Henry says much of the debate around COVID-19 research has been on the potential for danger from certain drugs, such as ACE inhibitors and angiotensin receptor blockers, because of the disruption of RAAS, while other researchers are testing those same drugs as therapies in patients with COVID-19.
“We were interested in trying to figure out what’s actually going on with RAAS,” Henry says. “There are a lot of clinical trials targeting RAAS, but no one has really examined if it is truly affected and disturbed in these patients. That was the focus of our investigation.”
When COVID-19 first hit, anyone presenting to University of Cincinnati Medical Center with potential symptoms of the virus was isolated in a separate part of the emergency department called the “Respiratory ED.” A lot of those people were getting blood work done, so researchers were able to pull a blood sample from those patients.
“This sets up a nice, natural experiment where all these patients are in the ED and they all have respiratory symptoms,” says Justin Benoit, MD, assistant professor in the Department of Emergency Medicine at the UC College of Medicine, who ran the logistics of the study. “Some have COVID, some do not, and we don’t know who does or doesn’t have COVID when you’re drawing the blood. Then you can start looking for differences. Since they all present similarly, when you find differences between these patient groups, you might be able to attribute that to COVID.”
Benoit says the researchers’ goal was to try to find pathways that are altered in patients with COVID-19 that have specific pharmacological targets that could be used in subsequent studies.
“We were trying to inform clinical trials because there are a lot of trials being proposed or up and running at UC and in other places, but most are based on theory and conjecture and not necessarily based on actual data,” Benoit says.