Researchers have identified an immune and lipid profile on the surface of the skin of infants that can predict the development of atopic dermatitis (AD) months before the onset of clinical illness.
The findings were published in the Journal of Allergy and Clinical Immunology.
“The holy grail to deal with atopic dermatitis is to prevent it,” said the study’s senior author Donald Leung, MD, PhD, in a press release. “It tends to come back when you treat it, so we really have to examine how to avoid getting it.” Dr. Leung is the division head of Pediatric Allergy and Clinical Immunology at National Jewish Health in Denver.
The researchers partnered with hospitals in the Republic of Korea, where physicians used non-invasive skin tapes to collect samples from the forearms of babies who were two months old, before signs of clinical AD typically present.
Study participants included those with and without a family history of atopic diseases. The babies were clinically monitored from birth until they reached age two years. Their skin cells were collected beginning at two months of age and were analyzed by mass spectrometry in the laboratory of Evgeny Berdyshev, PhD. Dr. Berdyshev is the lead author of the study and the head of the mass spectrometry laboratory at National Jewish Health who pioneered this analytical assay.
Overall, 22 of 74 (29.7%) infants in the risk group and five of 37 (13.5%) in the control group developed AD.
The researchers found decreased levels of protein-bound ceramides in the stratum corneum of infants who went on to develop AD. Unsaturated sphingomyelin species, “short-chain” NS- and AS-ceramides were elevated in the skin of these children compared to healthy children.
Thymic stromal lymphopoietin (TSLP) and interleukin-13 (IL-13) levels were also increased in the stratum corneum of future AD subjects.
Statistical analysis revealed that a combination of family history, type 2 cytokines and dysregulated lipids had a strong power for predicting AD.
“In order for us to introduce an effective preventative therapy, we must know the skin abnormalities before patients develop clinical rash. Now that we’ve discovered the biomarkers IL-13 and TSLP, we can find ways to prevent eczema by using targeted therapies, such as emollients or other biologics,” said Dr. Leung. “The disease begins because the skin barrier is leaky and allows allergens to come in through the skin. An abnormal skin barrier doesn’t protect a patient from environmental hazards.”
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