Epidemiology of occupational dermatoses associated with personal protective equipment use in the COVID-19 pandemic: Risk factors and mitigation strategies for frontline health care workers.

Background: Personal protective equipment (PPE)-related occupational dermatosis (PROD) represents a significant occupational burden to health care workers (HCWs), and understanding its epidemiology is imperative in formulating mitigation strategies. Objectives: To determine the prevalence of PROD in HCWs, characterize its manifestations, identify its risk factors, and evaluate behavioral modifications of HCW. Methods: A cross-sectional study using an online questionnaire was conducted from July to September 2020. HCWs who had direct contact with COVID-19 patients for a minimum of 2 weeks cumulatively were invited to participate. Results: The prevalence of PROD among 416 valid respondents was 73.8% (307/416), with face masks being the most common cause (93.8% [n = 288]). The most common PROD associated with face masks, protective eyewear, hairnets, gowns, and gloves were acne (71.5% [206/288]), pressure-related injuries (70.7% [99/140]), scalp itch (53.3% [16/30]), itch/rash (78.8% [26/33]), and xerosis (75.0% [27/36]), respectively. Exposure to PPE beyond an hour increased the odds of PROD by 4.8-fold. The majority of HCWs made behavioral modifications to mitigate PROD. Conclusions: We underscore evidence-based recommendations for HCWs to be (1) scheduled hourly breaks from PPE wear, (2) fitted to various PPE models, (3) screened for preexisting dermatoses before deployment, and (4) educated on mitigation strategies and avenues for help should they encounter PROD.

Antifibrotic properties of relaxin: in vivo mechanism of action in experimental renal tubulointerstitial fibrosis.

This study examined the efficacy and in vivo mechanism of action of the antifibrotic hormone, relaxin, in a mouse model of unilateral ureteric obstruction (UUO). Kidney fibrosis was assessed in recombinant human gene-2 relaxin-treated animals maintained for 3 and 9 d after UUO. Results were compared with untreated and unoperated animals (d 0). Total collagen, collagen subtypes (I, IV), TGF-ß2 production, mothers against decapentaplegic homolog 2 (Smad2) phosphorylation, myofibroblast differentiation, mitosis, and apoptosis were all progressively increased by UUO (all P<0.05 vs. d 0 group at d 3 and d 9), whereas TGF-ß1 production was increased and vascular endothelial growth factor expression (angiogenesis) decreased at d 9 (both P<0.05 vs. d 0). A progressive increase in matrix metalloproteinase (MMP)-2 after UUO suggested that it was reactive to the increased fibrogenesis. Conversely, MMP-9 was decreased at d 9, whereas its inhibitor tissue inhibitor of metalloproteinase-1 progressively decreased after UUO. Human gene-2 relaxin pretreatment of animals from 4 d prior to UUO ameliorated the increase in total collagen, collagen IV, Smad2 phosphorylation, and myofibroblasts at both time points (all P<0.05 vs. untreated groups) and inhibited TGF-ß2 production and cell proliferation (both P<0.05 vs. untreated groups) with a trend toward normalizing vascular endothelial growth factor expression at d 9, with no effect on TGF-ß1 production or apoptosis. The relaxin-mediated regulation of MMPs and tissue inhibitor of metalloproteinases in this model was not consistent with its antifibrotic properties. The beneficial effects of relaxin were lost when treatment was stopped. These findings establish that relaxin can inhibit both early and established phases of tubulointerstitial fibrosis, primarily by suppressing cell proliferation, myofibroblast differentiation, and collagen production. Not all of these effects paralleled changes to TGF-ß-Smad signaling.