ABSTRACT
The SARS-CoV-2 virus that caused the 2019 new coronavirus infection (COVID-19) pandemic has posed an unprecedented challenge to the global health system and scientific community. As of this literature review, the infection has claimed more than 6 million lives, and more than 500 million people worldwide have already been infected with SARS-CoV-2. In addition to the basic, pulmonary manifestations of the disease, as well as the severe, life-threatening complications of acute COVID-19, the long-term changes that occur in the postcovid period also affect other systems: endocrine, cardiovascular, nervous, and musculoskeletal. In this literature review, using data from current scientific publications obtained by searching <<covid-19 endocrine disorders>>, <<postcovid endocrine disorders>> and <<postcovid syndrome endocrine disorders>> in the MEDLINE (PubMed) database and <<endocrine pathology and covid-19>>, <<postcovid and endocrine pathology>> and <<postcovid syndrome and endocrine disorders>> in the e-Library database, we focused on describing and discussing the complications and consequences that SARS-CoV-2 infection can have on the endocrine glands, including the adrenals, thyroid, pituitary, gonads and pancreas. Copyright © 2022 Russian Association of Endocrinologists. All rights reserved.
ABSTRACT
Although more than 2 years have passed since the beginning of the pandemic of the new coronavirus infection, treatment and prediction of the course of SARS-CoV-2 infection remain pressing global problems. In this regard, the search for additional links in the pathogenesis of SARS-CoV-2 is currently one of the most important tasks. The aim. To assess the level of lipopolysaccharide-binding protein (LBP) and presepsin (sCD14-ST) in patients with SARS-CoV-2 viral lung disease in Crimea. Methods. We examined 121 patients with a positive PCR result for SARS-CoV-2 in the age group of 45 - 75 years who were hospitalized in the Department of Infectious Diseases, State Budgetary Healthcare Institution of the Republic of Crimea “N.A.Semashko Republican Clinical Hospital”. Patients were divided into 3 clinical groups according to the severity of SARS-CoV-2 infection: Group 1 - patients with moderate disease, Group 2 - patients with severe disease, and Group 3 - patients with fatal outcome. Peripheral blood levels of LBP, presepsin, ferritin, and C-reactive protein were determined upon admission to the infectious disease hospital. Results. A significant increase in all studied parameters was observed in the 1st, 2nd and 3rd clinical groups of patients with coronavirus infection. This finding corresponds to the state of lipopolysaccharide-binding systems and systemic infection in patients with SARS-CoV-2 viral lung disease. The highest levels of LBP, sCD14-ST, and ferritin were registered in the 3rd clinical group. We found a direct correlation between LBP and sCD14-ST levels in the 2nd group (r = 0.523, p < 0.05) and the 3rd group (r = 0.748, p < 0.05). Conclusion. Patients with SARS-CoV-2 lung disease were found to have an increased blood levels of LBP and presepsin upon admission. The highest values were observed in patients with fatal outcome. Severe SARSCoV-2 lung damage was associated with a direct correlation between levels of LBP and sCD14-ST. Presepsin, LBP, and ferritin are important prognostic markers for severe SARS-CoV-2 lung damage and risk of death in the early stages of hospital treatment.
ABSTRACT
This review presents data from the literature that provide insight into the role of the lipopolysaccharide (LPS) of the Gram-negative bacteria in pathogenesis of acute respiratory distress syndrome (ARDS) caused by the novel SARS-CoV-2 coronavirus infection. ARDS is a syndrome of severe respiratory failure, an acutely occurring diffuse inflammatory lesion of lung tissue that develops as a nonspecific reaction to various direct (aspiration, inhalation of toxic gases), and systemic (sepsis, polytrauma) damaging factors and leading to development of acute respiratory failure (ARF), due to impaired structure of the lung parenchyma, disturbances in vascular permeability, decreased area of ventilated lung tissue. ARDS from coronavirus infection appears to have worse outcomes than ARDS from other causes. Mortality from typical ARDS at the intensive care units and hospitals is 35.3% and 40.0%, respectively, while the lethality rates for COVID-19-associated ARDS, ranged from 26% to 61.5%. Among patients who underwent artificial ventilation of the lungs, the mortality rates can range from 65.7% to 94%. Risk factors for poor outcomes include, e.g., older age, presence of concomitant diseases such as hypertension, cardiovascular disease and diabetes mellitus;decreased number of lymphocytes, kidney injury, and increased D-dimer levels. Death with ARDS in COVID-19 occurs as a result of respiratory failure (53%), respiratory failure combined with heart failure (33%), myocardial damage and circulatory failure (7%), or death from an unknown cause. A large number of studies show that bacterial LPS is directly or indirectly involved in all pathogenetic links of ARDS caused by the SARS-CoV-2 virus, i.e., worsening the course of inflammatory lung diseases due to decreased level of angiotensin-converting enzyme 2 (ACE2);increasing generation of reactive oxygen species (ROS) via NADPH oxidase and subsequent inactivation of endothelial nitric oxide synthase (eNOS) and decreasing bioavailability of endothelial NO, thus leading to endothelial dysfunction;interacting with proteins of surfactants. SP-A and SP-D, promoting early destruction of the cellular monolayers and lowering surface tension, interact with soluble CD14 receptor, which also has a pro-inflammatory effect on epithelial and endothelial cells, leading to p38MAPK activation via TLR4 receptors, causing degradation of IκBα protein and subsequent translocation of p65 NF-κB into the nucleus, thus inducing transcription of IL-6 and adhesion molecules (ICAM-1, VCAM-1 and E-selectin), and, as shown by Petruk et al. (2020), causing direct binding to the viral S protein in combination with LPS, thus enhancing activation of nuclear factor-kappa B (NF-κB) in monocytic THP-1 cells and cytokine responses in mononuclear blood cells. These pathophysiological mechanisms require further in-depth study in order to understand the nature of changes that occur in the patients with new SARS-CoV-2 infection. © 2022 Russian Association of Allergologists and Clinical Immunologists, St. Petersburg Regional Branch (SPb RAACI). All rights reserved.
ABSTRACT
Background. Prescribing antibacterial drugs for the treatmentofa new coronavirus infection at the outpatient stage is often unreasonable and can also lead to an aggravation of the patient's condition due to the effect of this group of drugs on the intestinal microflora and lead to other undesirable effects. The aim: to assess the level of lipopolysaccharide-binding protein and indicators of systemic inflammation in patients with moderate viral SARS-CoV-2 lung disease on the background of antibiotic therapy. Materials and methods. 60 patients hospitalized in the infectious diseases departmentwitha positive PCRresultfor SARS-CoV-2in the age group 44-70 years oldwere examined. The patients were divided into 2 groups: group 1 (n = 26) - patients who didnotreceive antibacterialdrugs atthe outpatientstage, group 2 (n= 34)- patients who receivedantibiotic therapy. The control group was also selected(n= 20). Patients underwent a study of the level of lipopolysaccharide-binding protein (LBP), ferritin and C-reactive protein in the peripheral blood. Results. Inthe groupofpatientswithnewcoronavirusinfectionwhowereadmittedto the inpatientstage oftreatmentandreceivedantibacterialtherapy atthe outpatient stage, a significantly higher levels of LBP - 37.3 [13.8;50.4] µg/ml (p < 0.05) and ferritin- 276.00 [184.00;463.00] µg/ml (p < 0.05)were revealed, comparedwith group 1 and the control group. Conclusions. In the group of patients who received antibiotic therapy at the outpatient stage, a significantly higher level of LBP was revealed compared to the group in which this group of drugs was not used. These results indicate the possible impact of uncontrolled and early intake of antibacterial drugs on the gut microbiome andintestinal permeability, andalso prove the needfor a more responsible approach to the choice of starting therapy for new coronavirus infection. © 2022 by the authors.