Are the cutaneous manifestations during or due to SARS-CoV-2 infection/COVID-19 frequent or not? Revision of possible pathophysiologic mechanisms

Abstract

Background SARS-Cov-2 is a single-stranded RNA virus, a Betacoronavirus, composed of 16 non-structural proteins, with specific roles in replication of coronaviruses. The pathogenesis of COVID-19 is not yet fully understood. The virus and host factors interplay among distinct outcomes of infected patients. Methods Using MeSH (Medical Subject Headings) in PubMed, authors searched for articles cotaining information on COVID-19 and the skin. Results The pathophysiology of the disease is multifactorial: association with innate immune response, hypercoagulability state, lung tissue damage, neurological and/or gastrointestinal tract involvement, monocytic/macrophage activation syndrome, culminating in exaggerated cytokine secretion, called "cytokine storm", which leads to worsening and death. These systemic conditions may be associated with cutaneous lesions, that have polymorphic aspects, where at histopathological level show involvement in different skin changes. These lesions may be associated with multisystemic manifestations that could occur due to angiotensin-converting enzyme 2 receptor and transmembrane serine protease action, allowing the pulmonary infection and possibly skin manifestation. Several reports in literature show cutaneous lesions similar to chilblain, urticarial eruptions, diffuse or disseminated erythema, livedo racemosa, blue toe syndrome, retiform purpura, vesicle trunk, purpuric exanthema or exanthema with clinical aspects of symmetrical drug-related intertriginous and flexural exanthema (SDRIFE) and others. Conclusions This review describes the complexity of Covid-19, pathophysiological and clinical aspects, dermatological finding and other dermatological conditions associated with SARS-CoV-2 infection or COVID-19.

Clinical and Histopathological Features and Potential Pathological Mechanisms of Skin Lesions in COVID-19: Review of the Literature

“…The possible actions of SARS-CoV-2 on human skin and the resulting potential dermatological manifestations can be summarized as follows [ 63 ].…”

Cutaneous Manifestations of COVID-19: A Systematic Review

“…Criado et al mentioned that vesicular eruption could be a result of immune system overactivity causing a potential ''cytokine storm'' involving the skin. 30 The same study hypothesized a direct cytopathic effect of SARS-CoV-2 on endothelium dermal vessels could produce vesicular lesions. 30 Unlike maculopapular and urticarial lesions, vesicular lesions associated with COVID-19 are thought to be etiologically unrelated to antiviral drugs or other COVID-19 treatments.…”

“…30 The same study hypothesized a direct cytopathic effect of SARS-CoV-2 on endothelium dermal vessels could produce vesicular lesions. 30 Unlike maculopapular and urticarial lesions, vesicular lesions associated with COVID-19 are thought to be etiologically unrelated to antiviral drugs or other COVID-19 treatments. 48 Finally, vesicular lesions have been described as ''specific cutaneous manifestations'' of COVID-19; therefore, their identification could potentially be useful for diagnosis.…”

“…20 In addition to adverse drug effects, another possible pathophysiological mechanism leading to urticaria could be overactivity of the immune system, resulting in a potential ''cytokine storm'' involving the skin. 30 Interestingly, cases of delayed pressure urticaria have also been reported, although they are thought to be a result of vertical pressure caused by PPE. 31 Finally, a direct cutaneous effect by the SARS-CoV-2 virus is always a possibility, considering viral infections have sometimes been implicated as the primary agent in urticarial cases in the past.…”

Cutaneous Manifestations in Adult Patients with COVID-19 and Dermatologic Conditions Related to the COVID-19 Pandemic in Health Care Workers

“…SARS-CoV-2 can purportedly induce cutaneous manifestations via direct viral binding or secondarily through various allergic-immunologic mediated mechanisms [7]. Binding of SARS-CoV-2 to the angiotensin-converting enzyme 2 (ACE2) receptor facilitates viral entry into epithelial cells, primarily in the upper respiratory mucosa.…”