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Background: Coronavirus Disease 2019 (COVID‐19) is a viral illness caused by the novel coronavirus SARS‐CoV‐2 which spreads via droplets from an infected person. There has been an unprecedented rise in the use of personal protective equipment and practice of personal hygiene measures against COVID‐19. The extended use of protective measures (PM) can lead to ill effects on the skin. Our aim was to investigate PM‐induced dermatoses amongst healthcare workers and the general population during the COVID‐19 pandemic. Methods: A cross‐sectional study was conducted over a period of 2 months. The study subjects were patients who presented to dermatology outpatient clinics or sought teleconsultation for skin problems related to the use of PMs against COVID‐19. A detailed history was obtained and cutaneous examination was documented for all the patients in a pre‐set proforma. Diagnoses of the adverse skin effects were formulated based upon history and clinical examination. Results: A total of 101 cases with cutaneous adverse effects due to the use of PMs against COVID‐19 were included in the study. The general population and healthcare workers were affected similarly, comprising of 54.5% and 45.5%, respectively. The mean age of the study participants was 36.71 ± 15.72 years. The most common culprit material was soap and water (56.4%). Contact dermatitis was found to be the most common adverse effect in the majority of our patients (72.3%). The most common symptom reported was pruritus (45.5%). The wearing of personal protective equipment for a longer duration was significantly associated with multiple symptoms (P = 0.026). Conclusion: The enhanced use of different PMs against COVID‐19 can result in a variety of adverse skin effects. In our study, the use of soap and water was the most common culprit PM, and contact dermatitis was the most common adverse effect noted. [ABSTRACT FROM AUTHOR]

We investigated the functions of critical adhesion molecules ICAM-1 and VCAM-1 in a keratin-14 IL-4-transgenic (Tg) mouse model of atopic dermatitis, the skin lesions of which are characterized by prominent inflammatory cell infiltration, significantly increased mRNAs and proteins of ICAM-1, VCAM-1, E-selectin, P-selectin, L-selectin, and PSGL-1, and significantly increased numbers of dermal vessels expressing these adhesion molecules. We tested the hypotheses that deletion or blockade of these molecules may impede the inflammation by examining the disease progresses in the Tg mice crossed with ICAM-1-knockout mice and Tg mice received anti-VCAM-1-neutralizing antibody. Although the findings of the ICAM-1-knockout Tg mice (Tg/ICAM-1−/−) developed skin lesions similar to wide-type ICAM-1 Tg mice (Tg/ICAM-1+/+) were surprising, a compensatory mechanism may account for it: the frequency of VCAM-1 ligand, CD49d, on CD3+ T cells in the lesional skin significantly increased in the Tg/ICAM-1−/− mouse, compared with the Tg/ICAM-1+/+ mice. In contrast, anti-VCAM-1-treated Tg/ICAM-1−/− or Tg/ICAM-1+/+ mice had significantly delayed onset of skin inflammation compared with isotype antibody-treated groups. Moreover, anti-VCAM-1 significantly reduced the skin inflammation severity in Tg/ICAM-1+/+ mice, accompanied with reduction of mast cell, eosinophil, and CD3+ T cell infiltration. VCAM-1 is more critical in developing skin inflammation in this model. [ABSTRACT FROM AUTHOR]