should be considered when assessing the burden of AD on child and family.4 The social stigma of a visible skin condition can cause distress, anxiety, and embarrassment, which may result in limited social interactions, poor self-esteem, and lack of self-confidence.5
The etiology of AD involves complex skin barrier gene/environment interactions that undermine the structural and functional integrity of the skin barrier and its immune function.7-9 Early recognition of environmental risk factors and their exposure reduction may mitigate AD and support its prevention.5,7-9
The current review aims to explore early intervention in infants and young children with eczema and AD-prone skin by improving skin barrier function and controlling inflammation at the earliest time point using a moisturizer and a proactive treatment. This approach may help prevent AD and/or control its evolution; by slowing the atopic march with better control of sensitization emergence, early intervention may provide rapid and possible lasting improvement.5
Atopic Dermatitis Impacts Patients and Families
A cost-effectiveness analysis evaluated the average costs of total-body daily moisturizer application with one of seven commonly used moisturizers from birth to 6 months of age.10 The authors concluded that daily moisturiser use may represent a cost-effective, preventative strategy to reduce the burden of AD.10
A 2016 study surveyed 82 caretakers of children aged 6 months to 12 years with moderate to severe AD between 2011–2013 and asked questions about direct and indirect expenses.11 The authors reported a mean monthly personal cost of AD of US $274, with a high proportion spent on over the counter products, especially moisturizers.11 Indirect costs comprised the largest portion of the cost, with an average of US $199 expended due to lost caregiver workdays.11
AD significantly impacts patients and their families’ quality of life, burdening them financially and emotionally.12 Financial expenses can be divided into direct and indirect costs: Direct costs could include prescriptions, over-the-counter treatments, physician visits and hospitalizations, while indirect costs can consist of absenteeism from school or work, decreased productivity, and emotionally decreased quality of life.13
AD has profound effects on the lives of children due to scratching, pain, and sleep difficulties and is associated with secondary effects on caregivers.14 Reports have shown patients with AD have difficulties with sleep, work, and interpersonal relationships.4 AD is also associated with potential risk factors for obesity and high blood pressure, chronic inflammation, sleep disturbances, and mental health comorbidities, including suicide.14
Atopic Dermatitis Development in Early Childhood
The first phase or initial phase of AD commonly occurs in early childhood and may present without signs of sensitization; this phase is also referred to as non-atopic or intrinsic AD.5 A genetically predisposed child may present with non-pathological xerosis only, in the absence of positive specific serum immunoglobulin E (IgE) serology.5 The atopic child, in a second phase, also called true or extrinsic AD, presents as sensitive to allergens in the presence of an IgE response to environmental allergens, such as aeroallergens.5 There is a third phase, also referred to as auto-allergic AD, which only seems to affect those patients suffering from AD with sensitization and is characterized by the appearance of IgE response to endogenous proteins. This third phase involve very severe forms of AD.
AD may be regarded as a lifelong condition in which defects of the epidermal barrier play a central role (Figure 1).15,16 AD has been described as having genetic predispositions, including null mutations in FLG and having reactions to environmental triggers, climate, urban living, and diet.8,9,15
Kelleher and colleagues17 evaluated infants at 6 and 12 months of age for the presence of AD and assessed disease severity using SCORing Atopic Dermatitis (SCORAD) at 6 months and both SCORAD and Nottingham Severity Score (NSS) at 12 months. A total of 1903 infants were enrolled in the study and 1300 infants were genotyped for filaggrin (FLG) mutations. At 6 months, 18.7% of the infants presented with AD, and at 12 months, 15.53% had symptoms. The researchers concluded that enhanced TEWL at birth and at 2 months was shown to precede clinical AD.15
An infant’s stratum corneum (SC) is not fully developed and has an elevated pH of approximately 6.0, which acidifies in order to reach a physiological pH range of (4.1–5.8). During the first year of life, the SC‘s function and thickness will develop gradually.16 An in-vivo study on the physiology of infant epidermal skin and its adaptation after birth investigated the molecular composition of the SC and its water content using Raman spectroscopy, as well as non-invasive assays for measurement of transepidermal water loss (TEWL), SC hydration and skin surface pH.18 The 108 subjects were divided into six age groups: Full-term newborns (1–15 days), babies aged 5–6 weeks, babies aged 6±1 months, children aged 1–2 years, children aged 4–5 years and adults aged 20–35 years. The study showed skin surface acidification and changes in hydration take place during the first weeks after birth.18 A decreased water content was observed in newborns compared to all age groups.18 The investigators concluded that dynamic changes in the amount of natural moisturizing factor (NMF) take place during infancy, with lowest NMF amounts occurring at 6 months.18
A further study evaluated the maturation and organization of
The etiology of AD involves complex skin barrier gene/environment interactions that undermine the structural and functional integrity of the skin barrier and its immune function.7-9 Early recognition of environmental risk factors and their exposure reduction may mitigate AD and support its prevention.5,7-9
The current review aims to explore early intervention in infants and young children with eczema and AD-prone skin by improving skin barrier function and controlling inflammation at the earliest time point using a moisturizer and a proactive treatment. This approach may help prevent AD and/or control its evolution; by slowing the atopic march with better control of sensitization emergence, early intervention may provide rapid and possible lasting improvement.5
Atopic Dermatitis Impacts Patients and Families
A cost-effectiveness analysis evaluated the average costs of total-body daily moisturizer application with one of seven commonly used moisturizers from birth to 6 months of age.10 The authors concluded that daily moisturiser use may represent a cost-effective, preventative strategy to reduce the burden of AD.10
A 2016 study surveyed 82 caretakers of children aged 6 months to 12 years with moderate to severe AD between 2011–2013 and asked questions about direct and indirect expenses.11 The authors reported a mean monthly personal cost of AD of US $274, with a high proportion spent on over the counter products, especially moisturizers.11 Indirect costs comprised the largest portion of the cost, with an average of US $199 expended due to lost caregiver workdays.11
AD significantly impacts patients and their families’ quality of life, burdening them financially and emotionally.12 Financial expenses can be divided into direct and indirect costs: Direct costs could include prescriptions, over-the-counter treatments, physician visits and hospitalizations, while indirect costs can consist of absenteeism from school or work, decreased productivity, and emotionally decreased quality of life.13
AD has profound effects on the lives of children due to scratching, pain, and sleep difficulties and is associated with secondary effects on caregivers.14 Reports have shown patients with AD have difficulties with sleep, work, and interpersonal relationships.4 AD is also associated with potential risk factors for obesity and high blood pressure, chronic inflammation, sleep disturbances, and mental health comorbidities, including suicide.14
Atopic Dermatitis Development in Early Childhood
The first phase or initial phase of AD commonly occurs in early childhood and may present without signs of sensitization; this phase is also referred to as non-atopic or intrinsic AD.5 A genetically predisposed child may present with non-pathological xerosis only, in the absence of positive specific serum immunoglobulin E (IgE) serology.5 The atopic child, in a second phase, also called true or extrinsic AD, presents as sensitive to allergens in the presence of an IgE response to environmental allergens, such as aeroallergens.5 There is a third phase, also referred to as auto-allergic AD, which only seems to affect those patients suffering from AD with sensitization and is characterized by the appearance of IgE response to endogenous proteins. This third phase involve very severe forms of AD.
AD may be regarded as a lifelong condition in which defects of the epidermal barrier play a central role (Figure 1).15,16 AD has been described as having genetic predispositions, including null mutations in FLG and having reactions to environmental triggers, climate, urban living, and diet.8,9,15
Kelleher and colleagues17 evaluated infants at 6 and 12 months of age for the presence of AD and assessed disease severity using SCORing Atopic Dermatitis (SCORAD) at 6 months and both SCORAD and Nottingham Severity Score (NSS) at 12 months. A total of 1903 infants were enrolled in the study and 1300 infants were genotyped for filaggrin (FLG) mutations. At 6 months, 18.7% of the infants presented with AD, and at 12 months, 15.53% had symptoms. The researchers concluded that enhanced TEWL at birth and at 2 months was shown to precede clinical AD.15
An infant’s stratum corneum (SC) is not fully developed and has an elevated pH of approximately 6.0, which acidifies in order to reach a physiological pH range of (4.1–5.8). During the first year of life, the SC‘s function and thickness will develop gradually.16 An in-vivo study on the physiology of infant epidermal skin and its adaptation after birth investigated the molecular composition of the SC and its water content using Raman spectroscopy, as well as non-invasive assays for measurement of transepidermal water loss (TEWL), SC hydration and skin surface pH.18 The 108 subjects were divided into six age groups: Full-term newborns (1–15 days), babies aged 5–6 weeks, babies aged 6±1 months, children aged 1–2 years, children aged 4–5 years and adults aged 20–35 years. The study showed skin surface acidification and changes in hydration take place during the first weeks after birth.18 A decreased water content was observed in newborns compared to all age groups.18 The investigators concluded that dynamic changes in the amount of natural moisturizing factor (NMF) take place during infancy, with lowest NMF amounts occurring at 6 months.18
A further study evaluated the maturation and organization of
