27. The Skin Barrier in Atopic Dermatitis

  1. Alan D. Irvine MD, FRCPI, FRCP3,4,
  2. Peter H. Hoeger MD5,6 and
  3. Albert C. Yan MD, FAAP, FAAD7,8
  1. Simon G. Danby PhD, BSc (Hon)1 and
  2. Michael J. Cork BSc, MB, PhD, FRCP1,2

Published Online: 24 MAY 2011

DOI: 10.1002/9781444345384.ch27

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

How to Cite

Danby, S. G. and Cork, M. J. (2011) The Skin Barrier in Atopic Dermatitis, in Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition (eds A. D. Irvine, P. H. Hoeger and A. C. Yan), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444345384.ch27

Editor Information

  1. 3

    Trinity College, Dublin, Ireland

  2. 4

    Our Lady's Children's Hospital, Dublin, Ireland

  3. 5

    University of Hamburg, Hamburg, Germany

  4. 6

    Catholic Children's Hospital Wilhelmstift, Hamburg, Germany

  5. 7

    University of Pennsylvania School of Medicine, Philadelphia, PA, USA

  6. 8

    The Children's Hospital of Philadelphia, Philadelphia, PA, USA

Author Information

  1. 1

    The Academic Unit of Dermatology Research, Department of Infection and Immunity, The University of Sheffield, Sheffield, UK

  2. 2

    The Paediatric Dermatology Clinic, Sheffield Children's Hospital, Sheffield, UK

Publication History

  1. Published Online: 24 MAY 2011
  2. Published Print: 3 JUN 2011

ISBN Information

Print ISBN: 9781405176958

Online ISBN: 9781444345384



  • atopic dermatitis;
  • stratum corneum;
  • desquamation;
  • protease;
  • kallikrein;
  • pH;
  • filaggrin;
  • differentiation;
  • TEWL


Atopic dermatitis (AD) is a chronic, inflammatory disease of the skin characterised by xerosis, pruritus and erythematous lesions with increased trans-epidermal water loss (TEWL). AD is associated with a skin barrier defect, which permits the entry of irritants and allergens. Variants within three groups of genes, encoding structural proteins, degradatory proteases and protease inhibitors, predispose to a defective skin barrier. Environmental factors including exposure to house dust mite allergens, the use of soap and detergents and bacterial colonisation interact with these genetic factors to exacerbate skin barrier breakdown. At sites of natural predisposition, where the skin barrier is thinnest, gene-gene and gene-environment factors synergise to create optimum conditions for enhanced skin barrier breakdown. The risk of developing AD is greatest during infancy where the skin barrier is undergoing a period of development and optimisation.