|Year : 2019 | Volume
| Issue : 1 | Page : 7-8
Sr. Divisional Medical Officer Central Railway, Mumbai, Maharashtra, India
|Date of Web Publication||14-Mar-2019|
Dr. Dipti Jain
Sr. Divisional Medical Officer Central Railway, Mumbai, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Jain D. Atopic March. J Mahatma Gandhi Inst Med Sci 2019;24:7-8
“Much of what happens to us later in life is related to the exposures we encounter in early childhood,” said Sears.
Atopy is defined as a personal or familial propensity to produce IgE antibody and sensitization in response to the environmental triggers. The classical triad of atopic dermatitis (AD) or eczema, rhinitis, and asthma existing in the same child is more common than expected. In the International Study of Asthma and Allergies in Childhood, among the 56 countries, the prevalence of AD in children varied significantly from 0.3% to 20.5% but shows consistent trends in increasing disease prevalence over time. In India, the prevalence has been found to be 0.01% in North India and <5% in South India.
The term “Atopic March” (or “Allergic March”) refers to the natural history of atopic manifestations, which is characterized by a typical sequence of IgE antibody responses and clinical symptoms which may appear early in life, persist over years or decades and often remit spontaneously. It is supported by various cross-sectional and longitudinal studies. Atopic dermatitis is usually the first manifestation of the atopic diathesis. Occurring in genetically predisposed children, 80% of children with AD eventually develop allergic rhinitis and/or asthma later in childhood.
Ongoing studies about this classical triad suggested numerous pathophysiological mechanisms, including cyclic nucleotide regulatory abnormalities, immune cell alterations, and inflammatory and allergic triggers. This means that these diseases share causal mechanism. IgE sensitization though is independently associated with AD, rhinitis, and asthma, accounts only for 38% of comorbidity. That means IgE sensitization does not play a dominant causal role in the comorbidity of these diseases. It is further noted in a longitudinal study that early onset and persistent AD is associated with risk of other atopic diseases and sensitization to food and aeroallergens by the age of 7 years.
These recent genetic studies support strongly the role of filaggrin in the pathogenesis of AD and subsequent progression in the atopic march. A significant association is observed between the filaggrin gene mutations with asthma and allergic rhinitis, but only seen in subjects with the coexistence of AD. The filaggrin gene mutation causes epithelial barrier defect and reduced defense mechanisms that allow easy entry for pathogens, allergens, and other environmental insults (toxins, irritants, and pollutants), followed by enhanced Th2 lymphocyte responses with resultant chronic inflammation. Thus, filaggrin mutations seem likely to play a role in chronicity of the disease and IgE sensitization in patients with AD. It is further observed that the expression of filaggrin gene is downregulated in the skin with AD by Th2 cytokines (IL-4 and IL-13), suggesting that filaggrin defects can develop as an acquired and/or genetic defect.
Lung function trajectory in another study has demonstrated significant lung function impairment among subjects with asthma, AD, and allergic rhinitis from birth to 16 years of age, suggesting the onset of disease in utero rather than simply allergic sensitization.
The recent prospective Canadian Healthy Infant Longitudinal Development (CHILD) study evaluated the presence of AD sensitization at the age of 1 year and performed the clinical assessment at the age of 3 years for the presence of other atopic disorders like asthma, allergic rhinitis along with AD. It is observed that the children who have AD or eczema at the age of 1 year and who are sensitized to an allergen are seven times more likely to develop asthma than other infants. They are also more likely to have a food allergy at the age of 3 years.
Another significant finding which contradicts the previous medical advice to the parents to avoid cow's milk products, egg, and peanut during the 1st year recommends early introduction of these articles since it is beneficial in promoting tolerance and reducing risk of food sensitization and food allergy.
Dr. Anita Kozyrskyj, a CHILD investigator, found that children born to pregnant Caucasian mothers with asthma had the highest risk for developing asthma in early childhood and through further research concluded that it may not be genetic factor alone; it may also involve the gut microbiome with specific characteristics. She observed a significant reduction in the family of microbes called Lactobacillus in Caucasian babies born to asthmatic mothers, particularly if they had allergies or were overweight. With this research, it may be possible in the future to prevent asthma by modifying the gut microbiome. However, she cautioned that it is too early for the parents seeking probiotic treatment for their infants at this stage.
| References|| |
Carlsten C, Dimich-Ward H, Ferguson A, Watson W, Rousseau R, Dybuncio A, et al.
Atopic dermatitis in a high-risk cohort: Natural history, associated allergic outcomes, and risk factors. Ann Allergy Asthma Immunol 2013;110:24-8.
Asher MI, Montefort S, Björkstén B, Lai CK, Strachan DP, Weiland SK, et al.
Worldwide time trends in the prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and eczema in childhood: ISAAC phases one and three repeat multicountry cross-sectional surveys. Lancet 2006;368:733-43.
Kanwar AJ, De D. Epidemiology and clinical features of atopic dermatitis in india. Indian J Dermatol 2011;56:471-5.
] [Full text]
Zheng T, Yu J, Oh MH, Zhu Z. The atopic march: Progression from atopic dermatitis to allergic rhinitis and asthma. Allergy Asthma Immunol Res 2011;3:67-73.
Lødrup Carlsen KC, Mowinckel P, Hovland V, Håland G, Riiser A, Carlsen KH, et al.
Lung function trajectories from birth through puberty reflect asthma phenotypes with allergic comorbidity. J Allergy Clin Immunol 2014;134:917-23.e7.