Disease Trajectories in Childhood Atopic Dermatitis

An Update and Practitioner's Guide

A.D. Irvine; P. Mina-Osorio


The British Journal of Dermatology. 2019;181(5):895-906. 

In This Article


Associating specific observable AD phenotypes with a risk of disease progression or the development of comorbidities is relevant to clinical practice, as it has a profound impact on disease management. For instance, there is growing evidence that early restoration of skin barrier function could have an impact on the long-term prevention of AD,[104,105] and early referral or multidisciplinary management of patients at high risk of developing comorbidities would have a positive impact on patient care.[106]

Although clustering of atopic comorbidities is well recognized, the typical longitudinal atopic march occurs only in a small proportion of patients. Despite the absence of conclusive data to allow for precise prediction of the risk of AD progression, we have collated data on disease trajectories from various cohort studies to provide some guidance to practitioners for identifying infants and children with AD who may be at risk of developing other allergic diseases. In addition, we have presented a practitioner's guide, based on current data, to estimate the risk of patients with AD developing subsequent comorbid asthma and rhinitis.

Importantly, one of the most frequently identified risk factors for disease persistence and development of comorbidities, regardless of the methodology, is early-onset severe disease in patients with a family history of allergy.

Because patients with severe disease are typically under-represented in birth cohorts, trajectories of disease progression cannot be derived from birth cohorts alone. Longitudinal studies of patients with severe AD are needed,[7,57,75] especially those including identification of biomarkers of disease progression that could help clinicians more reliably identify patients at high risk.[107,108] For example, recent advances in AD research, including the use of systems biology, have led to the identification of a 'double switch', which provides mechanistic insights into common AD phenotypes, possibly explaining disease severity and the frequency of flares.[72]