AD hidden hematologic risk: clonal hematopoiesis of indeterminate potential (CHIP) ➜ DOI: 10.1111/all.16587 Patients with AD exhibit a significant increased prevalence of CHIP, particularly affecting lymphoid-lineage genes. These findings suggest an underrecognized predisposition to hematologic malignancies in AD, warranting closer surveillance and mechanistic investigation. A recent Nature paper indicates that metformin could prevent CHIP development (DOI: 10.1038/s41586-025-08871-w)
An unusual facial bump related to AD ➜ DOI: 10.1007/s10006-025-01384-w A previous report of anterior tibial bursitis—an atypical, nonarticular site—during an atopic dermatitis (AD) flare-up suggested a potential association between AD and bursitis. This paper now describes a striking case of mandibular bursitis occurring in a nonarticular region of the jaw in a patient with AD, further supporting this emerging link.
Switching off selectively skin lipid synthesis: a reversible human model of ceramide depletion ➜ DOI: 10.1016/j.xjidi.2025.100383 This study introduces the first human skin equivalent with inducible ceramide synthase 3 (CerS3) knockdown, enabling precise modeling of epidermal lipid deficiency. The system reveals that ceramide depletion alters lipid composition and chain length without affecting differentiation, offering a powerful platform to study barrier dysfunction and repair in vitro.
Beyond the skin: suicidal risk is real in AD ➜ DOI: 10.4088/JCP.24m15590 This nationwide Taiwanese cohort study reveals that patients with AD face over threefold increased risk of suicide attempts, particularly among young females and those with short-term systemic corticosteroid use. These findings underscore the need for integrated dermatologic and psychiatric care, even in patients with mild disease severity.
Complement, an overlooked driver of Th2 Immunity in AD ➜ DOI: 10.1172/JCI188352 Emerging evidence positions the complement system not only as a systemic antimicrobial cascade but as a potent, locally acting amplifier of Th2 responses at epithelial barriers, including the skin. In AD, elevated C3 and C3a levels are found even in non-lesional skin, implicating complement in systemic allergic priming. Genetic variants in complement components and mechanistic data from murine models suggest that dysregulated complement activation contributes directly to Th2 polarization, challenging conventional views of allergic disease pathogenesis and opening new therapeutic avenues.
