy. (C) 2020 The Authors. Published by Elsevier Inc. on behalf of the American Academy of Allergy, Asthma & Immunology.

Cinnamon contact stomatitis (CCS) is a rare delayed hypersensitivity reaction. We report two cases of contact stomatitis induced by cinnamon powder and cinnamon-flavored chewing gums. Case 1: A 31-year old female had been diagnosed with CCS by a stomatologist due to symptomatic episodes of pain, burning and redness of the tongue and the buccal mucosa at the occlusal level following use of cinnamon-flavored chewing gums. Case 2: A 39-year old female had been initially diagnosed with herpetic gingivostomatitis, due to the presence of widespread erosive lesions on the gingiva and buccal mucosa at initial intraoral examination, but this diagnosis was changed to probable CCS after negative cultures and serologic testing for HSV as well as recurrence of lesions upon rechallenge with cinnamon. Case 1: Patch tests for fragrance mix (including cinnamic alcohol and cinnamic aldeyde) were performed with positive results, while patch testing for cinnamon powder was negative. The patient was advised to avoid use of cinnamon-flavored chewing gums, with no recurrence of symptoms during a follow up period of 5 months. Case 2: Patch tests for fragrance mix were performed with negative results, while patch testing for cinnamon powder was positive. The patient was advised to avoid consumption of cinnamon powder and had no recurrence of stomatitis during a 4 month follow up period. Cinnamon contact stomatitis is a rare condition needing proper evaluation from a stomatologist as well as an allergologist in order to set the correct diagnosis.

BACKGROUND:Hazelnut allergy is birch pollen-driven in Northern/Western Europe and lipid transfer protein-driven in Spain and Italy. Little is known about other regions and other allergens.OBJECTIVE:Establishing a molecular map of hazelnut allergy across Europe.METHODS:In 12 European cities, subjects reporting reactions to hazelnut (n = 731) were evaluated and sensitization to 24 foods, 12 respiratory allergen sources, and latex was tested by using skin prick test and ImmunoCAP. A subset (124 of 731) underwent a double-blind placebo-controlled food challenge to hazelnut. Sera of 423 of 731 subjects were analyzed for IgE against 7 hazelnut allergens and cross-reactive carbohydrate determinants by ImmunoCAP.RESULTS:Hazelnut allergy was confirmed in 70% of those undergoing double-blind placebo-controlled food challenges. Birch pollen-driven hazelnut sensitization (Cor a 1) dominated in most cities, except in Reykjavik, Sofia, Athens, and Madrid, where reporting of hazelnut allergy was less frequent anyhow. In Athens, IgE against Cor a 8 dominated and strongly correlated with IgE against walnut, peach, and apple and against Chenopodium, plane tree, and mugwort pollen. Sensitization to seed storage proteins was observed in less than 10%, mainly in children, and correlated with IgE to nuts, seeds, and legumes. IgE to Cor a 12, observed in all cities (10% to 25%), correlated with IgE to nuts, seeds, and pollen.CONCLUSIONS:In adulthood, the importance of hazelnut sensitization to storage proteins, oleosin (Cor a 12), and Cor a 8 is diluted by the increased role of birch pollen cross-reactivity with Cor a 1. Cor a 8 sensitization in the Mediterranean is probably driven by diet in combination with pollen exposure. Hazelnut oleosin sensitization is prevalent across Europe; however, the clinical relevance remains to be established.

BACKGROUND:Kiwifruit is a common cause of food allergy. Symptoms range from mild to anaphylactic reactions. OBJECTIVE:We sought to elucidate geographic differences across Europe regarding clinical patterns and sensitization to kiwifruit allergens. Factors associated with the severity of kiwifruit allergy were identified, and the diagnostic performance of specific kiwifruit allergens was investigated. METHODS:This study was part of EuroPrevall, a multicenter European study investigating several aspects of food allergy. Three hundred eleven patients with kiwifruit allergy from 12 countries representing 4 climatic regions were included. Specific IgE to 6 allergens (Act d 1, Act d 2, Act d 5, Act d 8, Act d 9, and Act d 10) and kiwifruit extract were tested by using ImmunoCAP. RESULTS:Patients from Iceland were mainly sensitized to Act d 1 (32%), those from western/central and eastern Europe were mainly sensitized to Act d 8 (pathogenesis-related class 10 protein, 58% and 44%, respectively), and those from southern Europe were mainly sensitized to Act d 9 (profilin, 31%) and Act d 10 (nonspecific lipid transfer protein, 22%). Sensitization to Act d 1 and living in Iceland were independently and significantly associated with severe kiwifruit allergy (odds ratio, 3.98 [P = .003] and 5.60 [P < .001], respectively). Using a panel of 6 kiwifruit allergens in ImmunoCAP increased the diagnostic sensitivity to 65% compared with 20% for skin prick tests and 46% ImmunoCAP using kiwi extract. CONCLUSION:Kiwifruit allergen sensitization patterns differ across Europe. The use of specific kiwifruit allergens improved the diagnostic performance compared with kiwifruit extract. Sensitization to Act d 1 and living in Iceland are strong risk factors for severe kiwifruit allergy.