The turning point for people with COVID-19 typically comes in the second week of symptoms. As most people begin to recover, a few others find it increasingly difficult to breathe and wind up in the hospital. It has been theorized that those whose lungs begin to fail are victims of their own overactive immune systems.
A new study from Washington University School of Medicine in St. Louis and St. Jude Children’s Research Hospital in Memphis, TN, however, suggests that an out-of-control immune response is not the main problem for majority of hospitalized COVID-19 patients. Only 4 percent of patients in the study had the high levels of immune molecules that signify a so-called cytokine storm. The rest had inflammation, but not a remarkably high amount for people fighting infection. If anything, the COVID-19 patients had less inflammation than a comparable group of influenza patients.
The findings, published Nov. 13 in Science Advances, may help explain why anti-inflammatory medications, such as dexamethasone, benefit a subset of people with severe COVID-19, and suggest that more research is needed to identify the causes of respiratory failure in COVID-19 patients.
The researchers analyzed immune cells and molecules in blood samples from 168 COVID-19 patients, 26 influenza patients and 16 healthy people. The samples were drawn from influenza patients in 2019 or 2020, and from COVID-19 patients and healthy controls this year. They also collected information about how each patient fared — whether a patient ended up needing intensive care or mechanical ventilation — and whether he or she survived.
The numbers of inflammatory cells in the blood of COVID-19 and influenza patients were about the same. Seven of the COVID-19 patients (4 percent) showed signs of a cytokine storm, with extremely high levels of cytokines even when compared to other severely ill patients. The majority of the COVID-19 patients with acute respiratory failure not only did not have a cytokine storm, they had less inflammation than influenza patients who were equally ill.
The key will be to find a way to identify the people at high risk for a cytokine storm when they first arrive at the hospital, so that steroid treatment can be appropriately targeted to the ones most likely to benefit and least likely to be harmed, the researchers said. They ran a panel of routine lab tests — blood cell counts, measurements of common inflammatory markers — but could not find a signature of an impending cytokine storm. They are pursuing more in-depth analyses to find a way to predict who will develop a cytokine storm.
