Researchers review current knowledge on the management of flares in atopic dermatitis, including treatment and unmet needs.
Atopic dermatitis (AD) is characterized by a chronic remitting course, in which patients experience either minimal changes in symptoms over time or fluctuatations with periods of remission interrupted by acute exacerbations, also known as flares.
Despite being an integral part of the AD disease course, flares have been considered as solely a side effect of chronic disease in prior research, noted authors of a review published in Therapeutic Advances in Chronic Disease.
“Management of flares is crucial since their prevention is a key aim of long-term disease control. Nevertheless, difficulties related to this aspect are several, starting from the definition of flare itself, which is not always satisfactory or unambiguous, and needs clarification,” the researchers noted. “Deepening our knowledge on flares could be highly relevant to both clinicians and patients to provide adequate control of the disease through patient education and appropriate treatment.”
Seeking to improve comprehension of AD flares, they investigated research on the management of flares from definition to treatment, highlighted aspects that are still unclear, and identified any necessary unmet needs to better manage AD.
Researchers first conducted a systematic review of 22 AD flare definitions, in which none were indicated to have validation studies. “In 2020, the European Task Force of Atopic Dermatitis defined flare as an ‘acute, clinically significant worsening of signs and symptoms of AD requiring therapeutic intervention,‘” they noted.
They next explored flare triggering factors, including endogenous and environmental exposures. Besides inflammatory cytokines, such as interleukin (IL)-6 and IL-1, skin keratinocytes and fibroblasts were noted to also secrete cortisol, adrenocorticotropic and corticotropin-releasing hormones, and signal peptides upon stress—actively taking part in the onset and progression of flares.
“Stressors, either internal (ie, bacterial infections) or external (ie, psychological), have also been reported to impair the skin barrier function favoring a T helper type 2 cell/allergic response and may induce AD flare,” they added.
“Exposure to environmental factors in predisposed individuals may trigger AD flare by acting as pruritogens and irritants and can lead to the upregulation of inflammatory processes and deterioration of the skin barrier function.”
In lastly investigating clinical management and prevention of flares, the authors posited that strategies should consider clinical, pathogenic, and individual variability, and must target flare prevention. Recommended treatment strategies for AD should depend on disease severity, they said, with particular attention to difficult-to-treat areas.
Beyond disease severity, researchers noted that appropriate skin care must be adhered to, “with the use of emollients and mild skin cleansers providing the basis for continued skincare and addressing the dysfunctional epidermal barrier with hydrating/lubricating topical treatment, along with patient education programs and the avoidance of trigger factors.”
Regarding preventive strategies, a proactive approach was touted, but this is complicated by the lack of comparator studies identifying which class of topical anti-inflammatory therapy is more effective.
In concluding, researchers said that further research is warranted on how best to capture data on AD flares in real time and whether patient-reported outcome measures are superior for defining flares vs investigator-led assessment at scheduled clinical visits.
Girolomoni G, Busà VM. Flare management in atopic dermatitis: from definition to treatment. Ther Adv Chronic Dis. Published online January 13, 2022. doi:10.1177/20406223211066728