An international clinical trial has been launched after a cancer drug that targets the root cause of extreme inflammation showed promise in a preliminary study.
In some people with mild or moderate COVID-19, the illness caused by the SARS-CoV-2 virus, their condition briefly improves, only to suddenly worsen.
These people may then develop severe breathing difficulties, known as acute respiratory distress syndrome.
Scientists speculate that even when the infection is being brought under control, the virus can trigger an excessive immune response, causing hyper-inflammation of the lungs and other organs.
This type of inflammatory response is thought to begin when receptors in immune cells called macrophages recognize the genetic material of viruses such as SARS-CoV-2. They respond by initiating a massive release of immune-signalling molecules called cytokines.
This “cytokine storm” appears to cause the hyper-inflammation that damages the lungs and other organs of critically ill patients. Currently, no proven treatment can prevent or reverse the damage.
In macrophages, an enzyme called Bruton tyrosine kinase (BTK) is responsible for initiating the cytokine storm.
A drug that inhibits the activity of BTK — called acalabrutinib — is already in use as a treatment for certain blood cancers.
Researchers at the National Cancer Institute, in the United States, realized that because acalabrutinib inhibits BTK, it could potentially reduce inflammation in people with severe COVID-19.
To test the safety and efficacy of the drug in this context, they collaborated with scientists at the National Institute of Allergy and Infectious Diseases, the Walter Reed National Military Medical Center, and four other hospitals in the country.
The researchers have published the results of their trial in the journal Science Immunology.
For between 10 and 14 days, the team administered the drug to 19 people hospitalized for COVID-19. At the start of the study, 11 participants were breathing with the help of oxygen masks, and eight were on ventilators.
By the end of the follow-up period, eight of the 11 patients who had been receiving supplemental oxygen no longer needed help breathing and had been discharged from the hospital.
Of the eight patients on ventilators at the start of the treatment, four had been taken off the machines, or “extubated,” and two had been discharged. Two of the patients had died.
The drug, however, appeared to cause no toxic side effects.
The researchers also monitored two markers of inflammation in the blood — levels of a cytokine called interleukin 6 (IL-6) and C-reactive protein (CRP).
Of the 11 patients on supplemental oxygen at the start of the study, CRP levels returned to normal in 10 and were decreasing in one. Of the five patients who also had their IL-6 levels measured, the levels of three had returned to normal, and the levels of two had fallen sharply.
The picture was more mixed among the patients on ventilators. Reductions were smaller overall, and in some of these patients, the levels fluctuated.
Source: MedicalNews Today
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