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Severe skin inflammation and filaggrin mutation similarly alter the skin barrier in patients with atopic dermatitis
Author(s) -
Mócsai G.,
Gáspár K.,
Nagy G.,
Irinyi B.,
Kapitány A.,
Bíró T.,
Gyimesi E.,
Tóth B.,
Maródi L.,
Szegedi A.
Publication year - 2014
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.12743
Subject(s) - filaggrin , scorad , atopic dermatitis , haploinsufficiency , medicine , sensitization , inflammation , dermatology , spongiosis , immunology , biology , phenotype , psoriasis , biochemistry , dermatology life quality index , gene
Summary Background Filaggrin ( FLG ) deficiency is a well‐known predisposing factor for the development of atopic dermatitis ( AD ). Decreased FLG expression can be the result of haploinsufficiency or severe inflammation, which can cause acquired FLG alterations. FLG mutations are related to several clinical and laboratory parameters of AD ; however, some recent data seem to contradict these associations. Objectives Our aim was to determine which clinical and biochemical parameters are connected to FLG haploinsufficiency and which ones are also associated with acquired FLG alterations due to severe skin symptoms in patients with AD . Methods We introduced a novel classification of patients with AD , based on FLG mutations and SCORAD ( SCOR ing Atopic Dermatitis). Based on these parameters, we created three groups of patients with AD : mild‐to‐moderate wild‐type (A), severe wild‐type (B) and severe mutant (C). In all groups, we assessed laboratory and clinical parameters and performed immunohistochemical analyses. Results Groups B and C contained patients with equally severe symptoms based on the SCORAD . The two severe groups did not differ significantly with respect to barrier‐specific parameters, whereas group A had significantly better results for the barrier function measurements. However, significant differences were detected between groups B and C with respect to the allergic sensitization‐specific parameters. Conclusions These findings suggest that skin barrier function correlates with the severity of skin inflammation and can be equally impaired in patients with FLG mutant‐ and wild‐type AD with severe symptoms. Nevertheless, our results also suggest that patients with FLG mutant‐type AD may have a higher risk of allergic sensitization compared with patients with the wild‐type.