Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

The hen and the egg question in atopic dermatitis: allergy or eczema comes first

The hen and the egg question in atopic dermatitis: allergy or eczema comes first Atopic dermatitis (AD) as a chronic inflammatory systemic condition is far more than skin deep. Co-morbidities such as asthma and allergic rhinitis as well as the psychological impact influence seriously the quality of life of the patients. Recent studies have shown that only 10% of atopic patients undergo full manifestation of the atopic march, while 40% demonstrate concomitant food allergy. Exposure to food allergens in the environment causes sensitization and food allergy through the disruption of the skin barrier, as in AD. Food allergy and AD are closely related. While not all AD patients have a food allergy, 20–40% of children with moderate to severe AD will have an IgE-mediated food allergy. It is known that they may coexist but it is unclear if food allergy worsens the course of AD. Experimental, clinical, and epidemiological studies have provided evidence of the primary role of an epidermal barrier defect in the development of sensitization to environmental allergens and that this process occurs in the damaged skin barrier rather than the gastrointestinal or respiratory tract. There is strong evidence for a connection between early AD onset and the development of other allergic diseases later in life. Keywords Eczema, Atopy, Asthma, Atopic march, Treatment response (Th2 helper cells pathway), with the central Introduction role of interleukin (IL)-4 and IL-13 [3]. This complex of Being a chronic and systemic inflammatory condition pathologies in most cases in the life of patients with atopy atopic dermatitis (AD) affects not only the skin. A sig - is characterized by a consistent course, and the transition nificant deterioration in the quality of life of patients with of the pathological process from one organ and system AD is determined by the presence of comorbidities, such to another is called an «atopic march». Recent stud- as asthma and allergic rhinitis, as well as psychological ies have shown that only 10% of atopic patients undergo factors. In addition to skin eczema, the complex of atopic full manifestation of the atopic march, while 40% dem- diseases also includes asthma, allergic rhinoconjunc- onstrate concomitant food allergy [4]. Exposure to food tivitis, food allergy, and eosinophilic esophagitis [1, 2]. allergens in the environment causes sensitization and The unifying factor in this group is type 2 inflammatory food allergy through the disruption of the skin barrier, as in AD. However, immune tolerance can be achieved *Correspondence: by early oral exposure to food allergens [5]. The current Razvigor Darlenski darlenski@abv.bg vision of AD suggests two main directions in the disease Laboratory of Immune-Mediated Skin Diseases, I.M. Sechenov First pathophysiology: 1) disorders in the epidermal barrier as Moscow State Medical University (Sechenov University), Moscow, Russia a result of a genetically determined absence or violation Medical Research, and Education Center, M.V. Lomonosov Moscow State University, Moscow, Russia of the filaggrin synthesis — a protein involved in the con - Department of Dermatology and Venereology, Acibadem City Clinic struction of the stratum corneum and components of the Tokuda Hospital Sofia, 51B Nikola Vaptsarov Blvd., 1407 Sofia, Bulgaria natural moisturizing factor [6]; 2) immunological disor- Department of Dermatology and Venereology, Trakia University-Stara Zagora, Stara Zagora, Bulgaria ders with a predominance of the Th2-immune response with the key cytokines IL-1, IL-4, IL-5, IL-13, IL-31 but © The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. The Creative Commons Public Domain Dedication waiver (http:// creat iveco mmons. org/ publi cdoma in/ zero/1. 0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Allenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 2 of 4 the list of candidate cytokines and immune mediators of an important structural protein of the stratum corneum, inflammation is constantly expanding. The question that deficiency of antimicrobial peptides, changes in the inter - worries the scientific community for a long time is what cellular lipids of the stratum corneum, microbiome dys- exactly is the root cause of the atopic complex: allergy or biosis, and impaired immune regulation [7]. skin ezcema. In the last decade, much evidence has been Genetic defects encoding skin barrier proteins, as well provided supporting the idea that a defect in the epider- as abnormalities in lipid production or tight junctions, mal barrier plays the primary role in the initiation of sen- contribute to the epidermal barrier dysfunction that sitization to allergens from the environment and that this is a specific feature of AD. Mutations with loss of filag - process occurs through the damaged skin barrier rather grin function are associated with an earlier onset and than through the gastrointestinal tract or respiratory a more stable AD phenotype. It has been also reported system [7]. This fact has also been confirmed by large that polymorphism in the thymic stromal lymphopoietin cohort epidemiological studies of the age distribution (TSLP) gene and its receptor, as well as dysregulation of of the atopic spectrum diseases: a relationship has been genes involved in the metabolism of epidermal lipids, are shown between the early onset of AD and the develop- associated with an increased risk of AD, its resistance, ment of asthma and allergic rhinitis at school age [8]. The and food allergy. Other mutations of the skin barrier, risk appears to be even higher in children with persistent including the SPINK5 gene and сorneodesmosin muta- early-onset AD phenotype [9]. Clinical studies also sup- tions, are also associated with AD and the development port the concept of atopic march from early skin barrier of food allergy [7, 11]. Newborns with increased transepi- dysfunction to the development of food sensitization and dermal water loss (TEWL) in the first week of life had an clinical food allergy. Regarding inhaled allergens and AD, increased risk of developing AD at 12 months of age [12]. they are strongly related and often coexist. In certain These genetic factors, which play a significant role in the patients with AD and concomitant inhalation allergy, onset of AD, support the point of view that damage to the the skin condition was worsened during the provocation skin barrier may present at a very early age, even before season. These data are also confirmed by positive results the clinical onset of AD. in AD patients receiving immunotherapy inducing toler- ance to aeroallergens. Skin barrier dysfunction leads to epicutaneous sensitivity and food allergy Epidemiology data Currently, there is increasing evidence supporting the AD affects 15–20% of children and 2–10% of adults [1, view that allergic skin sensitization occurs more read- 10]. In recent decades, the incidence has been steadily ily through the damaged skin barrier. Several studies increasing. In 60% of patients AD develops in the first performed in mice describe immunological pathways year of life, and in 85% of patients’ skin changes develop involved in the progression from epicutaneous sen- by the age of 5. In severe cases, the disease persists after sitization to food allergy [13]. Now it is clear that the puberty. According to recent data, about one-third of AD mechanism of food allergy is through the epicutane- cases in adults appear much later - after age twenty. Most ous sensitization, while the oral exposure leads to toler- AD patients have a mild form of the disease, but about ance [13, 14]. Clinical studies also support the concept 10% have serious clinical manifestations. In adults, this of atopic march from early skin barrier dysfunction to percentage is higher than in children [2]. It is estimated the development of food sensitization and clinical food that about 50% of patients with AD also have other aller- allergy. It has been shown that an increase in TEWL on gic problems during the first year of life. Among them, the 2nd day of life is a predictor of food allergy at the age 85% show symptoms of other allergic diseases within the of two [15]. Newborns with a filaggrin defect have an first 5 years of life. In about 70% of patients, AD resolves increased risk of developing AD and asthma. People with spontaneously up to puberty. AD and filaggrin defects also have an increased risk of pollen allergy. Genetic predisposition to atopic dermatitis AD is undoubtedly characterized by strong genetic Allergy to respiratory and food haptens in AD patients effects. About 77% of identical and 15% of fraternal twins As is commonly known, food allergy and AD are closely develop AD [1, 2, 4, 10]. Intact healthy skin is an impor- related. While not all AD patients have a food allergy, tant physical and immunological barrier against the entry 20–40% of children with moderate to severe AD will have of allergens and microbes from the environment into an IgE-mediated food allergy [2, 7]. It is known that they the body. Defects of the skin barrier can be caused by a may coexist but it is unclear if food allergy worsens the variety of factors, including defects in terminal epithe- course of AD. Some studies show that in case of a posi- lial differentiation, such as deficiency of filaggrin (FLG), tive egg allergy test patient’s condition can improve if A llenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 3 of 4 they eliminate eggs from their diet. This creates some march, namely the use of emollients that restore the cause for concern since eliminating the allergen from skin barrier [1, 6, 7, 17], has recently been challenged the diet can interfere with the development of oral toler- [18]. It has been even shown that the use of emollients ance in patients. According to guidelines, children under increases the risk of food allergy development [19]. 5 years old with moderate to severe AD may be tested Whether this is an association or a causal relationship, for food allergies to milk, eggs, peanuts, wheat, and soy remains to be elucidated. if at least one of the following conditions is met: 1) the Regular use of emollients from the first day after birth child has a reliable history of an immediate reaction (e.g., reduces the risk of clinical AD and asthma development urticaria, swelling, itching, sneezing, coughing, wheez- by 30–55% until 2 years old [1, 6, 7, 17]. There is some ing, vomiting, and low blood pressure) after swallowing evidence that probiotic supplementation during preg- certain food; 2) the child has persistent AD despite opti- nancy or infancy may protect against AD development mized therapy. Food allergy develops in only around 30% but there is no proven protection against food allergies of AD patients [16]. However, many speculations about or other allergic disorders. There is still insufficient evi - cow’s milk protein allergy (CMPA) exist. AD and CMPA dence to support the use of other dietary components diagnostics are not equivalent. The only reliable method such as prebiotics, hydrolyzed formulas, or vitamin for confirming food allergy - it’s an elimination provoca - D supplements for the primary prevention of allergic tion test with the appropriate food. All other laboratory diseases [2, 7]. Several primary prevention strategies tests (skin prick test, in vitro immunoglobulin E test, etc.) for asthma and allergic rhinitis have also been stud- are of low diagnostic and prognostic value. Several ran- ied. These include avoiding contact with ticks in early domized controlled trials have shown that early admin- childhood and preventive sublingual immunotherapy istration of allergenic foods such as peanuts or eggs to in sensitized children. However, no sufficient evidence high-risk infants with severe AD or food sensitization for the admission of these methods into routine clinical may reduce the risk of developing peanut or egg allergy practice has been provided [5, 7]. Secondary prevention [12, 15]. Regarding inhaled allergens and AD, they are of allergic diseases includes interventions in high-risk strongly related and often coexist. Common allergens children or children with a disease, such as AD or sen- are pollen, mites, dogs, and cats. Several studies showed sitization, aimed at preventing progression to the next that AD patients who had a positive skin reaction to phase of the atopic march. dust mites and suffered a bronchial inhalation provoca - tion test with dust mites, developed skin symptoms in 50% of cases after this test, mainly in areas of the body Conclusion where eczema usually occurs. All of these patients also Experimental, clinical, and epidemiological studies have decreased pulmonary function. Other authors do have provided evidence of the primary role of an epi- not find a correlation between the inhalation provoca - dermal barrier defect in the development of sensitiza- tion test and AD aggravation. Our clinical observation tion to environmental allergens and that this process shows that in some patients with AD and concomitant occurs in the damaged skin barrier rather than the inhalation allergy, the skin condition worsens during the gastrointestinal or respiratory tract. There is strong provocation season. These data are also confirmed by evidence for a connection between early AD onset and positive results in AD patients receiving immunotherapy the development of other allergic diseases later in life. inducing tolerance to aeroallergens. Modern progress has Current preventive interventions, such as early regular led to the development of new drugs that suppress ele- use of emollients in high-risk infants, should be reap- ments of the pathological immune response (mediated praised and probably the future will disclose the opti- by Th2), characteristic of both AD and allergic rhinitis mal strategy to restore epidermal barrier effect - the and asthma. u Th s, in these patients, such drugs would primary event in AD. have a good effect on various comorbidities of the atopic Acknowledgements spectrum, and not only on the cutaneous or respiratory None. manifestations. Authors’ contributions RD and AA have equally contributed to the conceptualization, writing, and Preventive strategies: practice lessons editing of this paper. The author(s) read and approved the final manuscript. Many primary prevention interventions aim to reduce Funding the risk of AD by prophylactically protecting the None. skin barrier, starting at a very young age in high-risk Availability of data and materials infants. The generally recommended preventive inter - Available with the authorship. vention for the development of asthma and atopic Allenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 4 of 4 18. Kelleher MM, Phillips R, Brown SJ, Cro S, Cornelius V, Carlsen KCL, et al. Declarations Skin care interventions in infants for preventing eczema and food allergy. Cochrane Database Syst Rev. 2022;11(11):CD013534. Ethics approval and consent to participate 19. Perkin MR, Logan K, Marrs T, Radulovic S, Craven J, Boyle RJ, et al. Associa- Not applicable. tion of frequent moisturizer use in early infancy with the development of food allergy. J Allergy Clin Immunol. 2021;147(3):967–76 e1. Consent for publication Not applicable. Publisher’s Note Competing interests Springer Nature remains neutral with regard to jurisdictional claims in pub- None. lished maps and institutional affiliations. Received: 30 November 2022 Accepted: 30 January 2023 References 1. Darlenski R, Kazandjieva J, Hristakieva E, Fluhr JW. Atopic dermatitis as a systemic disease. Clin Dermatol. 2014;32(3):409–13. 2. Silverberg JI. Comorbidities and the impact of atopic dermatitis. Ann Allergy Asthma Immunol. 2019;123(2):144–51. 3. Gandhi NA, Pirozzi G, Graham NMH. Commonality of the IL-4/IL-13 path- way in atopic diseases. Expert Rev Clin Immunol. 2017;13(5):425–37. 4. Belgrave DC, Granell R, Simpson A, Guiver J, Bishop C, Buchan I, et al. Developmental profiles of eczema, wheeze, and rhinitis: two population- based birth cohort studies. PLoS Med. 2014;11(10):e1001748. 5. Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. 2008;121(6):1331–6. 6. O’Regan GM, Irvine AD. The role of filaggrin in the atopic diathesis. Clin Exp Allergy. 2010;40(7):965–72. 7. Tham EH, Leung DY. Mechanisms by which atopic dermatitis predisposes to food allergy and the atopic march. Allergy Asthma Immunol Res. 2019;11(1):4–15. 8. Saunes M, Oien T, Dotterud CK, Romundstad PR, Storro O, Holmen TL, et al. Early eczema and the risk of childhood asthma: a prospective, population-based study. BMC Pediatr. 2012;12:168. 9. Carlsten C, Dimich-Ward H, Ferguson A, Watson W, Rousseau R, Dybuncio A, et al. Atopic dermatitis in a high-risk cohort: natural history, associ- ated allergic outcomes, and risk factors. Ann Allergy Asthma Immunol. 2013;110(1):24–8. 10. Capozza K, Funk M, Hering M, Lang J, Merhand S, Manion R, et al. Patients’ and caregivers’ experiences with atopic dermatitis-related burden, medical care, and treatments in 8 countries. J Allergy Clin Immunol Pract. 2023;11(1):264-273.e1. https:// doi. org/ 10. 1016/j. jaip. 2022. 10. 032. Epub 2022 Nov 2. 11. Chiang C, Maibach HI. How many skin barriers haveth we: percutaneous egression of ions? Skin Res Technol. 2022;28(2):382–7. 12. Berents TL, Lodrup Carlsen KC, Mowinckel P, Skjerven HO, Rolfsjord LB, Bradley M, et al. Transepidermal water loss in infancy associated with atopic eczema at 2 years of age: a population-based cohort study. Br J Dermatol. 2017;177(3):e35–e7. 13. Brough HA, Nadeau KC, Sindher SB, Alkotob SS, Chan S, Bahnson HT, et al. Epicutaneous sensitization in the development of food allergy: what is the evidence and how can this be prevented? Allergy. 2020;75(9):2185–205. 14. Celebi Sozener Z, Ozbey Yucel U, Altiner S, Ozdel Ozturk B, Cerci P, Turk M, Re Read ady y to to submit y submit your our re researc search h ? Choose BMC and benefit fr ? Choose BMC and benefit from om: : et al. The external Exposome and allergies: from the perspective of the epithelial barrier hypothesis. Front Allergy. 2022;3:887672. fast, convenient online submission 15. Lack G, Fox D, Northstone K, Golding J, Avon Longitudinal Study of P, Chil- thorough peer review by experienced researchers in your field dren Study T. Factors associated with the development of peanut allergy rapid publication on acceptance in childhood. N Engl J Med. 2003;348(11):977–85. • 16. Papapostolou N, Xepapadaki P, Gregoriou S, Makris M. Atopic dermatitis support for research data, including large and complex data types and food allergy: a complex interplay what we know and what we would • gold Open Access which fosters wider collaboration and increased citations like to learn. J Clin Med. 2022;11(14):4232. maximum visibility for your research: over 100M website views per year 17. Fluhr JW, Darlenski R. Transepidermal water loss ( TEWL). In: Berardesca E, Maibach HI, Wilhelm K-P, editors. Non invasive diagnostic techniques in At BMC, research is always in progress. clinical dermatology. Berlin: Springer Berlin Heidelberg; 2014. p. 353–6. Learn more biomedcentral.com/submissions http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Asthma Research and Practice Springer Journals

The hen and the egg question in atopic dermatitis: allergy or eczema comes first

Loading next page...
 
/lp/springer-journals/the-hen-and-the-egg-question-in-atopic-dermatitis-allergy-or-eczema-8glxsV3lwg

References (23)

Publisher
Springer Journals
Copyright
Copyright © The Author(s) 2023
eISSN
2054-7064
DOI
10.1186/s40733-023-00090-2
Publisher site
See Article on Publisher Site

Abstract

Atopic dermatitis (AD) as a chronic inflammatory systemic condition is far more than skin deep. Co-morbidities such as asthma and allergic rhinitis as well as the psychological impact influence seriously the quality of life of the patients. Recent studies have shown that only 10% of atopic patients undergo full manifestation of the atopic march, while 40% demonstrate concomitant food allergy. Exposure to food allergens in the environment causes sensitization and food allergy through the disruption of the skin barrier, as in AD. Food allergy and AD are closely related. While not all AD patients have a food allergy, 20–40% of children with moderate to severe AD will have an IgE-mediated food allergy. It is known that they may coexist but it is unclear if food allergy worsens the course of AD. Experimental, clinical, and epidemiological studies have provided evidence of the primary role of an epidermal barrier defect in the development of sensitization to environmental allergens and that this process occurs in the damaged skin barrier rather than the gastrointestinal or respiratory tract. There is strong evidence for a connection between early AD onset and the development of other allergic diseases later in life. Keywords Eczema, Atopy, Asthma, Atopic march, Treatment response (Th2 helper cells pathway), with the central Introduction role of interleukin (IL)-4 and IL-13 [3]. This complex of Being a chronic and systemic inflammatory condition pathologies in most cases in the life of patients with atopy atopic dermatitis (AD) affects not only the skin. A sig - is characterized by a consistent course, and the transition nificant deterioration in the quality of life of patients with of the pathological process from one organ and system AD is determined by the presence of comorbidities, such to another is called an «atopic march». Recent stud- as asthma and allergic rhinitis, as well as psychological ies have shown that only 10% of atopic patients undergo factors. In addition to skin eczema, the complex of atopic full manifestation of the atopic march, while 40% dem- diseases also includes asthma, allergic rhinoconjunc- onstrate concomitant food allergy [4]. Exposure to food tivitis, food allergy, and eosinophilic esophagitis [1, 2]. allergens in the environment causes sensitization and The unifying factor in this group is type 2 inflammatory food allergy through the disruption of the skin barrier, as in AD. However, immune tolerance can be achieved *Correspondence: by early oral exposure to food allergens [5]. The current Razvigor Darlenski darlenski@abv.bg vision of AD suggests two main directions in the disease Laboratory of Immune-Mediated Skin Diseases, I.M. Sechenov First pathophysiology: 1) disorders in the epidermal barrier as Moscow State Medical University (Sechenov University), Moscow, Russia a result of a genetically determined absence or violation Medical Research, and Education Center, M.V. Lomonosov Moscow State University, Moscow, Russia of the filaggrin synthesis — a protein involved in the con - Department of Dermatology and Venereology, Acibadem City Clinic struction of the stratum corneum and components of the Tokuda Hospital Sofia, 51B Nikola Vaptsarov Blvd., 1407 Sofia, Bulgaria natural moisturizing factor [6]; 2) immunological disor- Department of Dermatology and Venereology, Trakia University-Stara Zagora, Stara Zagora, Bulgaria ders with a predominance of the Th2-immune response with the key cytokines IL-1, IL-4, IL-5, IL-13, IL-31 but © The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http:// creat iveco mmons. org/ licen ses/ by/4. 0/. The Creative Commons Public Domain Dedication waiver (http:// creat iveco mmons. org/ publi cdoma in/ zero/1. 0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Allenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 2 of 4 the list of candidate cytokines and immune mediators of an important structural protein of the stratum corneum, inflammation is constantly expanding. The question that deficiency of antimicrobial peptides, changes in the inter - worries the scientific community for a long time is what cellular lipids of the stratum corneum, microbiome dys- exactly is the root cause of the atopic complex: allergy or biosis, and impaired immune regulation [7]. skin ezcema. In the last decade, much evidence has been Genetic defects encoding skin barrier proteins, as well provided supporting the idea that a defect in the epider- as abnormalities in lipid production or tight junctions, mal barrier plays the primary role in the initiation of sen- contribute to the epidermal barrier dysfunction that sitization to allergens from the environment and that this is a specific feature of AD. Mutations with loss of filag - process occurs through the damaged skin barrier rather grin function are associated with an earlier onset and than through the gastrointestinal tract or respiratory a more stable AD phenotype. It has been also reported system [7]. This fact has also been confirmed by large that polymorphism in the thymic stromal lymphopoietin cohort epidemiological studies of the age distribution (TSLP) gene and its receptor, as well as dysregulation of of the atopic spectrum diseases: a relationship has been genes involved in the metabolism of epidermal lipids, are shown between the early onset of AD and the develop- associated with an increased risk of AD, its resistance, ment of asthma and allergic rhinitis at school age [8]. The and food allergy. Other mutations of the skin barrier, risk appears to be even higher in children with persistent including the SPINK5 gene and сorneodesmosin muta- early-onset AD phenotype [9]. Clinical studies also sup- tions, are also associated with AD and the development port the concept of atopic march from early skin barrier of food allergy [7, 11]. Newborns with increased transepi- dysfunction to the development of food sensitization and dermal water loss (TEWL) in the first week of life had an clinical food allergy. Regarding inhaled allergens and AD, increased risk of developing AD at 12 months of age [12]. they are strongly related and often coexist. In certain These genetic factors, which play a significant role in the patients with AD and concomitant inhalation allergy, onset of AD, support the point of view that damage to the the skin condition was worsened during the provocation skin barrier may present at a very early age, even before season. These data are also confirmed by positive results the clinical onset of AD. in AD patients receiving immunotherapy inducing toler- ance to aeroallergens. Skin barrier dysfunction leads to epicutaneous sensitivity and food allergy Epidemiology data Currently, there is increasing evidence supporting the AD affects 15–20% of children and 2–10% of adults [1, view that allergic skin sensitization occurs more read- 10]. In recent decades, the incidence has been steadily ily through the damaged skin barrier. Several studies increasing. In 60% of patients AD develops in the first performed in mice describe immunological pathways year of life, and in 85% of patients’ skin changes develop involved in the progression from epicutaneous sen- by the age of 5. In severe cases, the disease persists after sitization to food allergy [13]. Now it is clear that the puberty. According to recent data, about one-third of AD mechanism of food allergy is through the epicutane- cases in adults appear much later - after age twenty. Most ous sensitization, while the oral exposure leads to toler- AD patients have a mild form of the disease, but about ance [13, 14]. Clinical studies also support the concept 10% have serious clinical manifestations. In adults, this of atopic march from early skin barrier dysfunction to percentage is higher than in children [2]. It is estimated the development of food sensitization and clinical food that about 50% of patients with AD also have other aller- allergy. It has been shown that an increase in TEWL on gic problems during the first year of life. Among them, the 2nd day of life is a predictor of food allergy at the age 85% show symptoms of other allergic diseases within the of two [15]. Newborns with a filaggrin defect have an first 5 years of life. In about 70% of patients, AD resolves increased risk of developing AD and asthma. People with spontaneously up to puberty. AD and filaggrin defects also have an increased risk of pollen allergy. Genetic predisposition to atopic dermatitis AD is undoubtedly characterized by strong genetic Allergy to respiratory and food haptens in AD patients effects. About 77% of identical and 15% of fraternal twins As is commonly known, food allergy and AD are closely develop AD [1, 2, 4, 10]. Intact healthy skin is an impor- related. While not all AD patients have a food allergy, tant physical and immunological barrier against the entry 20–40% of children with moderate to severe AD will have of allergens and microbes from the environment into an IgE-mediated food allergy [2, 7]. It is known that they the body. Defects of the skin barrier can be caused by a may coexist but it is unclear if food allergy worsens the variety of factors, including defects in terminal epithe- course of AD. Some studies show that in case of a posi- lial differentiation, such as deficiency of filaggrin (FLG), tive egg allergy test patient’s condition can improve if A llenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 3 of 4 they eliminate eggs from their diet. This creates some march, namely the use of emollients that restore the cause for concern since eliminating the allergen from skin barrier [1, 6, 7, 17], has recently been challenged the diet can interfere with the development of oral toler- [18]. It has been even shown that the use of emollients ance in patients. According to guidelines, children under increases the risk of food allergy development [19]. 5 years old with moderate to severe AD may be tested Whether this is an association or a causal relationship, for food allergies to milk, eggs, peanuts, wheat, and soy remains to be elucidated. if at least one of the following conditions is met: 1) the Regular use of emollients from the first day after birth child has a reliable history of an immediate reaction (e.g., reduces the risk of clinical AD and asthma development urticaria, swelling, itching, sneezing, coughing, wheez- by 30–55% until 2 years old [1, 6, 7, 17]. There is some ing, vomiting, and low blood pressure) after swallowing evidence that probiotic supplementation during preg- certain food; 2) the child has persistent AD despite opti- nancy or infancy may protect against AD development mized therapy. Food allergy develops in only around 30% but there is no proven protection against food allergies of AD patients [16]. However, many speculations about or other allergic disorders. There is still insufficient evi - cow’s milk protein allergy (CMPA) exist. AD and CMPA dence to support the use of other dietary components diagnostics are not equivalent. The only reliable method such as prebiotics, hydrolyzed formulas, or vitamin for confirming food allergy - it’s an elimination provoca - D supplements for the primary prevention of allergic tion test with the appropriate food. All other laboratory diseases [2, 7]. Several primary prevention strategies tests (skin prick test, in vitro immunoglobulin E test, etc.) for asthma and allergic rhinitis have also been stud- are of low diagnostic and prognostic value. Several ran- ied. These include avoiding contact with ticks in early domized controlled trials have shown that early admin- childhood and preventive sublingual immunotherapy istration of allergenic foods such as peanuts or eggs to in sensitized children. However, no sufficient evidence high-risk infants with severe AD or food sensitization for the admission of these methods into routine clinical may reduce the risk of developing peanut or egg allergy practice has been provided [5, 7]. Secondary prevention [12, 15]. Regarding inhaled allergens and AD, they are of allergic diseases includes interventions in high-risk strongly related and often coexist. Common allergens children or children with a disease, such as AD or sen- are pollen, mites, dogs, and cats. Several studies showed sitization, aimed at preventing progression to the next that AD patients who had a positive skin reaction to phase of the atopic march. dust mites and suffered a bronchial inhalation provoca - tion test with dust mites, developed skin symptoms in 50% of cases after this test, mainly in areas of the body Conclusion where eczema usually occurs. All of these patients also Experimental, clinical, and epidemiological studies have decreased pulmonary function. Other authors do have provided evidence of the primary role of an epi- not find a correlation between the inhalation provoca - dermal barrier defect in the development of sensitiza- tion test and AD aggravation. Our clinical observation tion to environmental allergens and that this process shows that in some patients with AD and concomitant occurs in the damaged skin barrier rather than the inhalation allergy, the skin condition worsens during the gastrointestinal or respiratory tract. There is strong provocation season. These data are also confirmed by evidence for a connection between early AD onset and positive results in AD patients receiving immunotherapy the development of other allergic diseases later in life. inducing tolerance to aeroallergens. Modern progress has Current preventive interventions, such as early regular led to the development of new drugs that suppress ele- use of emollients in high-risk infants, should be reap- ments of the pathological immune response (mediated praised and probably the future will disclose the opti- by Th2), characteristic of both AD and allergic rhinitis mal strategy to restore epidermal barrier effect - the and asthma. u Th s, in these patients, such drugs would primary event in AD. have a good effect on various comorbidities of the atopic Acknowledgements spectrum, and not only on the cutaneous or respiratory None. manifestations. Authors’ contributions RD and AA have equally contributed to the conceptualization, writing, and Preventive strategies: practice lessons editing of this paper. The author(s) read and approved the final manuscript. Many primary prevention interventions aim to reduce Funding the risk of AD by prophylactically protecting the None. skin barrier, starting at a very young age in high-risk Availability of data and materials infants. The generally recommended preventive inter - Available with the authorship. vention for the development of asthma and atopic Allenova and Darlenski Asthma Research and Practice (2023) 9:1 Page 4 of 4 18. Kelleher MM, Phillips R, Brown SJ, Cro S, Cornelius V, Carlsen KCL, et al. Declarations Skin care interventions in infants for preventing eczema and food allergy. Cochrane Database Syst Rev. 2022;11(11):CD013534. Ethics approval and consent to participate 19. Perkin MR, Logan K, Marrs T, Radulovic S, Craven J, Boyle RJ, et al. Associa- Not applicable. tion of frequent moisturizer use in early infancy with the development of food allergy. J Allergy Clin Immunol. 2021;147(3):967–76 e1. Consent for publication Not applicable. Publisher’s Note Competing interests Springer Nature remains neutral with regard to jurisdictional claims in pub- None. lished maps and institutional affiliations. Received: 30 November 2022 Accepted: 30 January 2023 References 1. Darlenski R, Kazandjieva J, Hristakieva E, Fluhr JW. Atopic dermatitis as a systemic disease. Clin Dermatol. 2014;32(3):409–13. 2. Silverberg JI. Comorbidities and the impact of atopic dermatitis. Ann Allergy Asthma Immunol. 2019;123(2):144–51. 3. Gandhi NA, Pirozzi G, Graham NMH. Commonality of the IL-4/IL-13 path- way in atopic diseases. Expert Rev Clin Immunol. 2017;13(5):425–37. 4. Belgrave DC, Granell R, Simpson A, Guiver J, Bishop C, Buchan I, et al. Developmental profiles of eczema, wheeze, and rhinitis: two population- based birth cohort studies. PLoS Med. 2014;11(10):e1001748. 5. Lack G. Epidemiologic risks for food allergy. J Allergy Clin Immunol. 2008;121(6):1331–6. 6. O’Regan GM, Irvine AD. The role of filaggrin in the atopic diathesis. Clin Exp Allergy. 2010;40(7):965–72. 7. Tham EH, Leung DY. Mechanisms by which atopic dermatitis predisposes to food allergy and the atopic march. Allergy Asthma Immunol Res. 2019;11(1):4–15. 8. Saunes M, Oien T, Dotterud CK, Romundstad PR, Storro O, Holmen TL, et al. Early eczema and the risk of childhood asthma: a prospective, population-based study. BMC Pediatr. 2012;12:168. 9. Carlsten C, Dimich-Ward H, Ferguson A, Watson W, Rousseau R, Dybuncio A, et al. Atopic dermatitis in a high-risk cohort: natural history, associ- ated allergic outcomes, and risk factors. Ann Allergy Asthma Immunol. 2013;110(1):24–8. 10. Capozza K, Funk M, Hering M, Lang J, Merhand S, Manion R, et al. Patients’ and caregivers’ experiences with atopic dermatitis-related burden, medical care, and treatments in 8 countries. J Allergy Clin Immunol Pract. 2023;11(1):264-273.e1. https:// doi. org/ 10. 1016/j. jaip. 2022. 10. 032. Epub 2022 Nov 2. 11. Chiang C, Maibach HI. How many skin barriers haveth we: percutaneous egression of ions? Skin Res Technol. 2022;28(2):382–7. 12. Berents TL, Lodrup Carlsen KC, Mowinckel P, Skjerven HO, Rolfsjord LB, Bradley M, et al. Transepidermal water loss in infancy associated with atopic eczema at 2 years of age: a population-based cohort study. Br J Dermatol. 2017;177(3):e35–e7. 13. Brough HA, Nadeau KC, Sindher SB, Alkotob SS, Chan S, Bahnson HT, et al. Epicutaneous sensitization in the development of food allergy: what is the evidence and how can this be prevented? Allergy. 2020;75(9):2185–205. 14. Celebi Sozener Z, Ozbey Yucel U, Altiner S, Ozdel Ozturk B, Cerci P, Turk M, Re Read ady y to to submit y submit your our re researc search h ? Choose BMC and benefit fr ? Choose BMC and benefit from om: : et al. The external Exposome and allergies: from the perspective of the epithelial barrier hypothesis. Front Allergy. 2022;3:887672. fast, convenient online submission 15. Lack G, Fox D, Northstone K, Golding J, Avon Longitudinal Study of P, Chil- thorough peer review by experienced researchers in your field dren Study T. Factors associated with the development of peanut allergy rapid publication on acceptance in childhood. N Engl J Med. 2003;348(11):977–85. • 16. Papapostolou N, Xepapadaki P, Gregoriou S, Makris M. Atopic dermatitis support for research data, including large and complex data types and food allergy: a complex interplay what we know and what we would • gold Open Access which fosters wider collaboration and increased citations like to learn. J Clin Med. 2022;11(14):4232. maximum visibility for your research: over 100M website views per year 17. Fluhr JW, Darlenski R. Transepidermal water loss ( TEWL). In: Berardesca E, Maibach HI, Wilhelm K-P, editors. Non invasive diagnostic techniques in At BMC, research is always in progress. clinical dermatology. Berlin: Springer Berlin Heidelberg; 2014. p. 353–6. Learn more biomedcentral.com/submissions

Journal

Asthma Research and PracticeSpringer Journals

Published: Feb 10, 2023

Keywords: Eczema; Atopy; Asthma; Atopic march; Treatment

There are no references for this article.