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May COVID-19 outbreaks lead to a worsening of skin chronic inflammatory conditions?

ABSTRACT: The emergence of the novel betaCoronavirus has raised serious concerns due to the virus rapid dissemination worldwide. Many areas throughout the world are now experiencing the COVID 19 outbreaks with government and policy authorities taking many aggressive isolation or restriction measures, drastically reducing also patient's visits and limiting only to the most urgent ones such as oncological visits or emergencies. Several studies have demonstrated a relationship between increased weight, obesity, diabetes, hypertension and inflammatory skin diseases. Furthermore, weight loss interventions have been shown to improve psoriasis, as well as hidradenitis suppurativa, and increase responsiveness to treatment of this conditions. We suppose that due to aggressive isolation or restriction measures, in the next future dermatologist will face with a common worsening of chronic skin inflammatory conditions due to reduced physical activities, increased intake of calories with the derived increase body weight and always more frequent treatment discontinuation. It is time to start potential preventive strategies which could limit the expected negative impact of COVID-19 related quarantine on skin diseases.

SUBMITTER: Marasca C

PROVIDER: S-EPMC7236705 | biostudies-literature | 2020 Oct

REPOSITORIES: biostudies-literature

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May COVID-19 outbreaks lead to a worsening of skin chronic inflammatory conditions?

Marasca Claudio C Ruggiero Angelo A Napolitano Maddalena M Fabbrocini Gabriella G Megna Matteo M

Medical hypotheses 20200519

The emergence of the novel betaCoronavirus has raised serious concerns due to the virus rapid dissemination worldwide. Many areas throughout the world are now experiencing the COVID 19 outbreaks with government and policy authorities taking many aggressive isolation or restriction measures, drastically reducing also patient's visits and limiting only to the most urgent ones such as oncological visits or emergencies. Several studies have demonstrated a relationship between increased weight, obesi ...[more]

PMID: 32492559

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Project description:Background and study aims COVID-19 is a condition caused by the coronavirus (called SARS-CoV-2) that was first identified in late 2019. This virus can infect the respiratory (breathing) system. Some people do not have symptoms but can carry the virus and pass it on to others. People who have developed the condition may develop a fever and/or a continuous cough among other symptoms. This can develop into pneumonia. Pneumonia is a chest infection where the small air pockets of the lungs, called alveoli, fill with liquid and make it more difficult to breathe. Nearly 32 million people in the UK have received two doses of the COVID-19 vaccine. Research shows that this prevents infection in over 90% of people. However, these vaccines were tested in healthy people. Recent research in individuals with chronic health problems or cancer suggests that 30% are generating low antibody or T-cells (a type of white blood cell which fights infection) levels after two doses of the Pfizer or AstraZeneca COVID-19 vaccines. This raises the question of the potential benefit of a third dose (re-boost) of the vaccine in these vulnerable patients. A re-boost strategy has been successfully used for other vaccines but the limited research performed to date for COVID-19 has given variable results, so additional research is needed. This study aims to find out whether a re-boost vaccine strategy can induce an immune response in clinically vulnerable patients who have not produced an adequate antibody response after two doses of the COVID-19 vaccine. Who can participate? Patients aged 18 and over who have not produced an adequate antibody response after two doses of COVID-19 vaccine and have one of the following diseases: 1. Breast or lung cancer 2. Certain types of blood cancer 3. Immune-mediated rheumatic diseases (e.g. rheumatoid arthritis) 4. Chronic kidney disease 5. Chronic liver disease 6. Inflammatory bowel disease on immune suppressive therapy 7. Stem cell transplant 8. Primary immunodeficiency (a group of disorders characterized by poor or absent immune function) What does the study involve? Participants will be randomly allocated to receive an additional dose of Pfizer or Moderna COVID-19 vaccine (the main study) or, for a sub-set of patients with blood cancer, the Pfizer or Moderna or Novavax vaccine. Blood samples will be collected before and 21 days after the re-boost vaccine and the level of antibodies and T-cells determined. Patients will be followed up for 3 months to see if they go on to develop COVID-19.

Project description:BackgroundCoronavirus disease 2019 (COVID-19) is commonly associated with skin manifestations, and may also exacerbate existing skin diseases, yet the relationship between COVID-19 and skin diseases remains unclear.ObjectiveBy investigating this relationship through a multiomics approach, we sought to ascertain whether patients with skin conditions are more susceptible to COVID-19.MethodsWe conducted an epidemiological study and then compared gene expression across 9 different inflammatory skin conditions and severe acute respiratory syndrome coronavirus 2-infected bronchial epithelial cell lines, and then performed a genome-wide association study transdisease meta-analysis between COVID-19 susceptibility and 2 skin diseases (psoriasis and atopic dermatitis).ResultsSkin conditions, including psoriasis and atopic dermatitis, increase the risk of COVID-19 (odds ratio, 1.55; P = 1.4 × 10-9) but decrease the risk of mechanical ventilation (odds ratio, 0.22; P = 8.5 × 10-5). We observed significant overlap in gene expression between the infected normal bronchial epithelial cells and inflammatory skin diseases, such as psoriasis and atopic dermatitis. For genes that are commonly induced in both the severe acute respiratory syndrome coronavirus 2 infection and skin diseases, there are 4 S100 family members located in the epidermal differentiation complex, and we also identified the "IL-17 signaling pathway" (P = 4.9 × 10-77) as one of the most significantly enriched pathways. Furthermore, a shared genome-wide significant locus in the epidermal differentiation complex was identified between psoriasis and severe acute respiratory syndrome coronavirus 2 infection, with the lead marker being a significant expression quantitative trait locus for S100A12 (P = 3.3 × 10-7).ConclusionsTogether our findings suggest association between inflammatory skin conditions and higher risk of COVID-19, but with less severe course, and highlight shared components involved in anti-COVID-19 immune response.

Project description:BACKGROUND:High levels of serum interleukin-6 (IL-6) correlate with disease severity in COVID-19. We hypothesized that tocilizumab (a recombinant humanized anti-IL-6 receptor) could improve outcomes in selected patients with severe worsening COVID-19 pneumonia and high inflammatory parameters. METHODS:The TOCICOVID study included a prospective cohort of patients aged 16-80 years with severe (requiring >?6 L/min of oxygen therapy to obtain Sp02?>?94%) rapidly deteriorating (increase by ??3 L/min of oxygen flow within the previous 12 h) COVID-19 pneumonia with ??5 days of symptoms and C-reactive protein levels >?40 mg/L. They entered a compassionate use program of treatment with intravenous tocilizumab (8 mg/kg with a maximum of 800 mg per infusion; and if needed a second infusion 24 to 72 h later). A control group was retrospectively selected with the same inclusion criteria. Outcomes were assessed at D28 using inverse probability of treatment weighted (IPTW) methodology. RESULTS:Among the 96 patients included (81% male, mean (SD) age: 60 (12.5) years), underlying conditions, baseline disease severity, and concomitant medications were broadly similar between the tocilizumab (n?=?49) and the control (n?=?47) groups. In the IPTW analysis, treatment with tocilizumab was associated with a reduced need for overall ventilatory support (49 vs. 89%, wHR: 0.39 [0.25-0.56]; p?<?0.001). Albeit lacking statistical significance, there was a substantial trend towards a reduction of mechanical ventilation (31% vs. 45%; wHR: 0.58 [0.36-0.94]; p?=?0.026). However, tocilizumab did not improve overall survival (wHR?=?0.68 [0.31-1.748], p?=?0.338). Among the 85 (89%) patients still alive at D28, patients treated with tocilizumab had a higher rate of oxygen withdrawal (82% vs. 73.5%, wHR?=?1.66 [1.17-2.37], p?=?0.005), with a shorter delay before being weaned of oxygen therapy (mean 11 vs. 16 days; p?<?0.001). At D28, the rate of patients discharged from hospital was higher in the tocilizumab group (70% vs. 40%, wHR?=?1.82 [1.22-2.75]; p?=?0.003). The levels of CRP and fibrinogen post therapy (p?<?0.001 for both variables) were significantly lower in the tocilizumab group (interaction test, mixed model). Rates of neutropenia (35% vs. 0%; p?<?0.001) were higher in the tocilizumab group, yet rates of infections (22% vs. 38%, p?=?0.089) including ventilator-acquired pneumonia (8% vs. 26%, p?=?0.022) were higher in the control group. CONCLUSION:These data could be helpful for the design of future trials aiming to counter COVID-19-induced inflammation, especially before patients require admission to the intensive care unit.

Project description:BACKGROUND:Psoriasis and atopic dermatitis are two inflammatory skin diseases with a high prevalence and a significant burden on the patients. Underlying molecular mechanisms include chronic inflammation and abnormal proliferation. However, the cell types contributing to these molecular mechanisms are much less understood. Recently, deconvolution methodologies have allowed the digital quantification of cell types in bulk tissue based on mRNA expression data from biopsies. Using these methods to study the cellular composition of the skin enables the rapid enumeration of multiple cell types, providing insight into the numerical changes of cell types associated with chronic inflammatory skin conditions. Here, we use deconvolution to enumerate the cellular composition of the skin and estimate changes related to onset, progress, and treatment of these skin diseases. METHODS:A novel signature matrix, i.e. DerM22, containing expression data from 22 reference cell types, is used, in combination with the CIBERSORT algorithm, to identify and quantify the cellular subsets within whole skin biopsy samples. We apply the approach to public microarray mRNA expression data from the skin layers and 648 samples from healthy subjects and patients with psoriasis or atopic dermatitis. The methodology is validated by comparison to experimental results from flow cytometry and immunohistochemistry studies, and the deconvolution of independent data from isolated cell types. RESULTS:We derived the relative abundance of cell types from healthy, lesional, and non-lesional skin and observed a marked increase in the abundance of keratinocytes and leukocytes in the lesions of both inflammatory dermatological conditions. The relative fraction of these cells varied from healthy to diseased skin and from non-lesional to lesional skin. We show that changes in the relative abundance of skin-related cell types can be used to distinguish between mild and severe cases of psoriasis and atopic dermatitis, and trace the effect of treatment. CONCLUSIONS:Our analysis demonstrates the value of this new resource in interpreting skin-derived transcriptomics data by enabling the direct quantification of cell types in a skin sample and the characterization of pathological changes in tissue composition.

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May COVID-19 outbreaks lead to a worsening of skin chronic inflammatory conditions?

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May COVID-19 outbreaks lead to a worsening of skin chronic inflammatory conditions?

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