P014 Defining the barrier function of clinical treatment efficacy for atopic dermatitis

Abstract Atopic dermatitis (AD) is characterized by impaired epidermal barrier function. Portable devices are available to measure stratum corneum hydration (SCH) and transepidermal water loss (TEWL). These could be incorporated into clinical practice to measure barrier function to define treatment success in AD. Despite the importance, there is minimal evidence for objective biophysical measurements to assess treatment success. The aim of this study was to evaluate the role of SCH and TEWL in distinguishing treatment efficacy between methotrexate and topical treatments and their correlation with Eczema Area and Severity Index (EASI), Patient-Oriented Eczema Measure (POEM) and Dermatology Life Quality Index (DLQI). Patients with AD (n = 16) were recruited from a specialist eczema clinic, as well as healthy controls (n = 10). All cases were recruited when the current therapy switch was planned, namely at the point of treatment failure. Of the patients with AD, 56% (9 of 16) had not responded to topical therapy, and 44% (7 of 16) had not responded to methotrexate. EASI scores did not differ significantly between the groups with lack of response to topical treatment or methotrexate (mean 20.7, SD 10.9 vs. mean 18.2, SD 15.1, respectively; P = 0.70). Furthermore, DLQI and POEM scores did not significantly differ between topical or methotrexate treatment (P = 0.24 and P = 0.89, respectively). As expected, healthy control samples showed significantly better barrier function than both lesional (TEWL, P < 0.001; SCH, P = 0.002) and nonlesional skin (TEWL, P = 0.004; SCH, P = 0.02). EASI positively correlated with TEWL values in both lesional and nonlesional skin (r > 0.5, P < 0.05). However, SCH did not correlate well with EASI for lesional and nonlesional skin (r = 0.075 and 0.029, respectively). Interestingly, with topical treatment, lesions could be distinguished from nonlesions by both TEWL (P = 0.008) and SCH (P = 0.003), even in treatment failures. However, with methotrexate treatment, barrier function measures were equivalent between lesions and nonlesions for TEWL (P = 0.44) and SCH (P = 0.55). Skin barrier function correlated very weakly with patient-reported outcomes for both TEWL and SCH, with POEM (lesional r2 = 0.15 and 0.04, respectively; nonlesional r2 ≤ 0.005 and r2 = 0.04) and DLQI (lesional r2 = 0.11 and 0.22; nonlesional r2 = 0.06 and 0.21). In conclusion, barrier function, as defined by TEWL and SCH, was significantly impaired in AD compared with healthy controls, but only TEWL scores correlated with EASI. In the patients, SCH did significantly distinguish lesions from nonlesions, as did TEWL. However, unlike topical-treated cases, in those with methotrexate treatment, no difference was shown between lesional and nonlesional TEWL and SCH. These data suggest that systemic therapy with methotrexate may improve lesional skin barrier function to that of nonlesional skin, even in those who are deemed to have not responded to treatment. Therefore, additional measures may be required to automate the definition of therapeutic treatment success or failure.