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13 However, evidence was inconsistent regarding the preventive effect of emollient application.
#ADVANCED CARE SYSTEM 12.1 SKIN#
Compelling evidence indicated that emollients render the skin less susceptible to irritants and reduce flares of AD (secondary prevention) 12 and therefore was regarded as a cornerstone of AD therapy. To date, extensive research has been conducted on the therapeutic effect of barrier enhancement using emollients. Meanwhile, the role of epithelial-immune crosstalk in the atopic march needs to be further elucidated. 11 Granted that both the genetic predisposition and the atopic progression contribute to the development of atopic march, longitudinal studies are warranted to explore the impact of immune activation of AD on the development of other Th2 comorbidities. While the severity of subsequent allergic airway inflammation was affected by AD, abrogation of AD by topical treatment prevents worsening of subsequent airway inflammation by counteracting the Th17 pathway.
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10 Similarly, in asthmatic airways, disrupted junctional adhesion, mucus plugging develops due to Th2 polarisation. 7–9 Subsequently, sensitisations to food allergens develop in the setting of Th2 skewing, which is otherwise Th1 skewed in the gastrointestinal-homing T cells in tolerant subjects. Barrier dysfunction from both loss-of-function mutations in filaggrin and the itch-scratch cycle was postulated as the driving component for atopic march programming by promoting Th2 and Th17 differentiation. In the resting state, an intact skin barrier and a balance of immune cell populations, cytokines and chemokines promote immune tolerance, which is otherwise disrupted in AD patients. 5 6 The human skin is a functional immune organ with an abundance of immunocompetent cells. 5 The underlying mechanisms feature both a genetic susceptibility in which barrier dysfunction and immune dysregulation predispose atopic individuals to Th2 immunity, and a progression in which AD and its pathological changes function as instigating events to subsequent development of other atopic comorbidities. 1–4 The sequential occurrence of atopic dermatitis (AD), followed by one or more disorders characterised by allergen-specific type 2 (including T helper 2 (Th2)) responses are designated as atopic march. Biological samples will also be collected longitudinally.Ītopic disorders place a substantial burden on both individuals and the healthcare system. Data collection will be carried out using both electronic and paper questionnaires. Secondary outcomes will include other AD outcomes, atopic march outcomes, knowledge outcomes and other maternal and neonatal outcomes. The primary outcome will be infantile AD cumulative incidence at 2 years postpartum. Participants will be followed for 2 years. The PAEPAD group will receive a multidisciplinary education of neonatal care, including standard education as the control group and additional information on skincare of infants, sun protection, topical corticosteroids and an overview of atopic dermatitis (AD), whereas the standard care group will receive the standard neonatal care education carried out by obstetricians. The participants will be allocated into two groups (ie, the PAEPAD and the standard care group) by random allocation (1:1). Women at high risk for miscarriage or intend to have abortions will be excluded. Randomisation will take place at 30 weeks of gestation. Women aged≥18 years with less than 14+6 weeks of pregnancy who intends to remain resident in Daxing district for at least 2 years postpartum will be entered into the run-in phase. Expecting mothers enlisted in the birth registry of Daxing Teaching Hospital of Capital Medical University and intend to give birth at this location will be screened for eligibility. A total of 2266 expecting mothers will be recruited.
#ADVANCED CARE SYSTEM 12.1 TRIAL#
Methods and analysis This is a single-centre randomised controlled trial of expecting mother–children dyads in Daxing Teaching Hospital of Beijing, China.