Sandra G. Tedner

Background: Long‐time data of peanut allergy over time is sparse. We aimed to study the longitudinal development of sensitization to peanut extract and storage protein allergen molecules and associations with asthma status, airway and systemic inflammation markers.Methods: The Swedish birth cohort BAMSE followed 4089 participants with questionnaires, clinical investigations and blood sampling between 0 and 24 years. Information on (i) background factors at 2 months, (ii) peanut allergy symptoms and IgE data (ImmunoCAP) at 4, 8, 16, and 24 years, and (iii) IgE to storage proteins, lung function data including exhaled nitric oxide (FENO) as well as systemic inflammatory markers at 24 years of age were collected.Results: The prevalence of peanut extract sensitization, defined as IgE ≥ 0.35 kU_A/L, was 5.4%, 8.0%, 7.5%, and 6.2% at 4, 8, 16, and 24 years of age, respectively. Between 8 and 24 years of age, (33/1565) participants developed IgE‐ab to peanut extract (median 1,4, range 0.7–2.6 kU_A/L), and among those 85% were also sensitized to birch. Only six individuals developed sensitization to Ara h 2 (≥0.1 kU_A/L) between 8 and 24 years of age, of whom three had an IgE‐ab level between 0.1–0.12 kU_A/L. Storage protein sensitization was associated with elevated FENO, blood eosinophils and type 2 inflammation‐related systemic proteins.Conclusion: Sensitization to peanut extract after 4 years of age is mainly induced by birch cross‐sensitization and IgE to Ara h 2 rarely emerges after eight years of age. Storage protein sensitization is associated with respiratory and systemic inflammation.

Adverse reactions after food intake are commonly reported and a cause of concern and anxiety that can lead to a very strict diet. The severity of the reaction can vary depending on the type of food and mechanism, and it is not always easy to disentangle different hypersensitivity diagnoses, which sometimes can exist simultaneously. After a carefully taken medical history, hypersensitivity to food can often be ruled out or suspected. The most common type of allergic reaction is immunoglobulin E (IgE)–mediated food allergy (prevalence 5–10%). Symptoms vary from mild itching, stomach pain, and rash to severe anaphylaxis. The definition of IgE‐mediated food allergy is allergic symptoms combined with specific IgE‐antibodies, and therefore only IgE‐antibodies to suspected allergens should be analyzed. Nowadays, methods of molecular allergology can help with the diagnostic process. The most common allergens are milk and egg in infants, peanut and tree nuts in children, and fish and shellfish in adults. In young children, milk/egg allergy has a good chance to remit, making it important to follow up and reintroduce the food when possible. Other diseases triggered by food are non‐IgE‐mediated food allergy, for example, eosinophilic esophagitis, celiac disease, food protein‐induced enterocolitis syndrome, and hypersensitivity to milk and biogenic amines. Some of the food hypersensitivities dominate in childhood, others are more common in adults. Interesting studies are ongoing regarding the possibilities of treating food hypersensitivity, such as through oral immunotherapy. The purpose of this review was to provide an overview of the most common types of food hypersensitivity reactions.

Background: Factors predicting allergic sensitization in the first 6 months of life are poorly understood. We aimed to determine whether eczema, dry skin, and high transepidermal water loss (TEWL) at 3 months were associated with allergic sensitization at 6 months of age and, secondarily, to establish whether these characteristics predicted sensitization from 3 to 6 months of age.Methods: At 3 months of age, 1,994 infants from the population‐based PreventADALL birth cohort in Norway and Sweden were assessed for eczema and dry skin on the cheeks and/or extensors; impaired skin barrier function, defined as TEWL in the upper quartile (>9.4 g/m²/h), and allergen‐specific IgE levels A/L, available in 830. At 6 months, we assessed allergic sensitization to any food (egg, cow's milk, peanut, wheat, soy) or inhalant (birch, timothy grass, dog, and cat) allergen by a skin prick test wheal diameter ≥2 mm larger than negative control.Results: Any sensitization was found in 198 of the 1,994 infants (9.9%), the majority to food allergens (n = 177, 8.9%). Eczema, dry skin, and high TEWL at 3 months increased the risk of sensitization at 6 months; adjusted odds ratios 4.20 (95% CI 2.93–6.04), 2.09 (95% CI 1.51–2.90) and 3.67 (95% CI 2.58–5.22), respectively. Eczema predicted sensitization with 55.6% sensitivity and 68.1% specificity; dry skin with 65.3% sensitivity and 57.3% specificity; and high TEWL with 61.7% sensitivity and 78.1% specificity.Conclusion: Eczema, dry skin, and high TEWL at 3 months predicted allergic sensitization at 6 months of age.

Background: Tree nut allergy may cause anaphylaxis. There are limited population‐based studies on prevalence and early‐life risk factors.Methods: We evaluated the prevalence of reported symptoms and allergic sensitization to tree nuts at age 24 years in the BAMSE population‐based cohort study and assessed early‐life factors associated with the development of tree nut allergy.We estimated tree nut allergy prevalence, by analysing questionnaire data on tree nut ingestion and symptoms at age 12, 16 and 24 years, and IgE sensitization at age 24 years to hazelnut, walnut, pecan, cashew, pistachio, Brazil nut, almond extracts and allergen molecules Cor a 1, 9, 14 (hazelnut), Jug r 1 (walnut) and Ana o 3 (cashew). We evaluated eczema, asthma, food allergies, inherited risk of allergy and gender as potential early‐life risk factors.Results: Data were available for 2215/4089 (54%) BAMSE study participants, for estimation of the prevalence of tree nut sensitization (21.2%), tree nut allergy symptoms (9.8%) and combined sensitization and symptoms (7.9%, 2.1% for storage protein sensitization and symptoms, 4.3% for any sensitization and non‐mild symptoms). Sixty‐three per cent of sensitized individuals (295/470) were asymptomatic, but only 76/470 (16%) storage protein sensitized individuals. Egg allergy (OR_adj 8.50 95% CI 2.15–33.6), eczema (OR_adj 2.53 95% CI 1.21–5.32) and asthma (OR_adj 5.59 95% CI 2.35–13.3)) at pre‐school age were associated with future development of tree nut symptoms and storage protein sensitization. At age 24 years, tree nut allergy was associated with current eczema and with markers of current asthma severity. Sensitization to storage proteins was more strongly associated with symptoms than sensitization to whole extract for all tree nuts evaluated.Conclusions: In this Swedish cohort, we found tree nut whole extract sensitization is common but usually asymptomatic. Storage protein sensitization is a more reliable indicator of tree nut symptoms. Tree nut allergy is associated with early onset, persistent and severe atopic disease.

Background: More knowledge about sensitization patterns in early infancy, including impact of molecular allergology, is needed to help predict future allergy development more accurately.Objective: We aimed to determine the prevalence and patterns of allergic sensitization at 3 months of age, and explore possible associated factors.Methods: From the Scandinavian antenatally recruited PreventADALL mother–child cohort, we included 1110 3‐month infants with available serum. Sensitization was defined as s‐IgE of ≥0.1 kU_A/L by Phadiatop Infant^® (ThermoFisher Scientific) including birch, cat, grass, dog, milk, egg, peanut and wheat. Further ImmunoCAP analyses to ovomucoid, casein, Ara h 1‐3, omega‐5‐gliadin were performed in food extract s‐IgE‐positive children. Maternal sensitization was defined as s‐IgE ≥ 0.35 kU_A/L to Phadiatop^® (inhalant allergen mix) and/or Fx5 (food allergen mix) at 18‐week pregnancy.Results: Overall 79 (7.3%) infants had specific sensitization, many with low s‐IgE‐levels (IQR 0.16–0.81 kU_A/L), with 78 being sensitized to food extract allergens; 41 to egg, 27 to milk, 10 to peanut, and 25 to wheat. A total of 62/78 were further analysed, 18 (29%) had s‐IgE to ovomucoid, casein, Ara h 1‐3 and/or omega‐5‐gliadin. Eight infants (0.7%) were sensitized to inhalant allergens. Maternal sensitization to food allergens was associated with infant sensitization, odds ratio 3.64 (95% CI 1.53–8.68).Conclusion: Already at 3 months of age, 7% were sensitized to food, mostly without detectable s‐IgE to food allergen molecules, and <1% to inhalant allergens. Maternal food sensitization was associated with infants’ sensitization.

Summary: Background: Asthma is common in both children and adults in the Western world, just like anxiety and depression. While some research has revealed that these diseases might share important environmental and pathophysiological aspects, the exact mechanisms still remain unclear.Objective: To study the correlation firstly between depression or anxiety and asthma diagnosis in adult twins and secondly the association between parental depression or anxiety and offspring asthma in children of twins.Methods: In total, 24 685 adult twins aged 20–47 years were interviewed or completed a Web‐based questionnaire and their children were identified through the Multi‐Generation Register. Asthma diagnosis was obtained from the Patient Register and the Prescribed Drug Register. Assessment of depression and anxiety was obtained from questionnaires using Center for Epidemiologic Studies Depression Scale (CES‐D), major depression and generalized anxiety disorder (GAD) from DSM‐IV. The association between depression or anxiety and asthma was analyzed with logistic regression adjusting for confounders in twins and offspring. To address genetic and familial environmental confounding, we performed a cotwin analysis using disease‐discordant twin pairs.Results: We found an association between asthma and CES‐D, major depression and GAD, for example adjusted OR for major depression and register‐based asthma 1.56 (1.36–1.79). Most of the point estimates remained in the co‐twin control analysis, indicating that the association was likely not due to genetic or familial environmental factors. There was no association between parental depression and/or anxiety and asthma diagnosis in the offspring which implies lack of genetic confounding.Conclusions: We found an association between own asthma diagnosis and anxiety or depression, but not with offspring asthma. Our results indicate that the associations were not due to confounding from genes or environment shared by the twins.

Summary: Introduction: Early genetic and environmental factors have been discussed as potential causes for the high prevalence of asthma and allergic disease in the western world, and knowledge on fetal growth and its consequence on future health and disease development is emerging.Objective: This review article is an attempt to summarize research on fetal growth and risk of asthma and allergic disease. Current knowledge and novel findings will be reviewed and open research questions identified, to give basic scientists, immunologists and clinicians an overview of an emerging research field.Methods: PubMed‐search on pre‐defined terms and cross‐references.Results: Several studies have shown a correlation between low birth weight and/or gestational age and asthma and high birth weight and/or gestational age and atopy. The exact mechanism is not yet clear but both environmental and genetic factors seem to contribute to fetal growth. Some of these factors are confounders that can be adjusted for, and twin studies have been very helpful in this context. Suggested mechanisms behind fetal growth are often linked to the feto‐maternal circulation, including the development of placenta and umbilical cord. However, the causal link between fetal growth restriction and subsequent asthma and allergic disease remains unexplained. New research regarding the catch‐up growth following growth restriction has posited an alternative theory that diseases later on in life result from rapid catch‐up growth rather than intrauterine growth restrictionper se. Several studies have found a correlation between a rapid weight gain after birth and development of asthma or wheezing in childhood.Conclusion and clinical relevance: Asthma and allergic disease are multifactorial. Several mechanisms seem to influence their development. Additional studies are needed before we fully understand the causal links between fetal growth and development of asthma and allergic diseases.