From Gut to Skin: Can Fecal Transplants Tame Atopic Dermatitis? ➜ DOI: 10.1186/s12866-026-04717-1 + 10.3389/falgy.2025.1680658 Two studies from the same Chinese team explore washed fecal microbiota transplantation (WMT) in moderate to severe atopic dermatitis. Open-label cohorts report improvements in EASI, SCORAD, and itch, alongside shifts in gut and skin microbiota away from Staphylococcus dominance. A companion study links AD severity to intestinal barrier dysfunction and suggests D-lactate as a potential (but unvalidated) predictor of response. However, both studies lack controls, show modest immune signals, and rely on exploratory correlations.
Bottom line: Promising gut–skin biology, but WMT remains in the research domain.
IL-18 in Atopic Dermatitis: Going Upstream of Th2? ➜ DOI: 10.1111/all.70172 Interleukin-18 (IL-18) is released via the inflammasome by stressed keratinocytes after barrier damage and microbial exposure, linking innate immune activation to both Th2 and Th1 pathways. In a first placebo-controlled proof-of-concept study, the anti-IL-18 antibody aletekitug induced sustained improvements in EASI, itch, sleep disturbance, fatigue, and quality of life in adults with moderate-to-severe atopic dermatitis. Lesional skin transcriptomics shifted toward a non-lesional profile, with down-regulation of multiple inflammatory pathways extending beyond classical Th2 immunity. The treatment was well tolerated and showed prolonged biological activity after a single intravenous dose.
Bottom line: IL-18 inhibition emerges as a promising upstream strategy in AD, but its place alongside established biologics will depend on confirmation in larger, long-term trials.
Cannabidiol and Atopic Dermatitis: Experimental Signals, Clinical Questions ➜ DOI: 10.1016/j.jid.2025.11.023 Cannabidiol (CBD) targets the cutaneous endocannabinoid system and, in experimental models, modulates CB2 signaling, JAK/STAT pathways, inflammasome activation, and pruritus-related circuits. In a recent Journal of Investigative Dermatology study, topical CBD reduced inflammation, scratching behavior, and Th2-associated signaling in mouse models and showed biological activity in human AD skin samples. However, the work remains preclinical and mechanistic, with no controlled clinical efficacy data in patients with AD. Notably, despite widespread recreational and medicinal cannabis use worldwide, there is currently no robust real-world or pharmaco-epidemiological evidence demonstrating consistent improvement of AD symptoms.
Bottom line: CBD represents an interesting biological probe in AD, but its clinical relevance remains unproven and warrants carefully designed human studies before conclusions can be drawn.
Topical Steroid Withdrawal: Between Lived Experience and Biological Uncertainty ➜ DOI: 10.2196/85183 Two recent studies approach topical steroid withdrawal (TSW) from opposite angles: one documenting patient-reported suffering and healthcare disengagement, the other exploring biological mechanisms in “deeply” phenotyped patients, where the vast majority had a previous diagnosis of AD. Together, they show how difficult it is to disentangle TSW from severe or undertreated atopic dermatitis, given overlapping clinical features and the absence of validated diagnostic criteria. Social-media–driven narratives highlight real patient distress, while mechanistic studies remain exploratory and limited by small numbers. ISAD recognizes the need to listen carefully to the TSW community while avoiding premature conclusions.
Bottom line: Understanding TSW requires open dialogue and rigorous, unbiased research—not polarization.
When Prices Fall but Risks Rise: Veterinary vs Human JAK Inhibitors ➜ DOI: 10.1016/j.idcr.2025.e02459 A recent case report describes severe Pneumocystis jirovecii pneumonia in a human self-treating AD with long-term veterinary oclacitinib, highlighting the real immunosuppressive risks of such practices. Oclacitinib has been used for canine atopic dermatitis (CAD) for more than a decade and is now facing competition from several new veterinary JAK inhibitors, further driving prices down. For a typical 20–25 kg dog, monthly veterinary JAK-inhibitor costs (US market) are approximately €50–100 (≈ €2–5/kg/month), while human-approved JAK inhibitors for AD still cost €1,500–2,500/month (≈ €20–40/kg/month for a 70 kg adult), a one-to-two order of magnitude difference. This widening gap may incentivize unsafe procurement of veterinary drugs for human use.
Bottom line: Increased competition and falling prices in the veterinary JAKi market must not blur the boundary between animal and human medicines—safety and regulation remain non-negotiable, while also highlighting the need to reconsider the pricing of innovative small molecules in human medicine.
