Thank you so much for sharing your experience. That is pretty much the majority of what we have at hand to work with right now, and coming together to put out any helpful info to others treating patients is exactly what we all need. Anyone reading your post should know that you were not stating it as dogma, but trying to help. This kind of communication is what is going to get us all through this and help our patients the most. If you are a member of the Facebook Covid physician/APP group, it would be very helpful to many of us throughout the country who are trying to learn as we go along. We in the group are not allowed to repost anything without the original posters permission. If you do not have Facebook or you are not on that group, if you would allow me to repost this I would like to please.
Clinical Pearls Covid 19 for ER practitioners
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Last: 4 yr ago by plain_o_llama
Is it just me or does anybody else think Texags gonna figure this disease out first?
We know stuff...Freeze Frame said:
Is it just me or does anybody else think Texags gonna figure this disease out first?
This above is an important development to be aware of; Actemra (Tocilzumab) was observed to really help the cytokine storm in China; it impacts/calms the IL-6 receptors in a way my non-medical brain can't explain.lmarcus said:
Patients are dying because of a cytokine storm and inappropriate autoimmune response with raised IL-6 and CRP levels. The x rays are ground glass and similar to patients with immune checkpoint induced pneumonitis.
And I found a potential answer in THIS FORUM!
EXERPT FROM PREPRESS ARTICLE:
https://www.sitcancer.org/research/covid-19-resources/il-6-editorial
In any case here is a quote from the article as there is already an FDA approved drug Tocilizumab to treat this !!!
Tocilizumab also is already FDA-approved to manage cytokine release syndrome (CRS) in patients receiving CAR T cell therapy [4, 5]. In addition, tocilizumab has been shown to reduce toxicity in patients treated with ICI who were steroid refractory [6], and has been added to the ICI agents ipilimumab and nivolumab in an ongoing US phase II study (NCT03999749) to ameliorate immune-related toxicity. In Castleman's disease, a lymphoproliferative disorder caused by Kaposi's Sarcoma Herpesvirus, a pathogen that produces viral IL-6, tocilizumab has been shown to reduce viral loads [7]. Tocilizumab is also being explored as a potential supportive care measure for the management of CRS in cancer patients treated with a number of CD3-based bispecific molecules. Now, data from the frontlines of the pandemic indicates that the agent may offer lifesaving benefit for COVID-19 patients with respiratory distress.
Emerging evidence suggests that high levels of CRP and IL-6 are observed in patients infected with COVID-19 [1, 8]. Anecdotal experience on the use of tocilizumab at doses comparable to those used for the management of CRS from investigators in Italy [9] and from China [10] has reported rapid improvement in both intubated and non-intubated patients. In these reports, expeditious administration of anti-IL-6R therapy for patients in acute respiratory distress has been critical. A recent study protocol to evaluate the efficacy of tocilizumab in COVID-19 induced pneumonitis accrued over 300 patients worldwide in less than 24 hours. Additionally, Genentech will also provide 10,000 vials of tocilizumab to the U.S. Strategic National Stockpile [11]. Tocilizumab was also approved in China in March 2020, for the treatment of patients with COVID-19 with serious lung damage and elevated IL-6
Can we help Jimbo next?Freeze Frame said:
Is it just me or does anybody else think Texags gonna figure this disease out first?
Sincere and Profound Gratitude to ALL of you on the Frontlines !!!
This is easier than going 15-0.Jackal99 said:Can we help Jimbo next?Freeze Frame said:
Is it just me or does anybody else think Texags gonna figure this disease out first?
To your point "or other medicine ":
"Nov 13, 2018 In a placebo-controlled clinical trial, clemastine strongly reduced IL-6 and TNF- ... Clemastine fumarate"
This is from article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6243034/
I was highly upset when clemastine fumarate was taken off the market as an OTC medicine as it was working wonders on my daughter's eye sight. Myelin damage mitochondrial disease related.
"Nov 13, 2018 In a placebo-controlled clinical trial, clemastine strongly reduced IL-6 and TNF- ... Clemastine fumarate"
This is from article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6243034/
I was highly upset when clemastine fumarate was taken off the market as an OTC medicine as it was working wonders on my daughter's eye sight. Myelin damage mitochondrial disease related.
"Nov 13, 2018 In a placebo-controlled clinical trial, clemastine strongly reduced IL-6 and TNF- ... Clemastine fumarate"
This is from article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6243034/
I was highly upset when clemastine fumarate was taken off the market as an OTC medicine as it was working wonders on my daughter's eye sight. Myelin damage mitochondrial disease related.
This is from article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6243034/
I was highly upset when clemastine fumarate was taken off the market as an OTC medicine as it was working wonders on my daughter's eye sight. Myelin damage mitochondrial disease related.
Had not heard of a connection between vitamin D and cytokine storms before, but this article from Science Daily reports on a data analysis study led by Vadim Backman of Northwestern.
Vitamin D levels appear to play role in COVID-19 mortality rates
Dated May 7, the summary says,
"Researchers analyzed patient data from 10 countries. The team found a correlation between low vitamin D levels and hyperactive immune systems. Vitamin D strengthens innate immunity and prevents overactive immune responses. The finding could explain several mysteries, including why children are unlikely to die from COVID-19."
Vitamin D levels appear to play role in COVID-19 mortality rates
Dated May 7, the summary says,
"Researchers analyzed patient data from 10 countries. The team found a correlation between low vitamin D levels and hyperactive immune systems. Vitamin D strengthens innate immunity and prevents overactive immune responses. The finding could explain several mysteries, including why children are unlikely to die from COVID-19."
There is continuing interest in this topic. Here is a review article:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7276229/pdf/main.pdf
The article speculates on a number of possible relationships between Vitamin D, Immunity, and Covid 19.
1.13. Cytokine storm: Vitamin D, SARS-CoV-2, and ACE2
In patients with a severe disease course (ARDS) a cytokine storm is assumed to be the underlying cause [130]. SARS CoV-2 can lead to a downregulation of ACE2 in the lungs and to a shedding of the ectodo- main of ACE2. This soluble sACE2 shows enzymatic activity, but the biological role is unclear. The soluble form is believed to exert systemic influence on angiotensin II [131]; since SARS-CoV-2 induces shedding, it is assumed that sACE2 is directly related to the virus-induced in-flammatory response [132].
Downregulation of ACE2 expression by SARS-CoV infection is as- sociated with acute lung damage (edema, increased vascular perme- ability, reduced lung function) [ 133] and with RAS dysregulation leading to increased inflammation and vascular permeability. In-flammatory cytokines such as TACE (TNF-a-converting enzyme) induce increase shedding [134], which in turn can be also caused by spike protein of the virus, promoting virus uptake by ACE2 [135].
Comparative studies on mortality rates in different countries and analysis of the relationship between vitamin D and CRP (as a marker of cytokine storm) plasma levels, concluded that risk factors for severity of the clinical course, predicted by high CRP and low vitamin D (< 25 nmol) levels, were reduced by by 15.6% following vitamin D status normalization (> 75 nmol) [136].
It is interesting to note that calmodulin kinase IV (CaMK IV) stimulates vitamin D receptor (VDR) transcription and interaction with co-activator SRC (steroid receptor coactivator) [ 137]. According to the authors, this would explain the linkage of the genomic and non-genomic membrane pathways of vitamin D. The calmodulin binding domain at ACE2 [138] may explain why calmodulin inhibits the shedding of the ectodomain of ACE2 [139]. It is also conceivable that vitamin D may show significant effects either by stimulating VDR-mediated transcription, or by med- iating 1,25(OH)D calcium-dependent activity through CaMK II and phospholipase A [140].
There is a link to ongoing clinical trials
https://clinicaltrials.gov/ct2/results?cond=vitamin+D+and+Covid-19
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7276229/pdf/main.pdf
The article speculates on a number of possible relationships between Vitamin D, Immunity, and Covid 19.
1.13. Cytokine storm: Vitamin D, SARS-CoV-2, and ACE2
In patients with a severe disease course (ARDS) a cytokine storm is assumed to be the underlying cause [130]. SARS CoV-2 can lead to a downregulation of ACE2 in the lungs and to a shedding of the ectodo- main of ACE2. This soluble sACE2 shows enzymatic activity, but the biological role is unclear. The soluble form is believed to exert systemic influence on angiotensin II [131]; since SARS-CoV-2 induces shedding, it is assumed that sACE2 is directly related to the virus-induced in-flammatory response [132].
Downregulation of ACE2 expression by SARS-CoV infection is as- sociated with acute lung damage (edema, increased vascular perme- ability, reduced lung function) [ 133] and with RAS dysregulation leading to increased inflammation and vascular permeability. In-flammatory cytokines such as TACE (TNF-a-converting enzyme) induce increase shedding [134], which in turn can be also caused by spike protein of the virus, promoting virus uptake by ACE2 [135].
Comparative studies on mortality rates in different countries and analysis of the relationship between vitamin D and CRP (as a marker of cytokine storm) plasma levels, concluded that risk factors for severity of the clinical course, predicted by high CRP and low vitamin D (< 25 nmol) levels, were reduced by by 15.6% following vitamin D status normalization (> 75 nmol) [136].
It is interesting to note that calmodulin kinase IV (CaMK IV) stimulates vitamin D receptor (VDR) transcription and interaction with co-activator SRC (steroid receptor coactivator) [ 137]. According to the authors, this would explain the linkage of the genomic and non-genomic membrane pathways of vitamin D. The calmodulin binding domain at ACE2 [138] may explain why calmodulin inhibits the shedding of the ectodomain of ACE2 [139]. It is also conceivable that vitamin D may show significant effects either by stimulating VDR-mediated transcription, or by med- iating 1,25(OH)D calcium-dependent activity through CaMK II and phospholipase A [140].
There is a link to ongoing clinical trials
https://clinicaltrials.gov/ct2/results?cond=vitamin+D+and+Covid-19
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