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REVIEW ARTICLE Atopic dermatitis and the atopic march revisited S. C. Dharmage1,2, A. J. Lowe1,2, M. C. Matheson1, J. A. Burgess1, K. J. Allen2 M. J. Abramson3 1Centre for Molecular, Environmental, Genetic Analytic (MEGA) Epidemiology, School of Population and Global Health, The University of Melbourne, Carlton; 2Murdoch Childrens Research Institute Royal Children’s Hospital, Parkville; 3School of Public Health Preventive Medicine, Monash University, Melbourne, Vic., Australia To cite this article: Dharmage SC, Lowe AJ, Matheson MC, Burgess JA, Allen KJ, Abramson MJ. Atopic dermatitis and the atopic march revisited. Allergy 2014; 69: 17–27. Keywords allergic rhinitis; asthma; atopic dermatitis; atopic march; eczema. Correspondence Prof. Shyamali C. Dharmage, Centre for Molecular, Environmental, Genetic Analytic (MEGA) Epidemiology, School of Population Health, The University of Melbourne, 207, Bouverie Street, Carlton, Vic. 3052, Australia. Tel.: +61 3 8344 0737 Fax: +61 3 9349 5815 E-mail: s.dharmage@unimelb.edu.au Accepted for publication 15 August 2013 DOI:10.1111/all.12268 Edited by: Thomas Bieber Abstract Atopic dermatitis (AD) has become a significant public health problem because of increasing prevalence, together with increasing evidence that it may progress to other allergic phenotypes. While it is now acknowledged that AD commonly pre- cedes other allergic diseases, a link termed ‘the atopic march’, debate continues as to whether this represents a causal relationship. An alternative hypothesis is that this association may be related to confounding by familial factors or phenotypes that comanifest, such as early-life wheeze and sensitization. However, there is increasing evidence from longitudinal studies suggesting that the association between AD and other allergies is independent of confounding by comanifest allergic phenotypes. The hypotheses on plausible biological mechanisms for the atopic march focus on defective skin barrier function and overexp