Manifestations Of Allergic Disease Research Articles

Clinical epidemiology of IgE-mediated cutaneous and oculo-conjunctival allergic diseases

Background: IgE-mediated allergic disease may clinically manifest itself with either a single symptom or a multisymptomatic disease involving different organs. In this work we investigated whether gender and age of the patients and reactivity to specific allergens are related to different clinical presentations of IgE-mediated allergic disease, considering in particular eye-conjunctival and cutaneous symptoms, alone or in combination. Methods: Epidemiological and clinical data related to patients of the Local Health Unit of Torino and Alessandria were collected. Measuring of specific Immunoglobulin E (IgE) was carried out by using allergenic extracts and by the employment of the chemiluminescence method. Clinical outcomes were the presence of eye-conjunctival, cutaneous (with also other symptom), and only cutaneous symptoms. The covariates under study were the type of allergen (mite, epithelium, poaceae, food, trees and grasses), number and localisation of the allergic reactions, gender, age over 30 years. For each clinical outcome, a logistic regression analysis was performed. Statistical significance was set at p < 0.05. Results: 844 patients with allergic problems (clinical manifestations of allergic disease) entered the study. We found that exposure to epithelium [OR=3,61; IC 95% (2,17; 6,00)], poaceae [OR=2,24; IC 95% (1,46; 3,42)], grasses [OR=2,06; IC 95% (1.35; 3,14)] and age over 30 years [OR=2,05; IC 95% (1,35; 3,13)] are risk factors for the development of eye-conjunctival symptoms. With regard to cutaneous allergic reactions, exposure to mite [OR=1,49; IC 95% (1,07; 2,08)], food [OR=4,16; IC 95% (3,01; 5,75)] and multidistrict symptoms [OR=3,63; IC 95% (2,54; 5,20)] should be risk factors. Instead, considering only cutaneous reactions, possible risk factor is the exposure to food [OR=3,58; IC 95% (2,54; 5,03)]. The exposure to trees is associated with a reduction of the likelihood to have cutaneous [OR=0,45; IC 95% (0,26; 0,76)] and only cutaneous reactions [OR=0,24; IC 95% (0,11; 0,53)]. For only cutaneous symptoms, a reduction in probability is present for the exposure to the grasses [OR=0,60; IC 95% (0,38; 0,94)] too. Conclusions: The study highlighted significant associations between subgroups of allergens and specific symptoms. As a consequence, in the presence of cutaneous symptoms, IgE tests could be restricted to mite and food, and to epithelium, poaceae and grasses in the presence of oculo-conjunctival symptoms.

Sleep and allergic diseases among young Chinese adults from the Singapore/Malaysia Cross-Sectional Genetic Epidemiology Study (SMCGES) cohort

Background and objectiveSleep disruption has been shown to affect immune function and thus influence allergic disease manifestation. The specific effects of sleep on allergic diseases, however, are less well-established; hence, in a unique population of young Chinese adults, we investigated the association between sleep and allergic disease.MethodsYoung Chinese adults recruited from Singapore in the Singapore/Malaysia Cross-Sectional Genetic Epidemiology Study (SMCGES) were analyzed. We used the International Study of Asthma and Allergies in Childhood (ISAAC) protocol and a skin prick test to determine atopic dermatitis (AD), allergic rhinitis (AR), and asthma status. Information regarding total sleep time (TST) and sleep quality (SQ) was also obtained.ResultsOf 1558 participants with a mean age of 25.0 years (SD = 7.6), 61.4% were female, and the mean total sleep time (TST) was 6.8 h (SD = 1.1). The proportions of AD, AR, and asthma were 24.5% (393/1542), 36.4% (987/1551), and 14.7% (227/1547), respectively. 59.8% (235/393) of AD cases suffered from AD-related sleep disturbances, 37.1% (209/564) of AR cases suffered from AR-related sleep disturbances, and 25.1% (57/227) of asthma cases suffered from asthma-related sleep disturbances. Only asthma cases showed a significantly lower mean TST than those without asthma (p = 0.015). Longer TST was significantly associated with lower odds of AR (OR = 0.905, 95% CI = 0.820–0.999) and asthma (OR = 0.852, 95% CI = 0.746–0.972). Linear regression analyses showed that lower TST was significantly associated with asthma (β = − 0.18, SE = 0.076, p-value = 0.017), and AR when adjusted for AR-related sleep disturbances (β = − 0.157, SE = 0.065, p-value = 0.016). Only sleep disturbances due to AR were significantly associated with a poorer SQ (OR = 1.962, 95% CI = 1.245–3.089).ConclusionsWe found that sleep quality, but not sleep duration was significantly poorer among AD cases, although the exact direction of influence could not be determined. In consideration of the literature coupled with our findings, we posit that TST influences allergic rhinitis rather than vice versa. Finally, the association between TST and asthma is likely mediated by asthma-related sleep disturbances, since mean TST was significantly lower among those with nighttime asthma symptoms. Future studies could consider using objective sleep measurements coupled with differential expression analysis to investigate the pathophysiology of sleep and allergic diseases.

Food allergy and environmental contamination

The interaction between genetic potential and the environment, especially increased urbanization and inadequate waste management, contributes to the manifestation of allergic diseases. Pediatric patients are the most vulnerable, due to the immaturity of the respiratory and immune systems. Prenatal and postnatal exposure to air pollutants, both indoors and outdoors, accelerates or aggravates morbidity and mortality from allergic diseases. The "exposome," which encompasses all environmental exposures throughout life, influences health. Biological and chemical attacks alter the epithelial barrier, triggering inflammatory responses and favoring allergic diseases, such as food allergies. The uncontrolled use of toxic fuels, particulate matter, detergents and other factors contribute to the continuous deterioration of the intestinal epithelial barrier, increasing the risk of allergic diseases. It is important to take urgent action to address these issues and protect the health of the planet.

Fruit Pouch Consumption Does Not Associate with Early Manifestations of Allergic Disease.

Consumption of acidic fruit pouches in infancy may damage the epithelial barrier in the gastrointestinal tract and is suggested to increase allergy risk. We aimed to explore if a high fruit pouch consumption is associated with a higher incidence of early allergic manifestations. We included 2959 parent-child dyads from the Swedish prospective, population-based NorthPop birth cohort study with parentally reported data on frequency of fruit pouch consumption at 9 months of age, as well as parentally reported eczema, wheeze, physician-diagnosed asthma, and food allergy in the first 18 months of life. Immunoglobulin E levels (IgE) in serum (n = 1792), as response to a food mix and an inhalant mix, were determined at age 18 months. Compared with no consumption, daily consumption of one or more pouches at 9 months of age was associated with inhalant sensitization (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.06-4.87, n = 1792) but did not remain significant in the multivariable adjusted model (aOR 2.08, 95% CI 0.95-4.53, n = 1679). There were no associations between fruit pouch consumption and allergic manifestations at this young age. This study suggests that fruit pouch consumption is not associated with allergic phenotypes or IgE sensitization in early childhood.

Revised Swedish infant feeding guidelines are associated with earlier introduction of allergenic foods

Randomized controlled trials have demonstrated that early introduction of allergenic foods, such as peanut and egg, can reduce food allergy in high-risk children. Many international guidelines recommend introduction of allergenic foods in the first year of life, and accordingly, the Swedish National Food agency released updated guidelines in June 2019. Our aim was to examine whether the age at introduction and consumption frequency of allergenic foods have changed since release of the revised national guidelines on the introduction of solid foods in Sweden. Children born between June 2016 and December 2018 (n= 1925) were compared with children born between June 2019 and April 2021 (n= 1761) by using data from the NorthPop Birth Cohort study. Data on food introduction, eczema, and food allergy were prospectively collected until age 18 months by using web-based questionnaires. IgE sensitization was assessed at 18 age months. The proportion of participants who had been introduced to egg, legume, soy products, peanut, almond, and cashew nut during the first year of life increased after implementation of the revised national guidelines. The most significant changes were seen for legume (from 55.2% to 69.8% [adjusted odds ratio= 1.90 (95% CI= 1.62-2.24)]) and peanut (from 29.2% to 43.2% adjusted odds ratio= 1.87 (95% CI= 1.55-2.24)]); consumption frequency had also increased. No differences in the prevalence of eczema, food allergy, or sensitization to the foods of interest were found. Since release of the revised guidelines, infants in the general population are introduced to and consume a variety of allergenic foods earlier and more frequently; however, early manifestations of allergic disease have remained unchanged.

Dominant interfering CARD11 variants disrupt JNK signaling in T cells and impaired CARD11-JNK signaling increases expression of GATA3

CARD11 is a critical scaffold protein linking antigen receptor (AgR) engagement to transcriptional programs required for effector lymphocyte survival, proliferation, and differentiation. Prior work established that CARD11 mediates these effects by enabling AgR-induced signaling through NF-kB, mTORC1 and c-Jun N-terminal kinase 2 (JNK2). Although JNK influences helper CD4+ T cell differentiation, mechanisms governing JNK signal regulation and function in human lymphocytes remain incompletely understood. We therefore asked if/how dominant interfering (DI) CARD11 variants impact JNK signaling and JNK-specific transcriptomic changes in T cells. Wild-type (WT) and CARD11 knockout (KO) Jurkat T cells were transfected with plasmids expressing WT or DI CARD11 variants to assess effects on CARD11-dependent JNK signaling. Additionally, RNA sequencing was performed on mitogen-activated WT and CARD11 KO Jurkat T cells +/– JNK inhibition. Our results revealed that CARD11 is required for AgR-dependent activation of JNK1 and JNK2. Furthermore, heterozygous DI CARD11 mutations found in patients with CARD11-associated atopy with dominant interference of NF-kB signaling (CADINS) disease disrupted AgR-dependent JNK1/2 phosphorylation, c-Jun accumulation, and AP-1 transcriptional activity with variable potency, similar to the degree of impaired NF-kB activation. Intriguingly, JNK inhibition in Jurkat and primary CD4+ T cells enhanced AgR-induced expression of GATA3, the master transcriptional regulator of Th2 cell differentiation. These results were recapitulated in effector Tcells generated from CADINS patient PBMC, with greater GATA3 induction observed after mitogen activation relative to healthy controls. Intriguingly, simultaneous reactivation of JNK signaling through a CARD11-independent mechanism blunted AgR-induced GATA3 induction, suggesting JNK activity can directly modulate GATA3 expression. In summation, our novel findings imply that defective CARD11-dependent JNK signaling in CD4+ T cells contributes to enhanced Th2 differentiation and the atopic diathesis observed in CADINS patients, unveiling a new potential therapeutic target for ameliorating severe allergic disease manifestations.

Insights into the pathogenesis of allergic disease from dedicator of cytokinesis 8 deficiency.

Clinical observations and mechanistic studies in dedicator of cytokinesis 8 (DOCK8)-deficient patients and mice have revealed multiple mechanisms that could contribute to their unusually prevalent and severe allergic disease manifestations. Physical interactions of DOCK8 with STAT3 in B cells and T cells may contribute to increased IgE isotype switching or defective immune synapse formation that decreases T-cell receptor signal strength. A newly discovered TFH13 cell type promotes the development of life-threatening allergy via production of IL-13 and is increased in DOCK8 deficiency. Cytoskeletal derangements and cytothripsis, which were previously shown to account for the increased susceptibility to viral skin infection in DOCK8 deficiency, can lead to interplay between myeloid cells and T cells to ultimately increase production of IL-4, IL-5, and IL-13. Finally, theeffects on type-2 innate lymphoid cells may also contribute to allergic disease.

Comparison of Allergic Rhinitis and Bronchial Asthma Impacts on Tympanometric Parameters in Children at Kano, Nigeria

Background: Allergic rhinitis (AR) is a multifocal IgE-mediated type I hypersensitivity reaction that affects sino-nasal mucosa and is characterized by excessive sneezing, watery rhinorrhea, nasal itching, nasal stuffiness and eyes itching. Bronchial asthma (BA) is one of the common childhood diseases that affects the respiratory system characterized by recurrent cough, wheezing, chest tightness and difficulty with breathing. The two conditions are different manifestations of allergic disease of the airway; the composition of the inflammatory substrate in the mucosa of allergic patients is similar to the late-phase allergic response seen elsewhere in the respiratory tract, such as in bronchial asthma. Aim: The aim was to compare the impacts of allergic rhinitis and bronchial asthma on tympanometric parameters in children. Patients & Methods: This is a hospital based comparative cross-sectional study. Two groups of participants aged 4 - 12 years, one group with documented clinical diagnosis of allergic rhinitis and the other group with documented clinical diagnosis of bronchial asthma were consecutively selected from ear, nose and throat (ENT) and pediatrics cardiopulmonary outpatient clinics of Aminu Kano Teaching Hospital Kano respectively. Equal number of children aged 4 - 12 years with no history of ENT diseases or bronchial asthma that were selected from elementary schools within the same community served as a control group. An interviewer-administered questionnaire was filled out for all the participants, complete ENT and chest examinations were carried out and subsequently all the selected participants had tympanometry done, findings were recorded and analyzed. Results: The mean age of participants with bronchial asthma was found to be 7.5 ± 2.6 years while participants with allergic rhinitis had the mean age of 6.8 ± 2.1 years. The mean middle ear pressure (MEP) of participants with bronchial asthma was found to be -15.22 dapa and -40.32 dapa in those with allergic rhinitis. Acoustic reflex was found to be absent in 15.4% of the participants with bronchial asthma and 29.6% of allergic rhinitis participants. Type B tympanogram was found in 2.8% of bronchial asthma participants and 7.3% in participants with allergic rhinitis. Type C tympanogram was found in 4.6% of participants with bronchial asthma and 15.5% of participants with allergic rhinitis. Type A tympanogram was found in 90% of participants with bronchial asthma and 75% of participants with allergic rhinitis. The difference between type A, B and C tympanograms of participants with bronchial asthma and those with allergic rhinitis was found to be statistically significant (Type A χ2 = 14.62, df = 4, p value = 0.01, Type B χ2 = 14.06, df = 4, p value = 0.01, Type C χ2 = 17.01, df = 6, p value = 0.01). Conclusion: Participants with allergic rhinitis were found to have more abnormalities of tympanometric parameters compared to participants with bronchial asthma which signifies allergic rhinitis conferred an increased risk of having middle ear diseases and otitis media with effusion compared to bronchial asthma.

PD-1 blockade in T follicular helper cells protects mice from peanut allergy by promoting production of low-affinity antibodies

Abstract Food allergy, such as peanut allergy can cause life-threatening anaphylaxis. While T follicular helper (Tfh) cells play a major role in production of allergen-specific IgE and IgG antibodies, the immunologic mechanisms that regulate the production of antibodies that mediate anaphylaxis are not well understood. While PD-1 is highly expressed on Tfh cells, our knowledge is limited regarding the role of the molecule in Tfh cells. Thus, the objective of this study was to investigate the roles of PD-1 in allergic immune responses using a mouse model of peanut allergy. Naïve wild-type mice were exposed to peanut flour intranasally (i.n.) and then challenged by intraperitoneal (i.p.) injection of peanut extract. The mice exposed i.n. to peanut flour produced peanut-specific IgE and IgG antibodies and developed anaphylaxis when challenged i.p. with peanut extract. PD-1 blockade with anti-PD-1 treatment Tfh and germinal center B cell numbers in mice exposed to peanut flour. Nonetheless, anti-PD-1 or anti-PD-L1 fully protected mice from anaphylaxis. Anti-PD-1 or genetic deficiency of PD-1 in CD4+ T cells reduced and increased levels of peanut-specific IgE and IgG, respectively. Anti-PD-1 promoted production of low-affinity IgE and IgG antibodies with no effect on high-affinity antibodies. By passive cutaneous anaphylaxis, peanut-specific antibodies generated in anti-PD1 treated mice failed to induce anaphylaxis, and plasma from these mice prevented anaphylaxis. Therefore, blockade of the PD-1 pathway is protective against allergic immune responses. The interaction between Tfh cells and B cells may play a pivotal role in controlling antibody quality and clinical manifestation of allergic diseases.

Blocking the inhibitory receptor programmed cell death 1 prevents allergic immune response and anaphylaxis in mice

Food allergy and acute anaphylaxis can be life-threatening. While T follicular helper (Tfh) cells play a pivotal role in the allergic immune responses, the immunologic mechanisms that regulate the production of antibodies (Abs) that mediate anaphylaxis are not fully understood. The aim of this study was to investigate the role of the inhibitory receptor programmed cell death protein 1 (PD-1), which is highly expressed on Tfh cells, in allergic immune responses using an animal model of peanut allergy and anaphylaxis. Naive wild-type mice were exposed to peanut flour intranasally and then challenged with peanut extract to induce systemic anaphylaxis. The roles of PD-1 were examined by blocking Abs and using gene-deficient animals. Ahapten model and passive cutaneous anaphylaxis were used to characterize allergen-specific Abs. Treatment with anti-PD-1 enhanced development of Tfh cells and germinal center B cells in mice exposed to peanut flour. Nonetheless, anti-PD-1 or its ligand fully protected mice from developing anaphylaxis. Anti-PD-1 treatment or genetic deficiency of PD-1 in CD4+ T cells inhibited production of peanut-specific IgE and increased the levels of IgG. The passive cutaneous anaphylaxis showed that peanut-specific Abs generated in anti-PD-1-treated animals prevented, rather than provoked, anaphylaxis when transferred to naive animals. Anti-PD-1 promoted production of Abs with low affinity for an antigen in the hapten model. Blockade of the pathway between PD-1 and its ligand is protective against allergic immune responses. The direct interaction between Tfh cells and B cells may play a pivotal role in controlling Ab quality and clinical manifestation of allergic diseases.

Study of indicators of the immune status in HIV-infected patients with concurrent allergic pathology

Aim. To study the indicators of the immune status and manifestations of allergic diseases in HIV-infected patients in the Novgorod region. Methods. We studied the data of HIV-infected patients living in the Novgorod region for the years 20002021. A total of 1020 cases of HIV infection were studied, in which 121 (12%) patients were diagnosed with allergic reactions. In patients with allergic manifestations, the human immunodeficiency virus type 1 ribonucleic acid content was measured by the polymerase chain reaction method, and the indicators of the immune status (the content of lymphocytes, eosinophils, basophils, the levels of CD3+, CD3+CD4+, CD3+CD8+ cells, immunoregulatory index) were assessed. For statistical analysis, the Student's test (t) was used to assess the statistical significance of differences in immune status indicators, and the Pearson 2 test to assess the statistical significance of differences in allergic manifestations in patients with HIV. Results. The subjects of the study were divided into 2 groups based on the levels of HIV viral load. Analysis of these groups using the Pearson 2 test showed a statistically significant (p 0.012) correlation between high viral load and the development of drug hypersensitivity reaction in HIV-infected patients. The following etiology of allergic reactions was determined among the subjects: drug (59%), food (19%), pollen (5.7%), household (5.7%), chemical (1.9%), unspecified (6.7%). The study of the immune status in two groups did not reveal statistically significant differences (p 0.05). The study of the immune status indicators in HIV-infected patients with drug hypersensitivity reactions and different levels of viral load revealed a significantly higher level of CD3+ cells (p 0.003) in patients with drug hypersensitivity reactions and detectable viral load. Conclusion. The study revealed statistically significant differences in the immune status of HIV-infected patients with drug hypersensitivity reactions living in the Novgorod region compared with HIV-infected patients without drug allergies.

The Interplay Between Eczema and Breastfeeding Practices May Hide Breastfeeding’s Protective Effect on Childhood Asthma

Early allergic disease manifestations in infants may influence breastfeeding practices. In the current study, researchers sought to examine the relationship between breastfeeding duration and the development of asthma and allergic asthma phenotypes, stratified by a diagnosis of eczema during or after breastfeeding.Children who participated in the 6 year follow-up of the HealthNuts study, a population-based, longitudinal cohort study of allergic diseases in Australia.Children were enrolled between the ages of 11 and 15 months, and data regarding breastfeeding history, eczema diagnosis, environmental exposures, and family history of allergic disease were collected via questionnaire. At 6 years, information on wheeze, medication use, and parental report of physician-diagnosed asthma were obtained. Skin-prick testing to foods and aeroallergens at the age of 6 helped to stratify children with asthma into allergic and nonallergic phenotypes. From an original cohort of 5276 children, 3663 had completed questionnaires at 6 years, 3111 underwent skin testing, and 3632 had asthma data available for analysis. Children were characterized as never or ever breastfed. Of those breastfed, exclusive breastfeeding was categorized as never, <6 months, or >6 months. The overall duration of breastfeeding was treated as both a continuous (number of months) and categorical variable (<3 months, 3 to <6 months, 6 to <12 months, or >12 months).Children who did not participate in the full questionnaire at the age of 6 were more likely to be never breastfed, from a lower socioeconomic background, have one or both parents born outside of Australia, have no family history of allergic disease, and have had exposure to prenatal maternal or environmental smoking. Among children with asthma data, 96% were breastfed. At the age of 6, the prevalence of current asthma was 13%. Children with asthma were more likely to be male, have a parental history of asthma, have a family history of allergic disease, have been born preterm, have been born via cesarean delivery, and have been exposed to maternal smoking during pregnancy. Breastfeeding initiation was not associated with current asthma at the age of 6 years (adjusted odds ratio: 0.76) when compared with never breastfeeding. An increased duration of breastfeeding in children without eczema in infancy was associated with a reduced odds of asthma (per month increase; adjusted odds ratio: 0.98), which equates to a 0.86 reduced odds of asthma for a 6 month increase in breastfeeding. This association was not apparent in children who were diagnosed with eczema during breastfeeding.A longer duration of breastfeeding was associated with a reduced odds of asthma at the age pf 6 years among children without history of eczema in the first year. This association was masked before stratification of patients by history of eczema in infancy.Breastfeeding is known to be beneficial for improving many health outcomes. However, previous studies have not clearly demonstrated protective effects for breastfeeding on asthma. In the current study, a modest protective association was observed between an increased duration of breastfeeding and asthma but only among children who were not diagnosed with eczema in their first year. This association is complex because infantile eczema is a known risk factor for asthma and has also been shown to influence breastfeeding choices. Additional study is needed on the interplay between breastfeeding practices, early allergic manifestations, and the risk of subsequent allergic outcomes.

Crosstalk Between Circulating Follicular T Helper Cells and Regulatory B Cells in Children With Extrinsic Atopic Dermatitis.

Atopic dermatitis (AD) in early childhood is often the initial manifestation of allergic disease associated with high IgE. Accumulating evidences show that follicular helper T (Tfh) cells play a critical role in promoting B cell differentiation and IgE production, human regulatory B (Breg) cells participate in immunomodulatory processes and inhibition of allergic inflammation. However, the roles and interactions between IL-10-producing Breg cells and Tfh cells in childhood AD are unclear. In this study, we found that the percentage of CD19+IL-10+ Breg cells in children with extrinsic AD was significantly lower than that in age-matched healthy controls, and that it correlated negatively with enhanced CD4+CXCR5+PD-1+ICOS+ circulating Tfh cell responses and increased disease activity; however, there was no significant correlation with serum total IgE levels. A co-culture system revealed that Breg cells from patients with extrinsic AD cannot effectively inhibit differentiation of Tfh cells in an IL-10 dependent manner. Abnormal pSTAT3 signaling induced via Toll-like receptors (TLR), but not the B-cell receptor (BCR) signaling, might contribute to the defect of Breg cells in AD. Taken together, these observations demonstrate an important role for IL-10-producing Breg cells in inhibiting Tfh cell differentiation, and suggest that they may participate in the pathogenesis of AD.

Maternal energy-adjusted fatty acid intake during pregnancy and the development of cows' milk allergy in the offspring.

Cows' milk allergy (CMA) is one of the earliest manifestations of allergic diseases. Early dietary factors, like maternal diet during pregnancy, may play a role in the development of allergic diseases in the offspring. We aimed to investigate the association between maternal intake of fatty acids during pregnancy and the risk of CMA in the offspring. Our study was conducted in a population-based cohort, the Finnish Type 1 Diabetes Prediction and Prevention study. We collected the maternal dietary data by a validated FFQ. We obtained the information on CMA in the study participants (n 448) from registers and from the parents. Dietary data and information on CMA were available for 4921 children. We used logistic regression in the analyses, and fatty acid intakes were energy adjusted. The maternal intake of SFA, MUFA, PUFA, n-3 PUFA, n-6 PUFA, trans fatty acids, ratio of n-3 PUFA to n-6 PUFA or ratio of linoleic acid to α-linolenic acid was not associated with the risk of CMA in the offspring when adjusted for perinatal factors, background factors, parental history of asthma or allergic rhinitis and infant animal contacts. The intake of α-linolenic acid was associated with a decreased risk (OR 0·72; 95 % CI 0·56, 0·93) of CMA in the offspring of mothers without a history of allergic rhinitis or asthma. In conclusion, the maternal intake of fatty acids during pregnancy is not associated with the risk of CMA in the offspring.

Management of allergic diseases in pregnancy

Allergic diseases like asthma, allergic rhinitis, food allergy, hymenoptera allergy, or atopic dermatitis are highly prevalent in women of childbearing age and may affect up to 30% of this age group. This review focuses on the management of allergic diseases during pregnancy. Furthermore, we discuss the challenges of counseling women with allergic diseases in the reproductive age, including considerations relevant to the ongoing SARS-CoV-2 pandemic. To create the optimal milieu for the unborn child, a multitude of immunological changes occur during pregnancy which may favor type 2 responses and aggravate disease phenotypes. In co-occurrence with suboptimal preconception disease control, this elevated Th2 responses may aggravate allergic disease manifestations during pregnancy and pose a risk for mother and child. Due to limitations in conducting clinical trials in pregnant women, safety data on anti-allergic drugs during pregnancy are limited. The lack of information and concerns among pregnant patients demands counseling on the benefits of anti-allergic drugs and the potential and known risks. This includes information on the risk for mother and child of disease aggravation in the absence of treatment. By doing so, informed decisions and shared decision-making can take place.

A review on atopic dermatits

(AD) is common, chronic skin disorders that can significantly quality of life of affected individuals as well as their families. Although the pathogenesis of the disorder is not completely understood, it appears to result from the complex interplay between defects in skin barrier function, environmental &amp; infectious agents, &amp; immune deregulation. There are no diagnostic tests for AD; therefore, the diagnosis is based on specific clinical criteria that corticosteroids, Topical calcineurin inhibitors Atopic dermatitis(AD) is a chronic, highly pruritic(itchy) inflammatory skin disease, &amp; is one of the most common skin disorders in children. The disorder results in significant morbidity &amp; adversely affects quality of life.Not only are patients affected by the social stigma of a visible skin condition, but the intense itching characteristic of the disease often leads to skin trauma &amp; significant sleep disturbances. In addition, management of the condition necessitates the frequent application of emollients (agents that soothe, moisturize take into account the patient’s history &amp; clinical manifestations. Successful management of the disorder requires a multifaceted approach that involves education, optimal skin care practices, anti-inflammatory treatment with topical corticosteroids and/or topical calcineurin inhibitors, the management of pruritus, &amp; the treatment of skin infections. Systemic immunosuppressive agents may also be used, but are generally reserved for severe flare-ups or more difficult-to-control disease. Topical corticosteroids are the first-line pharmacologic treatments for AD, &amp; evidence suggests that these agents may also be beneficial for the prophylaxis of disease flare-ups. Although the prognosis for patients with AD is generally favourable, those patients with severe, widespread disease &amp; concomitant atopic conditions, such as asthma &amp; allergic rhinitis, are likely to experience poorer outcomes. Keywords: Atopic dermatitis, Diagnosis &amp; management, Emollients, Skin care practices, Topical &amp; soften the skin) &amp; topical medications, as well as physician visits. AD also poses a significant economic burden with an estimated annual cost in Canada of $1.4 billion. Current evidence suggests that AD is a primary skin barrier defect that facilitates the development of other atopic conditions., In fact, AD is often the initial step in the “atopic march” (the sequential development of allergic disease manifestations during early childhood), which leads to asthma and/or allergic rhinitis in the majority of afflicted patients.Early AD may also be a causative factor in the development of food allergy. Newer insights into AD suggest that both structural abnormalities of the skin &amp; immune dyregulation play important roles in the pathophysiology of the disease. Therefore, optimal management of AD requires a multifaceted approach aimed at healing &amp; protecting the skin barrier &amp; addressing the complex immune pathogenesis of the disease., This article provides an overview of current literature related to the epidemiology, pathophysiology, diagnosis, &amp; appropriate management of AD

Correlation Between Allergy History in Family and Allergy Manifestation in School Age Children

Background: Asthma, eczema and allergic rhinitis are influenced by both genetic factor and environtment factors. Based on family history of allergy, allergic trace cards can identify the level of allergic risk in children. The relationship between family history of allergy and manifestation of allergic disease as a single allergy disease and allergic multimorbidity still need to be explored. The objective of this study was to identify the associations between family history of allergic disease and manifestation of allergic disease in school-age children.Methods: We conducted a cross sectional study on school age children with 6-13 years old at eight elementary schools in Yogyakarta. Family history of allergy was defined as reported asthma, eczema and allergic rhinitis in a parent or sibling and classified the level of allergic risk based on allergic trace cards. Subjects were questioned by standardized ISAAC questionnaire. The relationship between the two was analyzed by the Chi-squared analysis to assess the prevalence ratio (PR).Results: A total of 272 children with an average age of 8.4 years, allergic manifestations occurred more as multimorbidity (53%) with the highest incidence of RA+asthma (9%) compared with one allergic disease (47%) with the highest incidence of RA (11%). There was a significant relationship between family history of allergy and all manifestations of allergic disease with an increased risk of developing allergies by 3.3 (PR 3.3; 95% CI 2.3-4.8) and 2.8 times (PR 2.8; IK95% 1.8-4.3) in the moderate and high-risk score group. Asthma, RA and DA have a risk for coexistence with 2 other diseases of 2.5 (RP 2.5 IK95%; 1.9-3), 2.25 (PR 2.25 IK95%; 1.7 -3) and 1.9 times (PR 2.5 IK95%; 1.45-2.4).Conclusion: Family history of allergic disease is a risk factors for the development of allergic manifestation both a single allergic disease and multimobidity.

The emerging role of neuroimmune interactions in atopic dermatitis and itch

Millions of people globally suffer from allergic diseases, and the cases have been rising in the past decades. One of the major manifestations of allergic diseases is itch, which is an unpleasant symptom that triggers the urge to scratch and greatly affects the quality of life. Thus, research on how sensation of itch is detected/transmitted from the contact of the allergen to the nervous system is crucial in mitigating itch. Recent studies have attempted to elucidate the mechanisms of itch in allergic diseases. Here, we aim to review the endogenous mediators released from immune/nonimmune skin cells (that are indirectly involved in the propagation of itch) and the sensory neurons that express receptors for these itch mediators that are associated with direct transmission of itch in cutaneous allergic diseases. As the mechanisms for allergic itch become clearer, new therapeutic approaches to relieve itch are likely to be developed. Recent clinical trials are testing numerous compounds that target the endogenous mediators and their receptors. These studies provide the possibility of more effective itch treatment for allergic diseases.

Kawasaki Disease and Allergic Diseases.

Background: Kawasaki disease (KD) is an inflammatory disorder with an unknown etiology. It is the leading cause of acquired heart disease, which leads to coronary vasculitis among children. Studies of frequent manifestation of allergic diseases in children with KD have been the subject of mounting clinical interest. However, evidence supporting the association between KD and allergies has yet to be systematically reviewed.Methods: In this article, we reviewed current literature regarding the association between KD and allergic diseases. References for this review were identified through searches of PubMed, Cochrane, and Embase through the end of August 2020.Results: The results of the analyses of immune repertoire, clinical, and epidemiological studies have indicated some of the characteristics of infectious disease for KD. Although some allergic disorders, such as asthma, may be exacerbated by viral infections, allergies are typically caused by an allergen that triggers an immune response, with the potential involvement of type 2 inflammation and immune disturbances leading to tissue remodeling in genetically susceptible hosts. The effect of intravenous immunoglobulin is multi-faceted and results in a decrease in activating Fc gamma receptor IIA and an increase in anti-inflammatory eosinophils. The findings from this review demonstrate that children who have suffered from KD are more likely to have allergic rhinitis than the general population and their siblings, a condition that lasts until the age of 17. When followed up as teenagers and adults, children with KD are more likely to develop urticaria.Conclusions: This review supports that allergic diseases, such as allergic rhinitis, have been demonstrated to increase following KD. Therefore, the importance of allergic diseases in patients with KD should be emphasized in long-term care. Interventions that include strategies for managing allergies in children with KD would be beneficial.

The Interplay Between Eczema and Breastfeeding Practices May Hide Breastfeeding's Protective Effect on Childhood Asthma

Longer duration of breastfeeding may be protective against asthma. However, early manifestations of allergic disease, such as eczema, are risk factors for asthma and can influence the duration of breastfeeding, and hence, may bias observable associations. To examine the relationship between breastfeeding ever and duration and the development of asthma and allergic asthma phenotypes, stratified by a diagnosis of eczema during or after the breastfeeding period. A total of 3663 children participated in the 6-year-old follow-up of the HealthNuts study, a population-based, longitudinal study of allergic diseases in Australia. At age 1 year, breastfeeding and eczema data were collected and at age 6 years, information on wheeze, medication use, and parental report of doctor-diagnosed asthma were obtained, both via questionnaire. Skin prick test responses to food and aeroallergens at age 6 years further distinguished asthmatic children into allergic and nonallergic phenotypes. Breastfeeding initiation was not associated with current asthma at age 6 years (adjusted odds ratio, 0.76; 95% CI, 0.45-1.29) when compared with never breastfeeding. Results were similar for length of exclusiveness and overall duration of breastfeeding, and allergic and nonallergic asthma phenotypes. However, increased duration of breastfeeding among children without eczema in infancy was associated with reduced odds of asthma (per month increase, adjusted odds ratio, 0.98; 95% CI, 0.95-1.0; P= .05), which equates to 0.86 (95% CI, 0.74-1.0) reduced odds of asthma for a 6-month increase in breastfeeding. This association was not apparent in children who were diagnosed with eczema during breastfeeding (adjusted odds ratio, 1.03; 95% CI, 0.98-1.08; P= .3). Longer duration of breastfeeding was associated with a reduced odds of asthma among children without eczema in the first year of life; this association was masked before stratification by eczema in infancy. Future studies examining breastfeeding practices and the risk of allergic outcomes in later childhood need to consider the presence of early-life allergic manifestations impacting on breastfeeding behavior.