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Abstract Introduction Treatments for atopic dermatitis (AD) often fail to achieve lasting disease control. In the CrisADe CONTROL phase III study (ClinicalTrials.gov: NCT04040192), participants aged ≥ 3 months with mild to moderate AD treated with once-daily (QD) crisaborole, following initial treatment success with crisaborole twice daily (BID), had longer periods of flare-free maintenance, a higher number of flare-free days, and a lower number of flares compared with those who received vehicle. The study was an exploratory analysis of data on the maintenance of response per Investigator’s Static Global Assessment (ISGA; ISGA score of 0 [clear] or 1 [almost clear]) during the CrisADe CONTROL study through week 52. Methods Exploratory endpoints were the time to ISGA response during the open-label run-in period, and the maintenance of ISGA response and the severity and duration of flares during the double-blind maintenance period. Outcomes were stratified by age (participants aged 3 months to

Abstract Atopic dermatitis (AD) is a chronic, relapsing immunoinflammatory skin condition characterized by sensations such as pruritis, pain, and neuronal hypersensitivity. The mechanisms underlying these sensations are multifactorial and involve complex crosstalk among several cutaneous components. This review explores the role these components play in the pathophysiology of atopic dermatitis. In the skin intercellular spaces, sensory nerves interact with keratinocytes and immune cells via myriad mediators and receptors. These interactions generate action potentials that transmit pruritis and pain signals from the peripheral nervous system to the brain. Keratinocytes, the most abundant cell type in the epidermis, are key effector cells, triggering crosstalk with immune cells and sensory neurons to elicit pruritis, pain, and inflammation. Filaggrin expression by keratinocytes is reduced in atopic dermatitis, causing a weakened skin barrier and elevated skin pH. Fibroblasts are the main cell type in the dermis and, in atopic dermatitis, appear to reduce keratinocyte differentiation, further weakening the skin barrier. Fibroblasts and mast cells promote inflammation while dermal dendritic cells appear to attenuate inflammation. Inflammatory cytokines and chemokines play a major role in AD pathogenesis. Type 2 immune responses typically generate pruritis, and the type 1 and type 3 responses generate pain. Type 2 responses and increased skin pH contribute to barrier dysfunction and promote dysbiosis of the skin microbiome, causing the proliferation of Staphyloccocus aureus. In conclusion, understanding the dynamic interactions between cutaneous components in AD could drive the development of therapies to improve the quality of life for patients with AD.

Abstract Stasis dermatitis (SD) is a chronic inflammatory dermatosis that typically presents with nonspecific signs and symptoms such as pruritic and xerotic skin, aching legs, and areas of dyspigmentation (red or brown in lighter skin tones and brown, purple, gray, or ashen in darker skin tones). These signs and symptoms are often misdiagnosed as other conditions, such as cellulitis. Moreover, within healthcare systems, SD is often overlooked due to a lack of understanding of the magnitude and impact of the condition, as well as incomplete recognition of the various presenting clinical manifestations. Inadequate or inappropriate management may lead to disease progression, including worsening edema, pain, and itch as well as complications such as venous leg ulcers. When patients do seek medical attention (often upon worsening of the condition), a diagnosis of SD is often challenging because of physician lack of expertise and the plethora of disorders that may manifest similarly to SD. Furthermore, upon diagnosis, evidence‐based treatment options are limited, and adherence to SD treatment regimens is often low. SD significantly impacts patient and caregiver quality of life (QoL), with far‐reaching psychosocial and socioeconomic effects. In this review, we describe the patient journey associated with SD and the challenges associated with diagnosis, the burden of disease and impact on patient QoL, and the unmet needs that remain with current therapeutic options.