Jean Paul Hamon, medical doctor and president of the Federation of French Doctors said on TV to NOT take NSAIDs (anti-inflammatory drugs) if #covid19 is suspected. The ONLY common point among young covid-19 patients they have witnessed in critical care centers in France was that they all took NSAIDs.
Under "What treatments are available to treat coronavirus?":
Currently there is no specific antiviral treatment for COVID-19. However, similar to treatment of any viral infection, these measures can help... ... Take acetaminophen, ibuprofen, or naproxen to reduce fever and ease aches and pains. Be sure to follow directions. If you are taking any combination cold or flu medicine, keep track of all the ingredients and the doses. For acetaminophen, the total daily dose from all products should not exceed 3,000 milligrams.
So it seems there is no widespread consensus on the matter for now. North American professionals, from what I've seen on social media, tend to disagree with their European colleagues on the matter.
Personally, I remain somewhat skeptical until there's more data available.
[0] https://www.health.harvard.edu/diseases-and-conditions/coron...
Edit: link to recommendation https://www.bag.admin.ch/bag/de/home/das-bag/aktuell/news/ne...
Normally when you see young people taking large doses of NSAIDs, it's because they're either elite athletes or have an autoimmune disease or something.
There are enough people who have no idea that hang-over + pop-2-advil is a deadly combination in this situation.
Also a lot of the "new year, new body" resolution folks start too hard at the gym & then push through with NSAIDs.
Young people, particularly the fit, do go through a lot of NSAIDs out of OTC convenience.
Does it make sense that a virus would evolve to favour these conditions? Or is it just an unfortunate coincidence? I guess it depends on whether the virus being "worse" means it helps spread faster, or just compromises the host faster - after all, the virus doesn't gain from killing its host. Also, animals don't get treated with NSAIDs to the same degree, so if nCovid-19 came from a non-human host that's another argument for it being coincidence.
If you're intending to take paracetamol long term, you can do worse than to reduce the stated maximum daily dose on the bottle by 1/4 or 1/2. You'll be less comfortable, sure. But it's called a "liver" because you need one to live. So it's worth a little extra discomfort to avoid the risk of breaking yours.
Paracetamol is probably as safe as it gets when it comes to drugs in its class. Overdosing is not all that simple and the numbers are high because of the availability and popularity of Paracetamol as a pain-killer and its silent use as a side ingredient in many products. Paracetamol is not as good as Ibuprofen when it comes to killing pain (IMHO), so maybe this causes a tendency to overdose in people who have built a tolerance to the drug.
To get liver damage, you have to exceed the daily recommended maximum of 4g of Paracetamol. Wiki says paracetomol toxicity is likely if your consumption exceeds 7g in a day [1]. Assuming you are a consuming Paracetamol in the form of OTC pills, say the super strength ones which are 500mg, you have to consume like 15 pills in a day. Overdosing from a combination of drugs containing paracetamol is much more likely. Most people don't realize the presence of the other ingredient.
For short term use, Ibuprofen is said to have a similar safety profile to Paracetamol, though its classification as an NSAID lends to its perception as a slightly less safe drug. Long term, it causes stomach and kidney damage.[2]
Anecdotally, Ibuprofen is much better at killing my pain, but I also have some negative reactions like increased reflux. Technically, Paracetamol also increases acidity but I tolerate it much better. I've mostly stopped using NSAIDs but I realize this is not possible for a lot of people.
[1]: https://en.wikipedia.org/wiki/Paracetamol_poisoning#Cause
I strongly doubt that COVID-19 has been exposed to NSAIDs long enough to result in evolution of any type. The paper suggests that NSAIDs make us more biocompatible, so it really is just a coincidence. Lots of medications have contra-indications.
NSAIDs are considerably more harmful than might be assumed from their availability and public perception. Over the past half decade, I've heard doctors recommending with increasing frequency against cessation of OTC NSAID use. Research available on Pubmed and NCBI seems to agree.
I'm also in a common but at-risk group for Covid-19 that should never use NSAIDs, but I think qualifications of their safety shouldn't be accepted outside of any but a very loose definition of 'generally'.
In related news, there have been cases of "severe" forms of Covid-19 among young people with no antecedents, all of them having taken ibuprofen.
Please don't take ibuprofen.
The commentator comes here with some assumptions, perhaps some hearsay, and an emotional attachment to their position and make the statement as though it's fact.
In this comment, you know what's missing? Actual knowledge, actual reasoning, and actual facts to back up the his/her claims. Perhaps worse, there are some facts (Ibuprofen suppresses some immune system responses to infection) which are used to draw unsubstantiated conclusions about the commentator's opinions (Ibuprofen can cause severe forms of Covid-19 in young people).
From where did this "related news" come from? On what rational basis do you draw the conclusion that an across-the-board recommendation not to take Ibuprofen is warranted? How does that trump other factors that may be at play?
What I really worry about though is how many people will read the comment I'm responding to and go on to post elsewhere, "in related news...", with a similar air of self-certainly and casting of opinions as facts. In other contexts of high emotion, people get lynched because of this sort of social media posting, people may cause themselves harm because of this kind of posting.
By the way, the commentator may actually be right... but there is nothing in the comment to make me believe that his/her being right would be anything more than coincidence.
I'll leave with the personal observation that this community is suppose to be made up of "the smart ones"; which we ourselves so often confidently believe to be true that we all too frequently think we should be able to engineer society and solve all its ills. If there is any one ponder-able to take away from reading Hacker News on regular basis, it's how decidedly average even "the smart ones" can be on any given topic.
I'm not sure what you're trying to say here - are you claiming that all young people with severe cases of COVID-19 (including, for instance, 33-year-old Wenliang Li) took ibuprofen?
Or simply that there exists a small group of people such that all people in that group took ibuprofen, and there are also other young people with severe cases who did not?
Given that standard advice for young people (who are expected not to have severe cases) is to take fever-reducing medication like ibuprofen, I feel like we need a lot more information here before we can turn this correlation into causation.
What makes you feel qualified to give medical advice on an Internet forum?
There might be negatives to taking ibuprofen in relation to COVID-19, but so far no official guidelines exist. Only internet stories. Responsible institutes have not handed out such advice, nowhere.
I’m not saying anyone should just stop taking their hypertension drugs, that’s a horrible idea. But if you do suspect that you might have COVID-19, you should probably call your doctor - there’s no shortage of other options.
One of those lists: https://www.medicinenet.com/top_drugs_prescribed_in_the_us/v...
https://twitter.com/angie_rasmussen/status/12389469408820060...
Btw, ACE2 expression is decreased in unmedicated diabetics and HTN patients and the elderly which would imply that those groups should have some degree of protection from the virus (ceteris paribus, obviously). In fact that seems to be exactly the opposite of what we see. Some research even indicates that ACE2 could help prevent ARDS-induced lung injury:
https://www.nature.com/articles/srep27911
But in that article the injury wasn't induced by COVID-19 so really we don't know enough yet.
(Ref. for decreased ACE2 expression in diabetes: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992757/)
ACE inhibitors have no effect on ACE2.
The relevant portion about ibuprofen, lightly edited to make it more readable, is:
> Coronaviruses bind to their target cells through ACE2. The expression of ACE2 is substantially increased in patients with diabetes, who are treated with ACE inhibitors and ARBs. Hypertension is also treated with ACE inhibitors and ARBs, which results in an upregulation of ACE2. ACE2 can also be increased by thiazolidinediones and ibuprofen. These data suggest that ACE2 expression is increased in diabetes and treatment with ACE inhibitors and ARBs increases ACE2 expression. Consequently, the increased expression of ACE2 would facilitate infection with COVID-19. We therefore hypothesise that diabetes and hypertension treatment with ACE2-stimulating drugs increases the risk of developing severe and fatal COVID-19.
More broadly, they're saying that many of the medical notes of patients who died mentioned that the patients also had diabetes or hypertension, and they're wondering if the correlation is about the treatment for those conditions and not about the conditions themselves.
It's not clear to me whether they're implying that anyone who takes ibuprofen (e.g. for a headache or even for a COVID-19 fever) will have more ACE2 and therefore be more susceptible to severe and fatal COVID-19, or if that effect only happens in the context of treatment for diabetes and hypertension. I can see how you can read it in the first way, but it feels like they would have titled it clearer if that were what they were actually saying.
In particular, there is plenty of advice for people with mild COVID-19 cases to do the normal things they'd do to take care of a flu at home, including take ibuprofen. If that's a bad idea, I feel like they would have said that more loudly.
(For instance - does it matter whether you've got more ACE2 if you're already infected and trying to keep the symptoms under control?)
EDIT: Thanks to 'FeteCommuniste in another comment for linking this Twitter thread https://twitter.com/angie_rasmussen/status/12389469379166822... which points out that this is an un-peer-reviewed hypothesis.
Ibuprofen /might/ be a bad idea. We currently have the time to notice that, and hopefully find out whether it's true by looking at hundreds of cases instead of tens of thousands.
We don't know how chronic the chronic is through. So to stay on the safe side, use as little as needed to control bigger fever and pain.
This unlike antibiotics (not for viral infections) where you are supposed to take exactly the recommended amount for recommended time, preventing resistance.
https://www.sciencedaily.com/releases/2011/11/111101130200.h...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869589/
I also think that this is part of the mechanism that makes zinc effective against viruses as a catalyst.
Generally, I think that it's good to keep fevers down for non-lethal infections like the common cold, especially for children. Just beware that aspirin may cause Reye's syndrome in the young:
https://www.healthline.com/health/headache-reyes-syndrome
But for serious infections like Covid-19, maybe it would be better to maintain a relatively safe temperature of say 101-102 F (38-39 C)? I'm honestly curious to know what doctors think of this.
There has been a huge PR push (in advertising etc) against Aspirin and for other NSAIDs.
Of course, take care, but don’t be sucked in by marketing.
They advise is to use acetaminophen.
It really comes down how covid-19 kills people, whether it is by directly attacking the body, or by triggering cytokine release syndrome (CRS).
In later case, medication that suppresses the immune system would be better, but in former case it could make things worse.
It seems to be both. Plausibly at least, CRS may be often involved in damage to the respiratory system, but COVID-19 is not unlike SARS in that severe forms can directly attack other parts of the body. So any treatment based on lowering inflammation or any other part of the immune response will have to be carefully tuned.
I've had my doctor recommend against cough suppressants in the past. But I've had trouble sleeping with a bad cough, and so if cough suppressants make sleep possible, it seems like a net-win. Is there any data yet?
The syndrome is called 'NSAIDs-Exacerbated Respiratory Disease'.
I felt equally proud and ashamed that the medical establishment officially diagnosed me as a NERD
https://en.wikipedia.org/wiki/NSAID_hypersensitivity_reactio...
https://news.ycombinator.com/item?id=22582568
https://news.ycombinator.com/item?id=22576721
stop spamming this
