Arthritis drug may help coronavirus patients by calming deadly inflammatory cytokine storms


Is Acterma the next severe COVID-19 treatment? All seven critically ill patients recovered from their fevers and needed less oxygen to breathe after treatment with arthritis drug in small new study

  • Researchers looked at coronavirus patients who have cytokine storms, which occur when the body attacks its own cells and tissues
  • They found these cytokines caused elevated levels of PAI-1, a protein which causes small blood clots in vessels throughout the body, including the lungs
  • Injections of arthritis drug tocilizumab decreased levels of PAI-1 in the blood as well as those of other cytokines
  • The drug also helped coronavirus patients break their fevers and come off of ventilators and oxygen therapy

A rheumatoid arthritis drug may help improve the conditions of severely ill patients, a new study suggests.  

Tocilizumab, sold under the brand names Actemra, is a medication with anti-inflammatory properties that scientists believe can control the immune system’s overreaction to the virus.    

Seven patients given doses of the drug saw severe symptoms reduce such a fevers and being able to come off of ventilators and oxygen therapy.

With no vaccines available yet, there is a pressing need to test both existing medicines and experimental therapies to stop the disease, which has killed more than 183,000 Americans, in its tracks. 

A new study found that tocilizumab (pictured), a drug used to treat rheumatoid arthritisd, helped coronavirus patients come off of ventilators and oxygen therapy

A new study found that tocilizumab (pictured), a drug used to treat rheumatoid arthritisd, helped coronavirus patients come off of ventilators and oxygen therapy

The drug decreased levels (above) of PAI-1, a protein which causes small blood clots in vessels throughout the body, including the lungs

The drug decreased levels (above) of PAI-1, a protein which causes small blood clots in vessels throughout the body, including the lungs

Tocilizumab belongs to a class of drugs called interleukin-6 (IL-6) inhibitors that could help mitigate a dangerous overreaction to the virus by the body’s immune system called a cytokine storm.

These so-called storms occur when the body doesn’t just fight off the virus but also attacks its own cells and tissues.

In cases of COVID-19, the disease caused by the virus, cytokine storms can trigger respiratory distress, which can lead to multi-system organ failure and death.

Currently, tocilizumab is not approved by the US Food and Drug Administration for use in coronavirus patients.

This overstimulation – also known as cytokine release syndrome (CRS) – can occur in people suffering microbial infections or trauma such as burns.

‘Despite knowing which cytokines are involved, there is still no specific immunotherapy for CRS and treatment is limited to supportive care,’ said lead author Sujin Kang, an assistant professor at Osaka University in Japan.

For the study, published in Proceedings of the National Academy of Sciences, the team looked at cytokines in 91 patients diagnosed with CRS.

Patients had high levels of of inflammatory cytokines IL-6, IL-8, IL-10, and MCP-10, as well as a protein called PAI-1, which causes small blood clots in vessels throughout the body, including the lungs.

Past studies have shown that increased PAI-1 levels are linked to more severe cases of pneumonia, a leading cause of death among those with COVID-19.  

‘Examination of cytokine profiles in severe COVID-19 patients revealed an increase in IL-6 early in the disease process, causing release of PAI-1 from blood vessels,’ said senior author Tadamitsu Kishimoto, a professor of immune regulation at Osaka.

‘Interestingly, PAI-1 levels were significantly higher in COVID-19 patients with severe respiratory impediment.’ 

This means that IL-6 is linked to the rise in levels of other cytokines and PAI-1, and that IL-6 signaling is crucial for patients to develop CRS.

Researchers gave the patients injections of tocilizumab, which decreased levels of PAI-1 in the blood as well as those of other cytokines.

Patients also saw an improvement in their clinical symptoms such as being able to come off ventilators or oxygen therapy. 

‘Notably, the decrease in PAI-1 levels and clinical improvements exhibited by COVID19 patients following tocilizumab injection suggest that tocilizumab treatment improved the vascular endothelial functions in these patients,’ the authors wrote.

‘Collectively, our findings suggest the possibility that elevated PAI-1 levels support the progression of endotheliopathy and coagulopathy in severe COVID-19 patients.’


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