Background: The heterogeneous course of moderate-to-severe atopic dermatitis necessitates treatment flexibility.Objective: We evaluated the maintenance of abrocitinib-induced response with continuous abrocitinib treatment, dose reduction or withdrawal, and response to treatment reintroduction following flare (JAK1 Atopic Dermatitis Efficacy and Safety [JADE] REGIMEN: National Clinical Trial 03627767).Methods: Patients with moderate-to-severe atopic dermatitis responding to open-label abrocitinib 200 mg monotherapy for 12 weeks were randomly assigned in a 1:1:1 ratio to blinded abrocitinib (200 or 100 mg) or placebo for 40 weeks. Patients experiencing flare received rescue treatment (abrocitinib 200 mg plus topical therapy).Results: Of 1233 patients, 798 responders to induction (64.7%) were randomly assigned. The flare probability during maintenance was 18.9%, 42.6%, and 80.9% with abrocitinib 200 mg, abrocitinib 100 mg, and placebo, respectively. Among patients with flare in the abrocitinib 200 mg, abrocitinib 100 mg, and placebo groups, 36.6%, 58.8%, and 81.6% regained investigator global assessment 0/1 response, respectively, and 55.0%, 74.5%, and 91.8% regained eczema area and severity index response, respectively, with rescue treatment. During maintenance, 63.2% and 54.0% of patients receiving abrocitinib 200 and 100 mg, respectively, experienced adverse events.Limitations: The definition of protocol-defined flare was not established, limiting the generalizability of findings.
Background
The generation of functional human epidermal melanocytes (HEM) from stem cells provides an unprecedented source for cell-based therapy in vitiligo. Despite the important efforts exerted to obtain melanin-producing cells from stem cells, pre-clinical results still lack the safety and scalability characteristics essential for their translational application.
Methods
Here, we report a rapid and efficient protocol based on defined culture conditions capable of differentiating adult adipose-derived stem cells (ADSC) to scalable amounts of proliferative melanocyte precursors (PreMel) within 30 days. PreMel were characterized in vitro through qPCR, Western blot, flow cytometry, biochemical assays, and in vivo assays in immunocompromised mice (NOD.Cg-Prkdc
scid
Il2rg
tm1Wjl
/SzJ, or NSG).
Results
After 30 days of differentiation, the stem cell-derived PreMel were defined as CD105
neg
CD73
low
according to immunophenotypic changes in comparison with parental stem cell markers. In addition, expression of microphthalmia-associated transcription factor (MITF), active tyrosinase (TYR), and the terminal differentiation-involved premelanosome protein (PMEL) were detected. Furthermore, PreMel had the potential to synthesize melanin and package it into melanosomes both in vitro and in vivo in NSG mice skin.
Conclusions
This study proposes a rapid and scalable protocol for the generation of proliferative melanocyte precursors (PreMel) from ADSC. These PreMel display the essential functional characteristics of bona fide HEM, opening a new path for an autologous cellular therapy for vitiligo patients.
Electronic supplementary material
The online version of this article (10.1186/s13287-019-1364-0) contains supplementary material, which is available to authorized users.
Tineas are frequent infections caused by dermatophytes that are able to invade keratinized tissue, causing rounded, erythematous, scaly lesions. Nonetheless, in tinea incognito the lesions are modified because of inappropriate use of topical corticosteroids or calcineurin inhibitors, making it difficult to diagnose. We present a case of a 12-year-old male child that presents with erythematous lesions on the right eyebrow, which at first was diagnosed as a contact dermatitis, so corticosteroids were indicated. The lesions became more inflammatory and a fungus culture was requested, which was positive for Tricophyton mentagrophytes. The conclusion of this report is that tineas can mimic other dermatologic conditions therefore caution should be taken when prescribing topical corticosteroids or calcineurin inhibitors without diagnostic certainty because if lesions are caused by tinea, diagnosis and treatment may become more difficult.
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