Dataset Information

Faltering of prenatal growth precedes the development of atopic eczema in infancy: cohort study.

ABSTRACT:

Background

Infants with atopic eczema have an increased risk of impaired growth, but the origin of this impairment is unclear. The aim of this study was to examine fetal and infant growth in relation to infantile atopic eczema.

Methods

Within the UK Southampton Women's Survey, 1,759 infants with known maternal menstrual data had anthropometric measurements at 11, 19, and 34 weeks' gestation, birth, and ages 6 and 12 months, enabling derivation of growth velocity SD scores. Infantile atopic eczema at ages 6 and/or 12 months was ascertained using modified UK Working Party diagnostic criteria.

Results

Expressed per SD increase, higher femur length and abdominal circumference at 34 weeks' gestation were associated with decreased risks of atopic eczema (eczema OR/SD increase 0.81 [95% CI 0.69-0.96], P=0.017 and 0.78 [95% CI 0.65-0.93], P=0.006, respectively), while every SD increase in head to abdominal circumference ratio (indicating disproportionate growth) was associated with an increase in risk of atopic eczema (1.37 [1.15-1.63], P=0.001). Lower velocities of linear growth from 11 weeks' gestation to birth and birth to age 6 months were associated with atopic eczema (atopic eczema OR/SD increase 0.80 [0.65-0.98], P=0.034 and 0.8 [1 0.66-1.00], P=0.051, respectively). Infants with atopic eczema at age 12 months had a larger head circumference in early gestation and faltering of abdominal growth velocity from 19 to 34 weeks' gestation (atopic eczema OR/SD increase 0.67 [0.51-0.88], P=0.003).

Conclusion

Infants with atopic eczema demonstrate altered patterns of fetal growth, including faltering of linear growth in utero, prior to the clinical onset of atopic eczema. These findings suggest growth falters prior to the start of clinical atopic eczema and its treatment.

SUBMITTER: El-Heis S

PROVIDER: S-EPMC6296686 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Publications

Faltering of prenatal growth precedes the development of atopic eczema in infancy: cohort study.

El-Heis Sarah S Crozier Sarah R SR Healy Eugene E Robinson Sian M SM Harvey Nicholas C NC Cooper Cyrus C Inskip Hazel M HM Baird Janis J Godfrey Keith M KM

Clinical epidemiology 20181212

<h4>Background</h4>Infants with atopic eczema have an increased risk of impaired growth, but the origin of this impairment is unclear. The aim of this study was to examine fetal and infant growth in relation to infantile atopic eczema.<h4>Methods</h4>Within the UK Southampton Women's Survey, 1,759 infants with known maternal menstrual data had anthropometric measurements at 11, 19, and 34 weeks' gestation, birth, and ages 6 and 12 months, enabling derivation of growth velocity SD scores. Infanti ...[more]

PMID: 30588116

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Project description:Background: Atopic eczema (AE) is a common chronic inflammatory skin disorder. In order to dissect the genetic background several linkage and genetic association studies have been performed. Yet very little is known about specific genes involved in this complex skin disease, and the underlying molecular mechanisms are not fully understood. Results: We used human DNA microarrays to identify a molecular picture of the programmed responses of the human genome to AE. The transcriptional program was analyzed in skin biopsy samples from lesional and patch-tested skin from AE patients sensitized to Malassezia sympodialis (M. sympodialis), and corresponding biopsies from healthy individuals. The most notable feature of the global gene-expression pattern observed in AE skin was a reciprocal expression of induced inflammatory genes and repressed lipid metabolism genes. The overall transcriptional response in M. sympodialis patch-tested AE skin was similar to the gene-expression signature identified in lesional AE skin. In the constellation of genes differentially expressed in AE skin compared to healthy control skin, we have identified several potential susceptibility genes that may play a critical role in the pathological condition of AE. Many of these genes, including genes with a role in immune responses, lipid homeostasis, and epidermal differentiation, are localized on chromosomal regions previously linked to AE. Conclusion: Through genome-wide expression profiling, we were able to discover a distinct reciprocal expression pattern of induced inflammatory genes and repressed lipid metabolism genes in skin from AE patients. We found a significant enrichment of differentially expressed genes in AE with cytobands associated to the disease, and furthermore new chromosomal regions were found that could potentially guide future region-specific linkage mapping in AE. A disease state experiment design type is where the state of some disease such as infection, pathology, syndrome, etc is studied. Disease State: Skin biopsies from normal ('normal') and lesional and patch-tested ('leisonal') skin from Atopic eczema patients sensitized to Malassezia sympodialis Organism Part: location of skin biopsy Keywords: disease state analysis

Dataset Information

Faltering of prenatal growth precedes the development of atopic eczema in infancy: cohort study.

Background

Methods

Results

Conclusion

Publications

Faltering of prenatal growth precedes the development of atopic eczema in infancy: cohort study.

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