Filaggrin (FLG) polymorphism appears to be linked with Molluscum contagiosum virus skin infection in children with atopic dermatitis (AD), reported Sara Manti, MD, of the University of Messina (Italy), and her associates.
“To the best of our knowledge, this is the first study” to describe this association, they said.
In an Italian study of 100 children with AD and 97 healthy children who served as controls, both clinical and laboratory data showed that FLG gene mutations were linked to early AD onset, a more severe clinical course of disease, and a significantly higher risk of Molluscum contagiosum virus (MCV)–associated skin infection.
In terms of the clinical onset of AD, the investigators also found that some FLG variants “exclusively predisposed” patients to early (less than 3 months), intermediate (3-6 months), or late (greater than 6 months) onset of disease. This revealed that the FLG mutations likely played a role in AD chronicity, especially in severe disease. Additionally, the researchers found that AD patients with specific FLG variants were more likely to have moderate and severe Scoring Atopic Dermatitis (SCORAD) indexes.The data “suggest that FLG gene may serve as a potential biomarker to screen the atopic population, identifying patients at high risk of AD, to adopt preventive measures that can restore the barrier function of the skin and reduce patients’ susceptibility to recurrent skin infection,” they wrote. “Our findings also indicate that the identified SNPs [single-nucleotide polymorphisms] might have clinically relevant implications with respect to a major MCV [M. contagiosum virus] colonization of skin, also permitting the identification of a new AD phenotype in children. However, to date, because of the existence of controversial data, we believe that further and needed insights into AD pathophysiology may also be gained by studying people with the FLG gene who do not have atopic predisposition and/or AD. Thus, a large population-based study is necessary to further validate these early interpretations and to gain detailed information about the role of FLG variants,” Dr. Manti and her coinvestigators concluded.
Read more in Manti S et al. Ann Allergy Asthma Immunol. 2017;119:446-51 .
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