Teledermatology Platforms Usage and Barriers: A Cross-Sectional Analysis of United States-Based Dermatologists Pre- and Post-COVID-19.

BACKGROUND: During the global COVID-19 pandemic, dermatologists increasingly adopted teledermatology to facilitate patient care. OBJECTIVE: To identify differences in teledermatology platform usage and functionality among dermatologists as a means of understanding the potential effect on virtual healthcare access. METHODS: Results from a 2021 cross-sectional pre-validated survey distributed to actively practicing United States dermatologists were analyzed based on timepoint when teledermatology was adopted relative to COVID-19, previous/currently used platforms, self-reported platform functionality, and barriers to teledermatology implementation. Analysis was performed using chi-square and odds ratios (OR) with 95% confidence intervals (95% CI) for categorical data and single-factor analysis of variance (ANOVA) with post-hoc Tukey-Kramer for continuous data. P<.05 was considered significant. RESULTS: Early adopters (EAs) trialed significantly more (2.3 vs 1.9, P=0.02) platforms than (post) COVID adopters (CAs) before choosing their current platform. More EAs reported using platforms capable of uploading images (P=.002), required a mobile application (P=.006), and allowed staff to join patient encounters (P<.001). While poor image quality was the most cited barrier to implementation, CAs and non-adaptors (NAs) were materially more likely to cite it as their largest barrier to teledermatology. LIMITATIONS: The retrospective nature of the study and potential response bias. CONCLUSION: Dermatologists' use of teledermatology materially correlates with their teledermatology-adoption timepoint, and future usage may be materially impacted by the end of the COVID-19 public health emergency. Future studies should aim at how implementation and barriers to teledermatology usage may impact access to care. J Drugs Dermatol. 2024;23(2): doi:10.36849/JDD.7819e.

Quality-of-Life Outcomes for Excision and Reconstruction of Periocular Nonmelanoma Skin Cancer.

Background: Understanding how periocular nonmelanoma skin cancer (NMSC) impacts quality of life (QoL) provides insight into the patient experience. Objective: To prospectively measure QoL of individuals with surgically treated periocular NMSC. Methods: Responses to the skin cancer index (SCI) and FACE-Q questionnaires were obtained at preoperative (PRE), postoperative week 1 (POW1), and postoperative month 3 (POM3) visits. Statistical analysis was performed using paired t-test and stepwise linear regression. Results: Forty-five patients participated in the study. Improved QoL as reflected in an increased mean difference of the total SCI score at PRE and POM3 visits (25.8, 95% confidence interval [CI 20.0 to 31.6]) and FACE-Q early life impact of treatment score at POW1 and POM3 visits (19.0, 95% CI [14.9 to 23.0), and a decreased mean difference of the FACE-Q adverse effects score at POW1 and POM3 visits (-1.3, 95% CI [-2.4 to -0.1]) was observed. Linear regression of the SCI and FACE-Q scores using demographic and clinical attributes revealed several predictors of postoperative QoL. Conclusions: Surgical management of periocular NMSC results in improved QoL, demonstrated at the final postoperative visit.

A novel function of p38-regulated/activated kinase in endothelial cell migration and tumor angiogenesis.

The p38 mitogen-activated protein kinase (MAPK) pathway has been implicated in both suppression and promotion of tumorigenesis. It remains unclear how these 2 opposite functions of p38 operate in vivo to impact cancer development. We previously reported that a p38 downstream kinase, p38-regulated/activated kinase (PRAK), suppresses tumor initiation and promotion by mediating oncogene-induced senescence in a murine skin carcinogenesis model. Here, using the same model, we show that once the tumors are formed, PRAK promotes the growth and progression of skin tumors. Further studies identify PRAK as a novel host factor essential for tumor angiogenesis. In response to tumor-secreted proangiogenic factors, PRAK is activated by p38 via a vascular endothelial growth factor receptor 2 (VEGFR2)-dependent mechanism in host endothelial cells, where it mediates cell migration toward tumors and incorporation of these cells into tumor vasculature, at least partly by regulating the phosphorylation and activation of focal adhesion kinase (FAK) and cytoskeletal reorganization. These findings have uncovered a novel signaling circuit essential for endothelial cell motility and tumor angiogenesis. Moreover, we demonstrate that the tumor-suppressing and tumor-promoting functions of the p38-PRAK pathway are temporally and spatially separated during cancer development in vivo, relying on the stimulus, and the tissue type and the stage of cancer development in which it is activated.