scholarly journals СУЧАСНІ АСПЕКТИ РОЗВИТКУ КОАГУЛОПАТІЇ У ПАЦІЄНТІВ ПРИ COVID‑19 ІНФЕКЦІЇ: ОГЛЯД ЛІТЕРАТУРИ

2021 ◽  
Vol 25 (5-6) ◽  
pp. 7-11
Author(s):  
М.О. Дудченко ◽  
С.М. Заєць ◽  
Р.А. Прихідько
Keyword(s):  
Blood Clotting ◽  
Bronchoalveolar Lavage Fluid ◽  
Current Knowledge ◽  
Lavage Fluid ◽  
Endothelial Damage ◽  
Multiple Organ ◽  
Local Damage ◽  
Blood Clots ◽  
Aggregation Of Platelets ◽  
Vessel Thrombosis

This review summarizes current knowledge about coagulation disorders associated with COVID-19 infection. Despite a significant amount of research, it is currently unclear whether COVID-19 is the direct cause of coagulopathic disorders or they occur as the infectious process progresses. Different authors have proposed several pathogenetic mechanisms for the development of coagulopathy in this disease. However, the most important is the release of a large number of cytokines that provoke interstitial inflammation, endothelial damage and activation of coagulation, in the pathogenesis of which the tissue factor plays a key role. Hyperinflammatory reactions lead to tissue damage, disruption of the endothelial barrier and uncontrolled activation of coagulation. In the lungs and, possibly, in other organs, under the influence of the virus, local damage to the vascular endothelium occurs, which leads to angiopathy, activation and aggregation of platelets with the formation of blood clots and concomitant consumption of platelets. Systemic hypercoagulation and hyperfibrinogenemia significantly increase the likelihood of large vessel thrombosis and thromboembolic complications, which are detected in 20–30% of patients in the intensive care units. Along with an increase in the level of cytokines in the blood, their content also increases in the lungs and in the bronchoalveolar lavage fluid. Cytokine storm leads to systemic intravascular coagulation, multiple organ failure and death. The review also provides the rationale for the principles of managing patients with coagulopathy based on the known mechanisms of unique disorders inherent in COVID-19. It has been shown that the problem of the pathogenesis of the development of blood clotting disorders in COVID-19 infection remains relevant.

Conventional Mechanical Ventilation Is Associated with Bronchoalveolar Lavage-induced Activation of Polymorphonuclear Leukocytes

2002 ◽  
Vol 97 (6) ◽  
pp. 1426-1433 ◽  
Author(s):  
Haibo Zhang ◽  
Gregory P. Downey ◽  
Peter M. Suter ◽  
Arthur S. Slutsky ◽  
V. Marco Ranieri
Keyword(s):  
Mechanical Ventilation ◽  
Bronchoalveolar Lavage ◽  
Polymorphonuclear Leukocytes ◽  
Bronchoalveolar Lavage Fluid ◽  
Distress Syndrome ◽  
Lavage Fluid ◽  
Surface Expression ◽  
Multiple Organ ◽  
Protective Strategy ◽  
Oxidant Production

Background Protective ventilatory strategies have resulted in a decreased mortality rate in acute respiratory distress syndrome, but the underlying mechanisms remain unclear. The authors hypothesized that (1) mechanical ventilation modulates activation of polymorphonuclear leukocytes (PMNs), (2) the consequent release of proteinases is correlated with a systemic inflammatory response and with multiple organ dysfunction, and (3) these deleterious effects can be minimized by a protective ventilatory strategy. Methods Human PMNs were incubated with bronchoalveolar lavage fluid obtained from patients at entry or 36 h after randomization to ventilation with either a conventional (control) or a lung-protective strategy. PMN oxidant production and surface expression of adhesion molecules and granule markers, including CD18, CD63, and L-selectin, were measured by flow cytometry. Extracellular elastase activity was quantified using a fluorescent substrate. Results Bronchoalveolar lavage obtained from both groups of patients at entry showed similar effects on PMN oxidant production and expression of surface markers. At 36 h, exposure of PMNs to bronchoalveolar lavage fluid from the control group resulted in increased PMN activation as manifested by a significant increase in oxidant production, CD18, and CD63 surface expression, and shedding of L-selectin. By contrast, these variables were unchanged at 36 h in the lung-protective group. There was a significant correlation between the changes of the variables and changes in interleukin-6 level and the number of failing organs. Conclusions Polymorphonuclear leukocytes can be activated by mechanical ventilation, and the consequent release of elastase was correlated with the degree of systemic inflammatory response and multiple organ failure. This result may possibly explain the decreased mortality in acute respiratory distress syndrome patients treated with a lung-protective strategy.

Identification of neutrophil chemotactic factors in bronchoalveolar lavage fluid of asthmatic patients

1997 ◽  
Vol 27 (4) ◽  
pp. 396-405 ◽  
Author(s):  
L. M. TERAN ◽  
M. G. CAMPOS ◽  
B. T. BEGISHVILLI ◽  
J.-M. SCHRODER ◽  
R. DJUKANOVIC ◽  
...  
Keyword(s):  
Bronchoalveolar Lavage ◽  
Bronchoalveolar Lavage Fluid ◽  
Lavage Fluid ◽  
Asthmatic Patients ◽  
Chemotactic Factors

scholarly journals Identification of Lung and Blood Microbiota Implicated in COVID-19 Prognosis

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1452
Author(s):  
Kypros Dereschuk ◽  
Lauren Apostol ◽  
Ishan Ranjan ◽  
Jaideep Chakladar ◽  
Wei Tse Li ◽  
...  
Keyword(s):  
Peripheral Blood Mononuclear Cell ◽  
Lung Biopsy ◽  
Bronchoalveolar Lavage Fluid ◽  
Human Microbiome ◽  
Lavage Fluid ◽  
Immune Dysregulation ◽  
Peripheral Blood Mononuclear ◽  
Inflammatory Pathways ◽  
Immune Therapies ◽  
Blood Microbiota

The implications of the microbiome on Coronavirus disease 2019 (COVID-19) prognosis has not been thoroughly studied. In this study we aimed to characterize the lung and blood microbiome and their implication on COVID-19 prognosis through analysis of peripheral blood mononuclear cell (PBMC) samples, lung biopsy samples, and bronchoalveolar lavage fluid (BALF) samples. In all three tissue types, we found panels of microbes differentially abundant between COVID-19 and normal samples correlated to immune dysregulation and upregulation of inflammatory pathways, including key cytokine pathways such as interleukin (IL)-2, 3, 5-10 and 23 signaling pathways and downregulation of anti-inflammatory pathways including IL-4 signaling. In the PBMC samples, six microbes were correlated with worse COVID-19 severity, and one microbe was correlated with improved COVID-19 severity. Collectively, our findings contribute to the understanding of the human microbiome and suggest interplay between our identified microbes and key inflammatory pathways which may be leveraged in the development of immune therapies for treating COVID-19 patients.

scholarly journals Severe pneumonia caused by Parvimonas micra: a case report

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qing Yu ◽  
Lingling Sun ◽  
Zuqing Xu ◽  
Lumei Fan ◽  
Yunbo Du
Keyword(s):  
Bronchoalveolar Lavage Fluid ◽  
Case Reports ◽  
Severe Pneumonia ◽  
Lavage Fluid ◽  
Due Date ◽  
Case Presentation ◽  
Abdominal Abscesses ◽  
Parvimonas Micra ◽  
Next Generation Sequencing Ngs ◽  
Generation Sequencing

Abstract Background Parvimonas micra (P. micra) is a gram-positive anaerobic coccus that is detected widely on the skin, in the oral mucosa and in the gastrointestinal tract. In certain circumstances, P. micra can cause abdominal abscesses, bacteraemia and other infections. To the best of our knowledge, there have been no case reports describing the biological characteristics of P. micra-related pneumonia. These bacteria do not always multiply in an aerobic organ, such as the lung, and they could be easily overlooked because of the clinical mindset. Case presentation A 35-year-old pregnant woman was admitted to the emergency department 4 weeks prior to her due date who was exhibiting 5 points on the Glasgow coma scale. A computed tomography (CT) scan showed a massive haemorrhage in her left basal ganglia. She underwent a caesarean section and brain surgery before being admitted to the ICU. She soon developed severe pneumonia and hypoxemia. Given that multiple sputum cultures were negative, the patient’s bronchoalveolar lavage fluid was submitted for next-generation sequencing (NGS) to determine the pathogen responsible for the pneumonia; as a result, P. micra was determined to be the causative pathogen. Accordingly the antibiotic therapy was altered and the pneumonia improved. Conclusion In this case, we demonstrated severe pneumonia caused by the anaerobic organism P. micra, and the patient benefited from receiving the correct antibiotic. NGS was used as a method of quick diagnosis when sputum culture failed to distinguish the pathogen.

scholarly journals Treatment with senicapoc in a porcine model of acute respiratory distress syndrome

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Asbjørn G. Petersen ◽  
Peter C. Lind ◽  
Anne-Sophie B. Jensen ◽  
Mark A. Eggertsen ◽  
Asger Granfeldt ◽  
...  
Keyword(s):  
Acute Respiratory Distress Syndrome ◽  
Lung Injury ◽  
Respiratory Distress Syndrome ◽  
Respiratory Distress ◽  
Bronchoalveolar Lavage ◽  
Primary Endpoint ◽  
Bronchoalveolar Lavage Fluid ◽  
Distress Syndrome ◽  
Pulmonary Hemorrhage ◽  
Lavage Fluid

Abstract Background Senicapoc is a potent and selective blocker of KCa3.1, a calcium-activated potassium channel of intermediate conductance. In the present study, we investigated whether there is a beneficial effect of senicapoc in a large animal model of acute respiratory distress syndrome (ARDS). The primary end point was the PaO2/FiO2 ratio. Methods ARDS was induced in female pigs (42–49 kg) by repeated lung lavages followed by injurious mechanical ventilation. Animals were then randomly assigned to vehicle (n = 9) or intravenous senicapoc (10 mg, n = 9) and received lung-protective ventilation for 6 h. Results Final senicapoc plasma concentrations were 67 ± 18 nM (n = 9). Senicapoc failed to change the primary endpoint PaO2/FiO2 ratio (senicapoc, 133 ± 23 mmHg; vehicle, 149 ± 68 mmHg). Lung compliance remained similar in the two groups. Senicapoc reduced the level of white blood cells and neutrophils, while the proinflammatory cytokines TNFα, IL-1β, and IL-6 in the bronchoalveolar lavage fluid were unaltered 6 h after induction of the lung injury. Senicapoc-treatment reduced the level of neutrophils in the alveolar space but with no difference between groups in the cumulative lung injury score. Histological analysis of pulmonary hemorrhage indicated a positive effect of senicapoc on alveolar–capillary barrier function, but this was not supported by measurements of albumin content and total protein in the bronchoalveolar lavage fluid. Conclusions In summary, senicapoc failed to improve the primary endpoint PaO2/FiO2 ratio, but reduced pulmonary hemorrhage and the influx of neutrophils into the lung. These findings open the perspective that blocking KCa3.1 channels is a potential treatment to reduce alveolar neutrophil accumulation and improve long-term outcome in ARDS.

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