scholarly journals Coronavirus: A Disease of the Haemoglobin? Suggested Therapeutic Approaches

2020 ◽  
Vol 10 (6-s) ◽  
pp. 1-2
Author(s):  
Moustapha Diedhiou ◽  
A. Dieye ◽  
D. Makalou ◽  
E.B. Ba ◽  
M.L. Fall ◽  
...  

The pathophysiology of the coronavirus infection is not yet fully understood. Several theories have been developed from the acute respiratory distress syndrome to antiphospholipid antibody syndrome to vascular thrombosis. It is in this context that we propose through brainstorming some proposals for the therapeutic management based on secondary haemoglobin damage by COVID-19. Keywords: coronavirus - haemoglobin - chloroquine - pathophysiology

2020 ◽  
Vol 49 (6) ◽  
pp. 758-760
Author(s):  
Emanuele Rossetti ◽  
Linda Appierto ◽  
Antonella Meschini ◽  
Giovanna Leone ◽  
Stefania Lazzaro ◽  
...  

We describe a 2 weeks corrected gestational age infant admitted in pediatric intensive care unit (PICU) for severe acute respiratory distress syndrome (ARDS) associated to <i>Bordetella pertussis</i> and Coronavirus infection. He developed leukocytosis as soon as ARDS required intubation and aggressive mechanical ventilation: hence he underwent 3 early therapeutic leukapheresis treatments in order to avoid the worsening of related cardiopulmonary complications, according to recent literature on pertussis infection in infants. The infant was discharged from PICU healthy.


2021 ◽  
Vol 12 ◽  
Author(s):  
Anna Kosyreva ◽  
Dzhuliia Dzhalilova ◽  
Anastasia Lokhonina ◽  
Polina Vishnyakova ◽  
Timur Fatkhudinov

Macrophages are cells that mediate both innate and adaptive immunity reactions, playing a major role in both physiological and pathological processes. Systemic SARS-CoV-2-associated complications include acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation syndrome, edema, and pneumonia. These are predominantly effects of massive macrophage activation that collectively can be defined as macrophage activation syndrome. In this review we focus on the role of macrophages in COVID-19, as pathogenesis of the new coronavirus infection, especially in cases complicated by ARDS, largely depends on macrophage phenotypes and functionalities. We describe participation of monocytes, monocyte-derived and resident lung macrophages in SARS-CoV-2-associated ARDS and discuss possible utility of cell therapies for its treatment, notably the use of reprogrammed macrophages with stable pro- or anti-inflammatory phenotypes.


2017 ◽  
Vol 141 (12) ◽  
pp. 1719-1727 ◽  
Author(s):  
Vera Luiza Capelozzi ◽  
Timothy Craig Allen ◽  
Mary Beth Beasley ◽  
Philip T. Cagle ◽  
Don Guinee ◽  
...  

Acute respiratory distress syndrome (ARDS) is a multifactorial syndrome with high morbidity and mortality rates, characterized by deficiency in gas exchange and lung mechanics that lead to hypoxemia, dyspnea, and respiratory failure. Histologically, ARDS is characterized by an acute, exudative phase, combining diffuse alveolar damage and noncardiogenic edema, followed by a later fibroproliferative phase. Despite an enhanced understanding of ARDS pathogenesis, the capacity to predict the development of ARDS and to risk-stratify patients with the disease remains limited. Biomarkers may help to identify patients at the greatest risk of developing ARDS, to evaluate response to therapy, to predict outcome, and to improve clinical trials. The ARDS pathogenesis is presented in this article, as well as concepts and information on biomarkers that are currently used clinically or are available for laboratory use by academic and practicing pathologists and the developing and validating of new assays, focusing on the assays' major biologic roles in lung injury and/or repair and to ultimately suggest innovative, therapeutic approaches.


2020 ◽  
Vol 34 (1) ◽  
Author(s):  
Chao Quan ◽  
Caiyan Li ◽  
Han Ma ◽  
Yisha Li ◽  
Huali Zhang

SUMMARY The outbreak of coronavirus disease 2019 (COVID-19) in December 2019 in Wuhan, China, introduced the third highly pathogenic coronavirus into humans in the 21st century. Scientific advance after the severe acute respiratory syndrome coronavirus (SARS-CoV) epidemic and Middle East respiratory syndrome coronavirus (MERS-CoV) emergence enabled clinicians to understand the epidemiology and pathophysiology of SARS-CoV-2. In this review, we summarize and discuss the epidemiology, clinical features, and virology of and host immune responses to SARS-CoV, MERS-CoV, and SARS-CoV-2 and the pathogenesis of coronavirus-induced acute respiratory distress syndrome (ARDS). We especially highlight that highly pathogenic coronaviruses might cause infection-associated hemophagocytic lymphohistiocytosis, which is involved in the immunopathogenesis of human coronavirus-induced ARDS, and also discuss the potential implication of hemophagocytic lymphohistiocytosis therapeutics for combating severe coronavirus infection.


2021 ◽  
Vol 5 (1) ◽  
pp. 1223-1233
Author(s):  
A.A. Pleshko ◽  
◽  
E.B. Petrova ◽  
S.V. Gunich ◽  
S.V. Rakovich ◽  
...  

Officially announced by the World Health Organization (WHO) in March 2020, the coronavirus disease 2019 (COVID-19) pandemic is terrifying with the unimaginable rate of spreading and the large number of deaths. More than 171 million COVID-19 cases including more than 3,6 million deaths have been confirmed worldwide since the start of the pandemic. The high incidence of venous thromboembolic events and non-ARDS (acute respiratory distress syndrome) associated death of patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, despite prophylactic antithrombotic therapy, may indicate the need for a more intensified personalized regime of preventive measures. Respiratory viruses such as influenza A H1N1, SARS-CoV, MERS-CoV and SARS-CoV-2 are known for their affinity for lung tissue and the ability to lead to viral pneumonia and acute respiratory distress syndrome (ARDS). The analyzed data bring up to the hypothesis that microvascular thrombosis, rather than decreased lung compliance, provides oxygenation impairment in COVID-19 patients. The accumulated experience in the management of patients with SARS-CoV-2 indicates that the pathophysiology of systemic microthrombosis associated with COVID-19 may differ from that in sepsis-induced disseminated intravascular coagulation (DIC). In contrast to sepsis-induced coagulopathy consumption of platelets, clotting factors, fibrinogen, and bleeding are rare in patients with severe SARS-CoV-2, suggesting that DIC is not a common complication of COVID-19. The development of micro- and macrovascular thrombosis of the venous and arterial bed in patients with SARS-CoV-2 makes it possible to consider COVID-19 as a systemic “thromboinflammatory” syndrome. According to the international analytical studies, the proportion of thrombosis and thromboembolic complications ranges from 0.9% to 6.5 in patients with a moderate COVID-19, and from 8% to 69% in patients treated in intensive care unit, the proportion of acute arterial obstruction in SARS-CoV-2 patients ranges 0.39% to 11.1%. The team of authors carried out a retrospective analysis of the medical records of 7607 patients hospitalized in 2020 in the infectious disease departments of the 4th city clinical hospital named after N.E. Savchenko. The proportion of patients with pulmonary embolism (PE) in the final diagnosis was 2.1% (n=163), the proportion of patients with deep vein thrombosis (DVT) was 0.9% (n=68), in the structure of patients with DVT the complication of PE was 58.8% (n=40). The variation in the data of national and foreign studies may apparently be related to different diagnostic tactics in verifying the diagnosis of VTE and DVT: the use of duplex ultrasound vascular examination and/or computed tomographic angiography (CTA) of the lungs as screening techniques, the inclusion of different clinical points (symptomatic and/or asymptomatic VTE) by authors in publications, the lack of uniform approaches to thromboprophylaxis, and population differences in the patient samples. There is an urgent need for more in-depth studies of the pathogenesis and molecular basis of thrombosis in patients with COVID-19 to establish the prognostic value of changes in the hemostasis system associated with SARS-CoV-2. Considering unknown long-term results in COVID-19 convalescents, many studies signaling the presence of disabling consequences and the need for subsequent full medical and non-medical rehabilitation, the search for new biomarkers, such as of coagulation, fibrinolysis, activation of endothelium, that are associated with the course, early outcomes and delayed complications in patients with coronavirus infection (SARS-CoV-2) remains relevant.


2020 ◽  
Author(s):  
YuV Lobzin ◽  
MB Ivanov ◽  
EB Shustov ◽  
VL Rejnyuk ◽  
AV Fomichev ◽  
...  

The article analyzes the links of pathogenesis of a new coronavirus infection that lead to severe clinical manifestations of the disease – acute respiratory distress syndrome, multiple organ failure and endotoxicosis. The sequence of development of the infectious process from the moment the virus enters the body from the external environment to the damage of the alveolar-capillary barrier and the development of acute respiratory distress syndrome is presented. Factors of initiation of pathological processes leading to the development of acute respiratory distress syndrome are described, among which special attention is paid to oxidative stress, hyperreactivity of the immune system, endothelial dysfunction and cytotoxic action of the virus. Possible pharmacotherapeutic directions of COVID-19 treatment are discussed, taking into account different pathogenesis links. Flowcharts for the sequence of events during COVID-19 infection have been developed.


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