Background: Data on the clinical patterns and histopathology of SARS-CoV-2 related skin lesions, as well as on their relationship with the severity of COVID-19 are limited. Methods and Materials: Retrospective analysis of a prospectively collected cohort of patients with SARS-CoV-2 infection in a teaching hospital in Barcelona, Spain, from 1 April to 1 May 2020. Clinical, microbiological and therapeutic characteristics, clinicopathological patterns of skin lesions, and direct immunofluorescence and immunohistochemical findings in skin biopsies were analyzed. Results: Fifty-eight out of the 2761 patients (2.1%) either consulting to the emergency room or admitted to the hospital for COVID-19 suspicion during the study period presented COVID-19 related skin lesions. Cutaneous lesions could be categorized into six patterns represented by the acronym “GROUCH”: Generalized maculo-papular (20.7%), Grover’s disease and other papulo-vesicular eruptions (13.8%), livedo Reticularis (6.9%), Other eruptions (22.4%), Urticarial (6.9%), and CHilblain-like (29.3%). Skin biopsies were performed in 72.4%, including direct immunofluorescence in 71.4% and immunohistochemistry in 28.6%. Patients with chilblain-like lesions exhibited a characteristic histology and were significantly younger and presented lower rates of systemic symptoms, radiological lung infiltrates and analytical abnormalities, and hospital and ICU admission compared to the rest of patients. Conclusion: Cutaneous lesions in patients with COVID-19 appear to be relatively rare and varied. Patients with chilblain-like lesions have a characteristic clinicopathological pattern and a less severe presentation of COVID-19.
Urea is a hygroscopic molecule (capable of absorbing water) present in the epidermis as a component of the natural moisturizing factor (NMF) and is essential for the adequate hydration and integrity of the stratum corneum. Urea improves skin barrier function including antimicrobial defense by regulating gene expression in keratinocytes relevant for their differentiation and antimicrobial peptide production. It also plays a fundamental role in regulating keratinocyte proliferation. One of the first uses of urea in modern medicine was the topical treatment of wounds due to its proteolytic and antibacterial properties. At present, urea is widely used in dermatology to improve skin barrier function and as one of the most common moisturizers and keratolytic agents. Urea-containing formulations are available in diverse formulations and concentrations. Multiple clinical trials on the use of ureacontaining formulations have shown significant clinical improvement in many of the dermatosis presenting with scaly and dry skin such as atopic dermatitis, ichthyosis, xerosis, seborrheic dermatitis and psoriasis, among others. Furthermore, urea can increase skin penetration and optimize the action of topical drugs. Ureabased products are well tolerated; their side effects are mild and are more frequent at high concentration. Here, we present a review of the use of urea in dermatology, discussing its mechanism of action, safety profile and frequent indications.
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Atopic dermatitis (AD) is a chronic inflammatory skin disease with an estimated prevalence of 10–15% in children and 2–10% in adults. Clinically, there is notable phenotypic variability driven by a complex interaction between genetics, immune function, and the environment. Impairment of the skin barrier plays a significant role in the pathogenesis of AD. The apparent beneficial effect of sunlight in patients with atopic eczema is questioned due to its capacity to disrupt the skin barrier and generate free radicals that can damage proteins, lipids, and DNA. The sum of the external factors that an individual is exposed to throughout their lifetime is termed the exposome. Environmental factors such as sun exposure, temperature, and humidity contribute to both AD flares and regional prevalence variation. Literature on photoprotection in atopic dermatitis is very scarce. The use of adequate sunscreens in atopic dermatitis can ensure the level of photoprotection required to prevent skin photoaging and skin cancer and to mitigate skin barrier dysfunction, decrease inflammation, and neutralize facial redness. Herein we discuss and review the role of UV radiation and the exposome in the etiology of AD, as well as the role of adequate photoprotection.
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