Atopic eczema or atopiform dermatitis.
Age period prevalence of atopic eczema (AE), a very common skin disease, has increased during the past decennia. This expansion seems to be ending in wealthy countries, while an increase is observed in developing nations, for which there is no firm explanation. Recent steps in understanding AE are the detection of skin barrier related filaggrin null mutations in approximately 25% of patients and the recognition of IL-31 as a molecule possibly involved in the itch (pruritus). Also interesting are the recognition of thymus and activation-regulated chemokine (TARC) and proliferating-inducing ligand (APRIL), as being associated with AE severity and activity. Immunocentric and corneocentric views on pathogenesis (the inside-outside paradigm) and the diagnostic entity atopiform dermatitis (AFD) are discussed here. We emphasize that diagnosing AE is not simple but challenging. We accentuate that a diagnosis of AE is only possible when there is allergen-specific IgE. Advice as to the need for elimination of allergens and adjustment of lifestyle are only proficient in patients having atopy and true AE, not in those having AFD.
Bos
Jan D
JD
Department of Dermatology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. j.d.bos@amc.uva.nl
Brenninkmeijer
Elian E A
EE
Schram
Mandy E
ME
Middelkamp-Hup
Maritza A
MA
Spuls
Phyllis I
PI
Smitt
J Henk Sillevis
JH
D003876:Dermatitis, Atopic / Q000175:diagnosis* / Q000453:epidemiology / Q000503:physiopathology / Q000628:therapy; D003937:Diagnosis, Differential; D000091344:Filaggrin Proteins; D006801:Humans; D007073:Immunoglobulin E / Q000276:immunology; D009626:Terminology as Topic
C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007073:Immunoglobulin E