Liver injury associated with acute respiratory distress syndrome and the prospects of mesenchymal stromal cells therapy for liver failure

The pathogenesis of acute respiratory distress syndrome (ARDS) includes neutrophilic alveolitis, alteration of alveolar epithelium and endothelium, formation of hyaline membranes and microvascular thrombosis, which results in an acute hypoxemic respiratory failure. ARDS results in major structural and cellular changes in organs and organ systems. It causes liver dysfunction in critical patients through paracrine action of cytokines and other pro-inflammatory mediators as well as hypoxemia, oxidative stress, toxins and hypoperfusion. Coronavirus disease 2019 (COVID-19)-associated ARDS affects liver through the development of systemic inflammatory response syndrome and hypoxia as well as cytokine storm. Liver injury manifests itself as increased plasma levels of hepatic transaminases and cholestatic liver enzymes. Stem cell therapy is one of the promising modern methods for treating ARDS-induced liver failure. Many studies showed the ability of multipotent mesenchymal stromal cells (MMSCs) to differentiate into functional hepatocyte-like cells, which were then successfully used for liver regeneration. MMSCs were proven to be able to prevent the apoptosis of hepatocytes, as well as have anti-fibrotic and anti-inflammatory activity which allows their successful use in the treatment of ARDS-induced liver injury. © 2021 The authors.

COVID-19-associated acute respiratory distress syndrome versus classical acute respiratory distress syndrome (a narrative review)

Coronavirus disease 2019 (COVID-19), caused by the novel coronavirus, Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), led to the ongoing global public health crisis. Existing clinical data suggest that COVID-19 patients with acute respiratory distress syndrome (ARDS) have worse outcomes and increased risk of intensive care unit (ICU) admission. The rapid increase in the numbers of patients requiring ICU care may imply a sudden and major challenge for affected health care systems. In this narrative review, we aim to summarize current knowledge of pathophysiology, clinical and morphological characteristics of COVID-19-associated ARDS and ARDS caused by other factors (classical ARDS) as defined by Berlin criteria, and therefore to elucidate the differences, which can affect clinical management of COVID-19-associated ARDS. Fully understanding the characteristics of COVID-19-associated ARDS will help identify its early progression and tailor the treatment, leading to improved prognosis in severe cases and reduced mortality. The notable mechanisms of COVID-19-associated ARDS include severe pulmonary infiltration/edema and inflammation, leading to impaired alveolar homeostasis, alteration of pulmonary physiology resulting in pulmonary fibrosis, endothelial inflammation and vascular thrombosis. Despite some distinct differences between COVID-19-associated ARDS and classical ARDS as defined by Berlin criteria, general treatment principles, such as lung-protective ventilation and rehabilitation concepts should be applied whenever possible. At the same time, ventilatory settings for COVID-19-associated ARDS require to be adapted in individual cases, depending on respiratory mechanics, recruitability and presentation timing.