there are two studies starting in Europe, one for stellate ganglion injection with procain 1% as an adjuvant therapy for viral pneumonia and one with local anaesthesia infusion therapy. Both are not regarded as promising from ICU chiefs point of view. As you can read in my own questions asked, I believe very much in these treatments, because they can, in my opinion, tune done sympathetic nerve hyperactivation
Article Cutting Edge: Sympathetic Nervous System Increases Proinflam...
and hopefully prevent cytokine storm and ARDS. Licocain 1%and Procain 1% are short term (60min and 20min) local anesthetics with anti-inflammatory potential.
Article Anti-inflammatory properties of local anesthetics and their ...
I suggested Procain 1% or Lidocain 1% inhalation therapy in small doses via dose aerosol without nebulizer, because there is the fear of contamination of the air with Sars-CoV-2 around the patient and the risk of infection for health care workers.
Another very easy treatment would be a series of wheals dorsal or ventral in the segments C8-Th4 using the cutivisceral reflex path (e.g. injection of Procain 1% intracutanously, each wheal with 0.5 to 1ml).
At that point, you are talking about something similar to SIRS, even though it may not necessary involve the entire system, when the inflammatory response is uncontrolled.
Strangely enough, if you look at the many many many studies over the years, trying to use anything as an anti-inflammatory counterpart and/or to modulate the immune response rarely, if ever, works. The new ideas in the neuro-immune field are interesting, but time will tell if this is what is missing in our understanding of what happens during such events. (My own personal opinion is that we rarely succeed because we are focusing on just one part of the issue. Once it hits that point, we probably have to control everything, meaning you need multiple drugs to target all factors involved.)
Right now, the trick is to do the treatment before it hits that threshold.
The cytokines storm is based mainly on TNF alpha and interleukin-6. That is the reason why tocilizumab (against IL6) seems to be working in COVID 19. Infliximab may be also a useful adjunct.
Emodin was never tested. On a theoreticall basis it may be useful because it down regulates both.
One of the defining features of Covid-19 is the excessive immune response that can occur in severe cases. This burst of immune overreaction, also called a cytokine storm, damages the lungs and can be fatal.
A new study researchers has developed specialized proteins, similar in structure to antibodies, that they believe could soak up these excess cytokines.
“The idea is that they can be injected into the body and bind to the excessive cytokines as generated by the cytokine storm, removing the excessive cytokines and alleviating the symptoms from the infection
Good health is the most effective way in preventing cytokine storm. And I believe that the gut microbiome is the key for a good health, as they provide us with the essential nutrients that we cannot get from any other food or supplements. If you are interested, following please find our recent paper on gut microbiome:
The cytokines storm is based mainly on TNF alpha and interleukin-6. That is the reason why tocilizumab (against IL6) seems to be working in COVID 19. Infliximab may be also a useful adjunct.
Emodin was never tested. On a theoreticall basis it may be useful because it down regulates both.
One of the defining features of Covid-19 is the excessive immune response that can occur in severe cases. This burst of immune overreaction, also called a cytokine storm, damages the lungs and can be fatal.
A team of MIT researchers has developed specialized proteins, similar in structure to antibodies, that they believe could soak up these excess cytokines.
“The idea is that they can be injected into the body and bind to the excessive cytokines as generated by the cytokine storm, removing the excessive cytokines and alleviating the symptoms from the infection,” says Rui Qing, an MIT research scientist who is one of the senior authors of the study.
The researchers have reported their initial findings in the journal Quarterly Review of Biophysics (QRB) Discovery, and they now hope to begin testing their proteins in human cells and in animal models of cytokine release and coronavirus infection.
The first hints that severe COVID-19 cases included a cytokine storm came out of Chinese hospitals near the outbreak’s epicenter. Physicians in Wuhan, in a study of 29 patients, reported that higher levels of the cytokines IL-2R and IL-6 were found in more severe Covid-19 infections.
IL-6 was also an early indicator of a cytokine storm-like condition in an 11-patient analysis by physicians in Guangdong. Another team, analyzing 150 cases in Wuhan, found that an array of molecular indicators for a cytokine storm — including IL-6, CRP and ferritin — were higher in those who died than in those who survived.
And immunologists in Hefei reported similar results among patients who died, as well as high levels of active, damaging immune cells spewing dangerous cytokines in the blood of Covid-19 patients who required intensive care.