Rituximab Administration in Coronavirus Pandemic Era: A Mini-Review of Clinical Evidence

Author(s):  
Ahmad Shamabadi ◽  
Hamidreza Mahmoudi ◽  
Maryam Daneshpazhooh

Rituximab (RTX), as a B cell-depleting agent, is indicated in treating several malignancies and autoimmune diseases. The management of patients currently receiving RTX and patients starting the medication raised concerns in the pandemic era. Theoretically, suppressing the immune response at the beginning of coronavirus disease 2019 (COVID-19) enhances viral replication, but it prevents acute respiratory distress syndrome as the disease progresses. This review aims to investigate the results of RTX administration in patients during the pandemic era. There is insufficient evidence to definitively conclude on the safety of RTX during the pandemic. For this purpose, high-quality controlled cohort studies, as well as registry-based studies, would be helpful.

2019 ◽  
Vol 32 (3) ◽  
pp. 347-360 ◽  
Author(s):  
Mitchell S. Buckley ◽  
Amy L. Dzierba ◽  
Justin Muir ◽  
Jeffrey P. Gonzales

Acute respiratory distress syndrome (ARDS) remains a common complication associated with significant negative outcomes in critically ill patients. Lung-protective mechanical ventilation strategies remain the cornerstone in the management of ARDS. Several therapeutic options are currently available including fluid management, neuromuscular blocking agents, prone positioning, extracorporeal membrane oxygenation, corticosteroids, and inhaled pulmonary vasodilating agents (prostacyclins and nitric oxide). Unfortunately, an evidence-based, standard-of-care approach in managing ARDS beyond lung-protective ventilation remains elusive, contributing to significant variability in clinical practice. Although the optimal therapeutic strategy for managing moderate to severe ARDS remains extremely controversial, therapies supported with more robust clinical evidence should be considered first. The purpose of this narrative review is to discuss the published clinical evidence for both pharmacologic and nonpharmacologic management strategies in adult patients with moderate to severe ARDS as well as to discuss practical considerations for implementation.


2009 ◽  
Vol 83 (14) ◽  
pp. 7062-7074 ◽  
Author(s):  
Barry Rockx ◽  
Tracey Baas ◽  
Gregory A. Zornetzer ◽  
Bart Haagmans ◽  
Timothy Sheahan ◽  
...  

ABSTRACT Several respiratory viruses, including influenza virus and severe acute respiratory syndrome coronavirus (SARS-CoV), produce more severe disease in the elderly, yet the molecular mechanisms governing age-related susceptibility remain poorly studied. Advanced age was significantly associated with increased SARS-related deaths, primarily due to the onset of early- and late-stage acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Infection of aged, but not young, mice with recombinant viruses bearing spike glycoproteins derived from early human or palm civet isolates resulted in death accompanied by pathological changes associated with ARDS. In aged mice, a greater number of differentially expressed genes were observed than in young mice, whose responses were significantly delayed. Differences between lethal and nonlethal virus phenotypes in aged mice could be attributed to differences in host response kinetics rather than virus kinetics. SARS-CoV infection induced a range of interferon, cytokine, and pulmonary wound-healing genes, as well as several genes associated with the onset of ARDS. Mice that died also showed unique transcriptional profiles of immune response, apoptosis, cell cycle control, and stress. Cytokines associated with ARDS were significantly upregulated in animals experiencing lung pathology and lethal disease, while the same animals experienced downregulation of the ACE2 receptor. These data suggest that the magnitude and kinetics of a disproportionately strong host innate immune response contributed to severe respiratory stress and lethality. Although the molecular mechanisms governing ARDS pathophysiology remain unknown in aged animals, these studies reveal a strategy for dissecting the genetic pathways by which SARS-CoV infection induces changes in the host response, leading to death.


2020 ◽  
Author(s):  
Devinder Toor ◽  
Aklank Jain ◽  
Shivani Kalhan ◽  
Harmesh Manocha ◽  
Vivek Kumar Sharma ◽  
...  

Hyper activation of macrophages contributes to acute respiratory distress syndrome, respiratory failure, and subsequent death of COVID-19 cases. Given this, tempering macrophage plasticity is paramount and the highest priority for the management of COVID-19 cases. In this context we here propose that either exchange or in situ re-programming of derailed Th17+ alveolar macrophages/ Slan+ DC with Th1 programmed counterpart would potentially mitigate or abolish pulmonary fibrosis. This approach is also anticipated to afford antiviral immune response and promote recovery in the patients and hold tremendous potential for managing severely infected patients by both curbing viruses and enhancing post-treatment recovery.


Author(s):  
Youenn Jouan ◽  
Antoine Guillon ◽  
Loïc Gonzalez ◽  
Yonatan Perez ◽  
Stephan Ehrmann ◽  
...  

AbstractCovid-19 can induce lung infection ranging from mild pneumonia to life-threatening acute respiratory distress syndrome (ARDS). Dysregulated host immune response in the lung is a key feature in ARDS pathophysiology. However, cellular actors in Covid-19-driven ARDS are poorly understood. Here, we dynamically analyzed the biology of innate T cells, a heterogeneous class (MAIT, γδT and iNKT cells) of T lymphocytes, presenting potent anti-infective and regulatory functions. Patients presented a compartmentalized lung inflammation paralleled with a limited systemic inflammation. Circulating innate T cells of critically ill Covid-19 patients presented a profound and persistent phenotypic and functional alteration. Highly activated innate T cells were detected in airways of patients suggesting a recruitment to the inflamed site and a potential contribution in the regulation of the local inflammation. Finally, the expression of the CD69 activation marker on blood iNKT and MAIT cells at inclusion was predictive of disease severity. Thus, patients present an altered innate T cell biology that may account for the dysregulated immune response observed in Covid-19-related acute respiratory distress syndrome.


Author(s):  
Ghazaleh Khalili-Tanha ◽  
Majid Khazaei ◽  
Saman Soleimanpour ◽  
Gordon A Ferns ◽  
Amir Avan

Abstract: The outbreak of COVID-19 that began in Wuhan, China, has constituted a new emerging epidemic that has spread around the world. There are some reports on illustrated the patients getting reinfected after recovering from COVID-19. Here we provide an overview of the biphasic cycle of COVID-19, genetic diversity, immune response and chance of reinfection after recovering from COVID-19. The new generation of COVID-19 is highly contagious and pathogenic infection can lead to acute respiratory distress syndrome. Whilst most patients suffer from a mild form of the disease, there is a rising concern that patients who recover from COVID-19 may be at risk of reinfection. The proportion of the infected population, is increasing worldwide; meanwhile, the rate and concern of reinfection by the recovered population are still high. Moreover, there are a few evidence on the chance of COVID-19 infection even after vaccination, which is around one per cent or less. Although the hypothesis of zero reinfections after vaccination has not been clinically proven, further studies should be performed on the recovered class in clusters to study the progression of the exposed with the re-exposed subpopulations to estimate the possibilities of reinfection and, thereby, advocate the use of these antibodies for vaccine creation.


2014 ◽  
Vol 21 (4) ◽  
pp. 213-215 ◽  
Author(s):  
William R Henderson ◽  
Donald EG Griesdale ◽  
Paolo Dominelli ◽  
Juan J Ronco

The emergence of computed tomography imaging more than 25 years ago led to characterization of acute respiratory distress syndrome (ARDS) as areas of relatively normal lung parenchyma juxtaposed with areas of dense consolidation and atelectasis. Given that this heterogeneity is often dorsally distributed, investigators questioned whether care for ARDS patients in the prone position would lead to improved mortality outcomes. This clinical review discusses the physiological rationale and clinical evidence supporting prone positioning in treating ARDS, in addition to its complications and contraindications.


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