Atopic Dermatitis
Conditions
Keywords
Skin Barrier, Atopic Dermatitis, Dermatology, Skin Physiology
Brief summary
Effects of abrocitinib treatment of atopic dermatitis on skin barrier function.
Detailed description
Open-label, non-randomized, single-arm, 12-weeks observational clinical and translational study
Interventions
OTHERNo Intervention
Non Interventional
Sponsors
Prof. Dr. Stephan Weidinger
Study design
Observational model
COHORT
Time perspective
PROSPECTIVE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
No
Inclusion criteria
1. Written informed consent obtained from the subject prior to performing any protocol-related pro-cedures, including screening evaluations 2. Age ≥ 18 years at time of study entry. 3. Diagnosis of chronic atopic dermatitis for at least 1 year prior to enrollment based on American Academy Criteria 4. Eczema Area and Severity Index (EASI) score ≥12 at baseline visit (Week 0) 5. Investigator Global Assessment (IGA) ≥3 at baseline visit (Week 0) 6. Subject is willing and able to comply with the protocol for the duration of the study 7. Subject receives abrocitinib by the treating dermatologist within routine care
Exclusion criteria
1. 1\. Subject is unable to provide written informed consent or comply with the protocol 2. Concurrent enrolment in another clinical trial where the subject is receiving an IMP or participation in another clinical trial with investigational product during the last 30 days before inclusion or 7 half-lives of previously used trial medication, whichever is longer. 3. Active dermatologic conditions that may confound the diagnosis of AD or would interfere with as-sessment of treatment, such as scabies, cutaneous lymphoma, or psoriasis. 4. Known active allergic or irritant contact dermatitis that is likely to interfere with the assessment of severity of AD. 5. Having used systemic immunosuppressive/immunomodulating therapy (e.g. systemic corticoster-oids methotrexate, cyclosporine, azathioprine, mycophenolate mofetil, JAK inhibitors) or tanning beds or phototherapy during any week within the 4 weeks or receipt of any marketed biologic ther-apy (e.g., dupilumab, tralokinumab) within 3 months or 5 half-lives, whichever is longer, prior to baseline 6. Treatment of selected marker skin areas (non-lesional skin at volar forearm and extensor forearm, lesional skin) with topical corticosteroid or topical calcineurin inhibitor 1 week prior to baseline visit and throughout the study. 7. Treatment of skin areas of examination with emollients 24 hours prior to baseline visit and throughout the study. 8. Involvement in the planning and/or conduct of the study.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Change in transepidermal water loss (TEWL) at one non-lesional and one lesional marker skin area at week 2 and week 12 compared to baseline/week 0 (day 0). | 12 Weeks | To determine the mean change of TEWL in g/m2/h at one non-lesional and one lesional marker skin site at week 2 and week 12 compared to baseline |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Number of epidermal barrier-related genes/pathways differentially expressed in a marker lesional skin site at week 2 and week 12 compared to baseline | 12 Weeks | To compare the expression of epidermal barrier-related genes at the transcriptome level at a marker lesional skin site at week 2 and week 12 to baseline and to non-lesional skin |
| Epidermal thickness and epidermal differentiation markers in a marker lesional skin site at week 2 and week 12 compared to baseline | 12 Weeks | To compare epidermal thickness (in µm) and the percentage of marker-positive cells (KRT 16, Ki67, FLG) in a marker skin site with reference to the number of cells in the basal layer at week 2 and 12 to baseline and to non-lesional skin |
| Stratum corneum biomarker (cytokine) levels (pg/μg protein) in marker skin sites at week 2 and week 12 compared to baseline | 12 Weeks | To compare stratum corneum biomarker (cytokine) levels (pg/μg protein) in a marker lesional skin site at week 2 and week 12 compared to baseline and to non-lesional skin |
| Composition of Bacterial Taxa of one lesional and non-lesional marker skin area at week 2 and week 12 compared to baseline | 12 Weeks | To identify changes in community composition and diversity at one lesional and one non-lesional marker skin site at week 2 and week 12 as compared to baseline using Next Generation Sequencing techniques |
Countries
Germany
Contacts
PRINCIPAL_INVESTIGATORStephan Weidinger, MD
UKSH Kiel, University of Kiel
Outcome results
None listed