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This review aims at summarizing state-of-the-art knowledge on glycocalyx and SARS-CoV-2. The endothelial glycocalyx is a dynamic grid overlying the surface of the endothelial cell (EC) lumen and consists of membrane-bound proteoglycans and glycoproteins. The role of glycocalyx has been determined in the regulation of EC permeability, adhesion, and coagulation. SARS-CoV-2 is an enveloped, single-stranded RNA virus belonging to β-coronavirus that causes the outbreak and the pandemic of COVID-19. Through the respiratory tract, SARS-CoV-2 enters blood circulation and interacts with ECs possessing angiotensin-converting enzyme 2 (ACE2). Intact glycolyx prevents SARS-CoV-2 invasion of ECs. When the glycocalyx is incomplete, virus spike protein of SARS-CoV-2 binds with ACE2 and enters ECs for replication. In addition, cytokine storm targets glycocalyx, leading to subsequent coagulation disorder. Therefore, it is intriguing to develop a novel treatment for SARS-CoV-2 infection through the maintenance of the integrity of glycocalyx. This review aims to summarize state-of-the-art knowledge of glycocalyx and its potential function in SARS-CoV-2 infection. [ABSTRACT FROM AUTHOR]

Since its emergence, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) remains a public health threat worldwide. While the majority of patients recover in 3–4 weeks, complications in severely ill patients, including acute respiratory distress syndrome, cardiac injury, thrombosis, and sepsis, can lead to death. Several biomarkers, in addition to cytokine release syndrome (CRS), have been associated with severe and fatal outcomes in coronavirus disease 2019 (COVID-19) patients. The aim of this study is to assess clinical characteristics and cytokines profiles in hospitalized COVID-19 patients in Lebanon. A total of 51 hospitalized COVID-19 patients were recruited between February 2021 and May 2022. Clinical data and sera were collected at two time points: at hospital presentation (T0) and last collected results during hospitalization (T1). Our results showed that 49% of participants were >60 years with males accounting for the majority (72.5%). Hypertension, followed by diabetes and dyslipidemia, were the most frequent comorbid conditions among study participants accounting for 56.9% and 31.4%, respectively. Chronic obstructive pulmonary disease (COPD) was the only significantly different comorbid condition between intensive care unit (ICU) and non-ICU patients. Our results also showed that the median level of D-dimer was significantly elevated among patients in ICU and those who died compared to non-ICU patients and those who survived. Moreover, C-reactive protein (CRP) levels were significantly higher at T0 compared to T1 in ICU and non-ICU patients. The median level of IL-12p70 was significantly higher in patients >60 years compared to those ≤60 years (p = 0.0209). Our data are in agreement with previous reports suggesting the importance of IL-6, CRP, and IL-12p70 in the assessment of risk of severe disease and mortality. [ABSTRACT FROM AUTHOR]

What is known and objective: The coronavirus disease 2019 (COVID‐19) associated cytokine activation can lead to a rapid progression into respiratory failure, shock and multiorgan failure. Interleukin‐6 (IL‐6) is a pro‐inflammatory cytokine that likely contributes to the pathogenesis of cytokine release syndrome. It is hypothesized that modulating IL‐6 levels or its effects with tocilizumab, a recombinant humanized anti‐IL‐6 receptor monoclonal antibody, may alter the course of disease. Methods: We examined the association between tocilizumab use and intubation or death at a community hospital in New York City. Data were obtained regarding consecutive patients hospitalized with COVID‐19. The primary end point was a composite of intubation or death in a time‐to‐event analysis. We compared outcomes in patients who received tocilizumab with those in patients who did not, using a multivariable Cox model with inverse probability weighting according to the propensity score. Results and Discussion: In this single‐centre retrospective cohort study involving 1225 hospitalized patients with SARS‐CoV‐2 infection, the probability to respiratory failure, which was measured as intubation or death, was less frequent in patients who received tocilizumab. What is new and conclusion: Tocilizumab and other IL‐6 receptor monoclonal antibodies may evolve as a viable option in treating patients with moderate and severe COVID‐19. [ABSTRACT FROM AUTHOR]

The novel coronavirus is not only causing respiratory problems, but it may also damage the heart, kidneys, liver, and other organs; in Wuhan, 14 to 30% of COVID-19 patients have lost their kidney function and now require either dialysis or kidney transplants. The novel coronavirus gains entry into humans by targeting the ACE2 receptor that found on lung cells, which destroy human lungs through cytokine storms, and this leads to hyperinflammation, forcing the immune cells to destroy healthy cells. This is why some COVID-19 patients need intensive care. The inflammatory chemicals released during COVID-19 infection cause the liver to produce proteins that defend the body from infections. However, these proteins can cause blood clotting, which can clog blood vessels in the heart and other organs; as a result, the organs are deprived of oxygen and nutrients which could ultimately lead to multiorgan failure and consequent progression to acute lung injury, acute respiratory distress syndrome, and often death. However, there are novel protein modification tools called the QTY code, which are similar in their structure to antibodies, which could provide a solution to excess cytokines. These synthetic proteins can be injected into the body to bind the excess cytokines created by the cytokine storm; this will eventually remove the excessive cytokines and inhibit the severe symptoms caused by the COVID-19 infection. In this review, we will focus on cytokine storm in COVID-19 patients, their impact on the body organs, and the potential treatment by QTY code-designed detergent-free chemokine receptors. [ABSTRACT FROM AUTHOR]

Immunosuppressive and immunomodulatory therapies are important in dermatology, but indications are influenced by SARS‐CoV‐2. We will focus on skin disorders such as autoimmune connective tissue disorders, neutrophilic dermatoses, and vasculitis. Immunomodulators such as colchicine and antimalarials can easily be preferred taking their beneficial effects on COVID‐19 into consideration and also given their wide spectrum of action. Among the conventional therapies, methotrexate, azathioprine, and mycophenolate mofetil increase the risk of infection, and thus their use is recommended only when necessary and at low doses. On the other hand, use of cyclosporine is also not recommended as it increases the risk of hypertension, which is susceptible to COVID‐19. Anti‐TNF agents from among the biological therapies appear to be slightly risky in terms of susceptibility to infection. However, there are ongoing studies which suggest that some biological treatments may reduce cytokine storm impeding the COVID‐19 progression as a result, in spite of their susceptibilities to COVID‐19. Patients, who will be started on immunosuppressive therapy, should be tested for COVID‐19 prior to the therapy, and in the event that COVID‐19 is suspected, the therapy should be discontinued. [ABSTRACT FROM AUTHOR]

Late-onset AGEP-like skin pustular eruption following COVID-19: A possible association Dear Editor, The new coronavirus (SARS-CoV-2), the cause of the 2019 corona virus disease (COVID-19), is very infectious and is the primary cause of the current pandemic. The prominent AGEP-like pustular eruptions following COVID-19 recovery in our patient might be a distinctive late-onset skin manifestation associated with COVID-19 or a delay-onset unusual reaction to the prescribed drug. [Extracted from the article]