Benea Vasile MD
Clinical Hospital for Infectious and Tropical Diseases “Victor Babeş” Bucharest
What’s new in atopic dermatitis?
Author: Vasile Benea
Atopic dermatitis is a common inflammatory skin disease affecting up to 25% of children and up to 10% of adults in Western industrialized countries. With each year, more advances have been made in regard to understanding the pathophysiology of the disease and developing more targeted therapies.
Atopic dermatitis is a complex multifactorial disease encompassing defects in skin architecture, immune dysregulation, and skin flora changes. Gene polymorphisms and mutations are associated with defects of the epidermal barrier function and are crucial in patients. In adults, the acute phase is characterized by a strong T helper 2/T helper 22 activation and the contribution of T helper 17 cells, whereas the chronic phase by a marked T helper 1 polarization, although the T helper 2 pathway had still an important role. More T helper 17-related cytokines and antimicrobial peptides were detectable in the skin of atopic dermatitis children than in the skin of adults. Human skin is densely colonized by a variety of natural flora (microbiome) influenced by the host and the surrounding environment. In atopic dermatitis (AD), the skin microbiome is dominated by Staphylococcus aureus and less diverse than in healthy skin.
There’s a significantly increased risk for major comorbidities in adult patients with atopic dermatitis; the risk difference was predominantly found in patients with severe disease and among smokers.
The standard treatment of atopic dermatitis focuses on the severity of skin inflammation and consists of topical treatment with corticosteroids and calcineurin inhibitors, ultraviolet light or systemic immunosuppression. A new step forward was made with the introduction, in 2017, of dupilumab (which binds to the α-subunit of the IL-4 receptor, part of both the IL-4 and IL-13 receptor complex) in the treatment of adult atopic dermatitis. There are a lot of new agents in the pipeline: the interleukin 13 inhibitors; Janus kinase inhibitors; phosphodiesterase 4 inhibitors; TRPV1 (transient receptor potential cation channel subfamily V member 1) inhibitors; neurokinin 1 inhibitors; T-cell inhibitors; arachidonic acid, leukotriene, and prostaglandin inhibitors; 5HT2B antagonists; antihistamines, etc.