Official websites use. Share sensitive information only on official, secure websites. Correspondence: laura. Here, we review current evidence suggesting a systemic impact of the cutaneous inflammation in AD together with a higher risk of asthma and other comorbidities, especially in severe and persistent AD.
Thus, early therapy of AD to restore the impaired skin barrier, modified microbiome, and target type 2 inflammation, depending on the endo phenotype, in a tailored approach is crucial.
We discuss what we can learn from the comorbidities and the implications for preventive and therapeutic interventions from precision dermocosmetics to precision medicine. Keywords: asthma, atopic dermatitis, atopic march, biologic therapies, comorbidities, dermocosmetics, emollient, immunity, precision medicine, systemic disease.
The inherent complexity of genetic factors, environmental influences, skin barrier dysfunction, immune dysregulation, microbial dysbiosis, as well as the resulting cutaneous inflammation and its potential systemic impact, are not fully understood. Furthermore, the complex pathophysiology of AD may lead to atopic and non-atopic comorbidities. AD is considered the starting point of the atopic march, leading to the development of comorbidities such as asthma, food allergies FA , and allergic rhinitis AR [ 4 , 5 ].
Experiments in different mouse models [ 6 , 7 ] have suggested that genetics, epigenetics, and non-type 2 unspecific inflammation from the innate immune response likely con-tribute to the pathophysiologic makeup of the initial phase of AD in the early years. Loss of barrier integrity has been hypothesized to enable penetration of allergens, pollutants and microbes, and initiation of an inflammatory immune cascade of events leading to sensitization and a proinflammatory atopic state.
