Posted on 04/08/2020 8:47:52 PM PDT by SeekAndFind
A hospital in France has had to stop an experimental treatment using hydroxychloroquine on at least one coronavirus patient after it became a "major risk" to their cardiac health.
The University Hospital Center of Nice (CHU de Nice) is one of many hospitals trialing hydroxychloroquine in COVID-19 patients. It announced it had been selected for the trial on March 22. A statement from the hospital said it was testing four experimental treatments, one of which included hydroxychloroquine. It hoped to establish its effectiveness and side effects of this and the other treatments being tested.
In an interview with the French daily newspaper Nice-Matin, Professor Émile Ferrari, the head of the cardiology department at the Pasteur hospital in Nice, said the side effects had already been identified, with some patients having to stop treatment because of the risk posed.
He said electrocardiogram recordings of patients involved with the trial were being constantly monitored. An ECG measures electrical activity in the heart, and represents this on a graph as a QT interval. Ferrari said these recordings are interpreted and, if anomalies are reported, treatment is stopped.
Asked if this had happened yet, he said: "Yes, from the start of the trial. Thanks to this ECG follow-up, we highlighted the major risks of a very serious accident in a patient, and the treatment was immediately stopped."
The potential cardiac side effects of hydroxychloroquine were highlighted by the Mayo Clinic at the end of March. An article on its website said the drug has potential to lead to sudden cardiac death in some patients. In a small number of patients it has the potential to lead to prolonged QTc , which can result in an abnormal heart rhythm.
Hydroxychloroquine, Mayo Clinic said, blocks one of the channels that controls the heart's electrical recharging systems.
(Excerpt) Read more at newsweek.com ...
“You’re also wrong about antibiotics having no effect upon viruses. There are numerous examples of antibiotics having an antiviral effect. “
I’ll bite. Please source.
“It’s you and your tiresome devil’s advocate nonsense that’s BS. You’re wrong constantly, absolutely cannot admit it and continue on with the asinine rude corrections no matter what.”
I see you got the notification from Osage Orange!
R-on-T Vtach and can trip into vfib. The QT prolongs and interferes with the next “P” causing early depolarization of the next “Beat cycle”...there can be a whole following cascade of faster and faster early depolarizations that trip the heart into vatch. The heart has to be shocked back into rhythm and meds given to control the arrhythmia from occurring again...amiodarone or lidocaine.
Are you obtuse or do search engines just confuse you? Here, try this one regarding Azithromycin:
https://erj.ersjournals.com/content/45/2/428
Clinical studies are needed to elucidate the potential of azithromycin in the management and prevention of RV-induced CF pulmonary exacerbations.
Well, you can read at least. Can you explain why you believe that statement means Azithromycin does not have antiviral effect? Because that is what you’re claiming.
The bottom line is there’s no evidence outside of this publication that would suggest that there’s going to be some bang out of giving azithromycin to our patients. There’s no in vitro data against any coronaviruses, let alone SARS-CoV-2. There’s no clinical data. There’s no animal data.
When you start to walk through that process, in my opinion, it gets really hard to get to a logical place that azithromycin is playing a role here.
Both drugs can be associated with QT prolongation. If you give them both, that’s an additive adverse event that you could see in a patient. So without a real good reason to think that there is a benefit. Again, there’s no other data that supports it.
We talked about the limitations and what happens when you compare like therapies. It’s my opinion that there’s no rationale to give this combination right now, and the risk absolutely outweighs the benefits.
In my opinion, there’s nothing in this study that really supports that combination therapy would be a good thing.
“Well, you can read at least. Can you explain why you believe that statement means Azithromycin does not have antiviral effect? Because that is what you’re claiming.”
I believe you have misstated my position.
Seeing a small effect in a petri dish. is a far distance from using it as a cure for a virus.
Please review in the document the mechanism discussed.
Why do doctors prescribe z-packs for colds? As I said, I was quoting doctors who were describing the regimen of treatment and the reasons for it. Argue with them. Their bonofides far exceed mine.
“As I said, I was quoting doctors”
hmmm .., what quotes?
“Why do doctors prescribe z-packs for colds? As I said, I was quoting doctors who were describing the regimen of treatment and the reasons for it. Argue with them. Their bonofides far exceed mine.”
The Z pack is a 5-day antibiotic treatment that does not work on the common cold. Viral infections cause the common cold, but the Z pack only works on bacterial infections.
https://www.medicalnewstoday.com/articles/323770
“Why do doctors prescribe z-packs for colds? As I said, I was quoting doctors who were describing the regimen of treatment and the reasons for it. Argue with them. Their bonofides far exceed mine.”
First of all who keeps giving you the Z-Pack for a simple cold? It;s true antibiotics don’t work for viruses in fact nothing can cure a viruse. That’s why Aids has been so horrific and hard to treat because antibiotics only kill bacteria. I’m thinking that when you get these colds and you take the Z-pack (Azithromycin) that it is just a coincidence becasue a true cold will only last 2-5 days. So, you could be just assuming that it’s the pills. The only time a doctor SHOULD give us any type of antibiotic for a cold or flu is after you’ve had it for about 2 weeks and it’s not going away, OR if you are getting sicker, then the doctor will assume that a secondary infection from a bacteria set in. I blame the doctors for all of these super-bugs which are antibiotic resistence because many doctors didn’t want to lose their patients so they would oblige them by giving them what they asked for and that is usally antibiotics. I know that 40 to 50 years ago doctors never imagined that this day would come and I am sure that they didn’t think by giving people all of these antibiotics for things that they don’t work for would cause such horrible deadly problems today. It was hard for me once to comprehend the idea that what other people did with antibiotics could affect me intil a few years ago. Meaning that if one person has a bacterial infection and he gets antibiotics for it and only takes half of them what happens is the bugs start to die but the ones that didn’t die yet become immuned to the antibiotics and they flee from that persons body and go on to the next person which is called a host.
https://www.medications.com/azithromycin-5-day-dose-pack/seem-work-cold
"Along with other medications, it may also be used for malaria.[3] It can be taken by mouth or intravenously with doses once per day." [ "Azithromycin". The American Society of Health-System Pharmacists. Archived from the original on 5 September 2015. Retrieved 1 August 2015.]
According to the Chinese research study, Covid 19 acts much like malaria in its interaction with hemoglobin. Ergo the combination of a malaria drug and azythromycin just as in the treatment of Malaria. Is the Chinese study Gospel? I don't know, but it was a well structured study, came to reasonable conclusions based on the evidence and it matches well with real world evidence like the fact that 80% of patients placed on a ventilator end up dying. 85%+ of covid 19 patients placed on a regimen of hydroxycloroquine, azythromycin (or doxycycline) and zinc end up living.
Still waiting for your references to doctors prescribing antibiotic for the common cold.
Hydroxychloroquine increases[32] lysosomal pH in antigen-presenting cells. In inflammatory conditions, it blocks toll-like receptors on plasmacytoid dendritic cells (PDCs).[citation needed] Toll-like receptor 9 (TLR 9), which recognizes DNA-containing immune complexes, leads to the production of interferon and causes the dendritic cells to mature and present antigen to T cells. Hydroxychloroquine, by decreasing TLR signaling, reduces the activation of dendritic cells and the inflammatory process.[medical citation needed]
In 2003, a novel mechanism was described wherein hydroxychloroquine inhibits stimulation of the toll-like receptor (TLR) 9 family receptors. TLRs are cellular receptors for microbial products that induce inflammatory responses through activation of the innate immune system.
[3
wiki
No references, totally anecdotal. I see no value in belaboring the point.
I am not testifying this study is correct. It is however the most complete and thorough that i have seen related to the actual Covid 19 attack mechanism. It also conforms to the observations and results reported from hospitals on hydroxy vs. non-hydroxy patient outcomes. I'll leave it to experts and clinicians to argue it.
This paper is only for academic discussion, the correctness needs to be confirmed by other laboratories.
“No references, totally anecdotal. I see no value in belaboring the point.
Except it is the basis of your argument!
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