Corona Virus How To Treat

GenericName86

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Jun 30, 2018
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Also with Vitamin C being more and more talked about I've seen more "experts" come out saying it's no good because high doses stops kidneys from clearing properly?
 

S.Seneff

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Mar 18, 2020
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A recent Chinese survey revealed that the median duration of viral shedding was 20.0 days
(IQR 17.0–24.0) in survivors, but SARS-CoV-2 was detectable until death in non-survivors.
The shortest observed duration of viral shedding among survivors was eight days, whereas the
longest was 37 days (18). Therefore, a treatment enabling the viral carriage to be cleared and
COVID-patients to be clinically cured at an early stage would help limit the transmission of
the virus.

COVID treatment
Patients with no contraindications (Supplementary document 1) were offered a combination
of 200 mg of oral hydroxychloroquine sulfate, three times per day for ten days combined with
azithromycin (500mg on D1 followed by 250mg per day for the next four days). For patients
with pneumonia and NEWS score≥5, a broad spectrum antibiotic (ceftriaxone) was added to
hydroxychloroquine and azithromycin. Twelve-lead electrocardiograms (ECG) were
performed on each patient before treatment and two days after treatment began. All ECGs
were reviewed by senior cardiologists. The treatment was either not started or discontinued
when the QTc (Bazett’s formula) was > 500 ms and the risk-benefit ratio was estimated to be
between 460 and 500 ms. The treatment was not started when the ECG showed patterns
suggesting a channelopathy and the risk-benefit ratio was discussed when it showed other
significant abnormalities (i.e., pathological Q waves, left ventricular hypertrophy, left bundle
branch block). In addition, any drug potentially prolonging the QT interval was discontinued
during treatment. Symptomatic treatments, including oxygen, were added when needed. An
ionogram and verification of serum potassium levels in particular, was systematically
performed upon admission. When needed, standard blood chemistry was checked.

Criteria for discharge
Criteria for discharge changed over the course of the study. Initially, patients with two
successive negative nasopharyngeal samples resulting from PCR assay (CT value ≥35) were
discharged. From 18 March, patients with a single nasopharyngeal sample with a PCR CT
value ≥34 were discharged to their homes or transferred to other units for continuing
treatment, Ultimately, because of a crucial need to admit new, untreated inpatients, inpatients
already receiving treatment with a PCR CT value <34, with good clinical outcome and good
adherence to treatment were also discharged. When possible, further follow-up was continued
in other units or through out-patient consultations.


Contagiousness as assessed by PCR Ct value and culture (Figures 1 and 2)
A rapid fall of nasopharyngeal viral load tested by qPCR was noted, with 83% negative at
was observed after six days of treatment. After ten days, two patients only were still
presumably contagious with Ct values of 32 and 29 respectively. The proportion of patients
with a Ct value >34 significantly decreased overtime (R2 = 0.9). Virus cultures from patient
respiratory samples were negative in 97.5% patients at Day5. The number of contagious
patients (with positive culture) early decreased after three days of treatment (Figure 2). After
five days of treatment, two patients only were contagious. On Day8 post-treatment only one
of these two patients was contagious and ceased to be contagious on Day9. The proportion of
negative culture significantly decreased overtime (R
2 = 0.8).
Day7, and 93% at Day8. The number of patients presumably contagious (with a PCR Ct value
<34) steadily decreased overtime and reached zero on Day12 (Figure 1). A marked decrease


These data are important to compare with that of
the literature which shows that the viral RNA load can remain high for about three weeks in
most patients in the absence of specific treatment (18;22)
The second challenge is the rapid spread of the disease in the population through contagious
individuals. The elimination of viral carriage in the human reservoir of the virus has recently
been recognised as a priority (25).
Chloroquine and hydroxychloroquine are extremely well-known drugs which have already
been prescribed to billions of people. Because of anecdotical reports of heart complications
with such drugs in patients with underlying conditions, it would be useful to perform an ECG
before or at the very beginning of the treatment (26). This problem is solved by hospitalising
patients at risk with multiples pathogens in continuing care units with ECG monitoring
allowing for the early detection and treatment of these rare but possible cardiac side-effects.
Azithromycin is the drug that has been the most widely prescribed against respiratory
infections and a recent (2010) study showed that one in eight American out-patients, has been
prescribed azithromycin (27). Indeed, there have probably been more than a billion
azithromycin prescriptions around the world since it was first discovered. The toxicity of each
of these two drugs does not, therefore, pose a major problem. Their possible toxicity in
combination has been suggested in a few anecdotal reports but, to our knowledge, has never
been demonstrated.
In conclusion, we confirm the efficacy of hydroxychloroquine associated with azithromycin
in the treatment of COVID-19 and its potential effectiveness in the early impairment of
contagiousness. Given the urgent therapeutic need to manage this disease with effective and
safe drugs and given the negligible cost of both hydroxychloroquine and azithromycin, we
believe that other teams should urgently evaluate this therapeutic strategy both to avoid the
spread of the disease and to treat patients before severe irreversible respiratory complications
take hold.
https://www.mediterranee-infection.com/wp-content/uploads/2020/03/COVID-IHU-2-1.pdf
 

LeeLemonoil

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Sep 24, 2016
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Olive leaf extract seems to be anti-viral „directly“, without meddling with the host immune response and tissue by attacking the viral abilities to become proteolytic. See links provided above.


I read that outbreaks in Italy and Madrid (which sees many deads) are suspected to originate in nursing homes and hospitals.

I can only square the higher death-rates there with theses circumstances.
The virus attacks a weakened host organism and has more time to proliferate. Also, old and sick patients often show a deranged immune-response a la cytokine storm. I suspect that a massive inflammatory immune response actually helps the virus to become more aggressive or mutate even, it’s a known mechanism of some viruses that humans can’t handle well.

So, in a nursing home you might find a more aggressive, infectious virus, that exists for a longer Time in the host (which probsbly also increases infectiousness, transmission)
and is surrounded by many other potential ideal hosts/victims.

Take on the other end of the spectrum populations like in Germany with relatively few severe cases.
More testing led to isolation of transmitters ave the virus doesn’t find such a vulnerable, target rich environment there.
How and why the virus set put originally in nursing homes or not and with it the subsequent development might simply be a matter of chance / bad luck
 

Kunstruct

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Sep 6, 2018
Messages
902
Olive leaf extract seems to be anti-viral „directly“, without meddling with the host immune response and tissue by attacking the viral abilities to become proteolytic. See links provided above.

I started taking some today as I have some olive leaf extract capsule.
I actually have mild flu like symptoms for several days now.
 

thomas00

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Nov 14, 2016
Messages
872
Today I heard a renowned pulmonology specialist explaining that in his opinion, patients with COVID-19 in Italy are dying due to excessive use of oxygen respirators. He cited some studies that showed a larger percentage of patients survive if not put on respirators.

Do you have a link to that sir? am interested to read....
 
M

metabolizm

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How much Lysine have you taken to get that effect?

If I feel an outbreak coming, I’ll usually take a 1-1.5g dose. That often stops it altogether. Otherwise I’ll usually take 500mg three times a day, or more, and that massively speeds up the healing process.
 

David PS

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If I feel an outbreak coming, I’ll usually take a 1-1.5g dose. That often stops it altogether. Otherwise I’ll usually take 500mg three times a day, or more, and that massively speeds up the healing process.

I am glad that this strategy works for you. I think that it may be best to make sure that you get more lysine than arginine in your diet. You may find that you do not need to supplement everyday.

It is the ratio of the two amino acids that counts. Supplementation with lysine can change the ratio and that is one way to keep the level of the viruses low. The other way is to keep arginine low. Chronometer can show you how much of lysine and arginine is in your diet. Here is a pdf if you want to plan ahead to insure that your ratio for the day will be desirable.
http://eiwellness.com/wp-content/uploads/2017/04/Lysine-and-Arginine-Food-Guide.pdf
 
M

metabolizm

Guest
I am glad that this strategy works for you. I think that it may be best to make sure that you get more lysine than arginine in your diet. You may find that you do not need to supplement everyday.

It is the ratio of the two amino acids that counts. Supplementation with lysine can change the ratio and that is one way to keep the level of the viruses low. The other way is to keep arginine low. Chronometer can show you how much of lysine and arginine is in your diet. Here is a pdf if you want to plan ahead to insure that your ratio for the day will be desirable.
http://eiwellness.com/wp-content/uploads/2017/04/Lysine-and-Arginine-Food-Guide.pdf

Yes, I only really supplement lysine when I get a coldsore outbreak, which is less common now that I try to get it in my diet, and try to keep arginine in balance.
 

SeamusR

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Feb 26, 2018
Messages
28
2 weak points stand out for Virus infections.

1. Hijack the cell metabolism to be more proliferative (so that the Virus can leverage biosynthetic metabolites & proliferate itself).
2. Inflammatory response of the immune system.

So the following simple therapy would be a great start.

1. Thiamine - Glycolysis Inhibitor.
2. Cannabidiol _ Glutamine uptake inhibitor.
3. Inflammation Inhibitor - EGCG (Also inhibitor of CCR5, the primary target of the latest wonder drug candidate LeronLimab for CoronaVirus)
 

S.Seneff

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Mar 18, 2020
Messages
215
SARS-CoV-2 invades host cells via a novel route: CD147-spike protein

"First, in vitro antiviral tests indicated Meplazumab, an anti-CD147 humanized antibody, significantly inhibited the viruses from invading host cells, with an EC50 of 24.86 μg/mL and IC50 of 15.16 μg/mL."

Basigin (BSG) also known as extracellular matrix metalloproteinase inducer (EMMPRIN) or cluster of differentiation 147 (CD147) is a protein that in humans is encoded by the BSG gene.[4][5][6] This protein is a determinant for the Ok blood group system. Basigin has been shown to be an essential receptor on red blood cells for the human malaria parasite, Plasmodium falciparum.[7]
Meplazumab treats COVID-19 pneumonia: an open-labelled, concurrent controlled add-on clinical trial

Abstract

: SARS-CoV-2 is a novel human coronavirus, there is no specific antiviral drugs. It has been proved that host-cell-expressed CD147 could bind spike protein of SARS-CoV-2 and involve in host cell invasion. Antibody against CD147 could block the infection of SARS-CoV-2. We aimed to assess the efficacy and safety of meplazumab, a humanized anti-CD147 antibody, as add-on therapy in patients with COVID-19 pneumonia. Methods: All patients received recommended strategy from Diagnosis and Treatment for 2019 Novel Coronavirus Diseases released by National Health Commission of China. Eligible patients were add-on administered 10 mg meplazumab intravenously at days 1, 2, and 5. Patients hospitalized in the same period were observed as concurrent control. The endpoints include virological clearance rate, case severity, chest radiographic, and laboratory test. This trial was approved by the Ethics Committee of Institution at the Tangdu hospital, and registered with ClinicalTrials.gov, NCT 04275245. Findings:17 patients were enrolled and assigned to meplazumab group between Feb 3, 2020 and Feb 10, 2020. 11 hospitalized patients served as concurrent control. Baseline characteristics were generally balanced across two groups. Compared to control group, meplazumab treatment significantly improved the discharged (p=0.006) and case severity (p=0.021) in critical and severe patients. The time to virus negative in meplazumab group was reduced than that in control group (median 3, 95%CI[1.5-4.5] vs. 13, [6.5-19.5]; p=0.014, HR=0.37, 95%CI[0.155-0.833]). The percentages of patients recovered to the normal lymphocyte count and CRP concentration were also increased remarkably and rapidly in meplazumab group. No adverse effect was found in meplazumab-treated patients. Interpretation:Meplazumab efficiently improved the recovery of patients with SARS-CoV-2 pneumonia with a favorable safety profile. Our results support to carry out a large-scale investigation of meplazumab as a treatment for COVID-19 pneumonia. Funding:National Science and Technology Major Project.

Competing Interest Statement

PZ, ZNC, HB, and ZZ were the inventors of the patent Humanized Anti-Basigin Antibodies and the Use Thereof (PCT/CN2017/082713), and all of the above authors were not the applicant or patentee of the patent. PZ, ZNC, HB, DW, ZZ, and XMY were the inventors of patent Humanized Anti-Basigin Antibody for use of coronavirus disease 2019 (COVID-19) therapy (202010166717.9, China), and all of the above authors were not the applicant or patentee of the patent. Other authors declare no competing interests.

Meplazumab treats COVID-19 pneumonia: an open-labelled, concurrent controlled add-on clinical trial



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Opioidus

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May 22, 2019
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Update III : so I went back to the hospital for my persistent chest pain. Huge mistake as the hospital was completely overrun this time. I had to wait for three hours to be examined, this is way beyond the norm in here, last time I was examined within 15 minutes. They had no beds with those big hospital ventilators next to them, last time they immediately put me on one of those beds, instead, they had a bunch of bi-pap machines that looked like home devices next to newly made beds.

There wasn't a special wing designed for corona patients like last time, the entire hospital had become a huge corona wing, with beds everywhere. There was one guy that was really bad and his situation was just horrible, he was very young too, younger than me for sure(I'm in my 30s). He was jumping up and down on his bed gasping for air and waving his hands frantically, fighting invisible enemies and asking for help. It looked really really horrible. I have no idea how these doctors and nurses stay sane and keep coming back to work. They couldn't do anything for him as he was able to still "breath" on his own, he wasn't hooked to a machine just oxygen.

I couldn't wait there for long and went outside to a special area they have designed with open-air that's for patients that are better, I would check back every ten minutes or so to see if the doctor had become available.

Anyway, the doctor finally came and took my bp and listened to my breathing and wrote another chest ct from my lungs and heart. The ct showed medium lung involvement but no heart enlargement. He asked whether I want to start treatment with chloroquine and be admitted or can I go home. I just wanted to gtho of there asap so I refused. He said I should immediately get back and start treatment if I get even slightly worse. He also reviewed the other doctor's recommendations and said I should stop taking vitamins c, d and e because they put a strain on my body. There was no time to ask him about other things I've started taking like reishi and b complex.

Yesterday I didn't take any vitamins but instead took around 10-15 grams of dried reishi mushroom about 5 hours before bed. Last night was the first night in two weeks that I didn't wake up gasping for air several times. Very glad about that. Also, my chest pain has become more centralized and is no longer located on the left side.

Today I had shortness of breath all day long but it wasn't as bad as say, five or six days ago. This is by far the longest I have been sick and it's definitely the strongest bug I have ever had. It is incredible that more than two weeks after the start of my symptoms I sometimes feel like the disease is making a comeback, like it's moving to another part of my body or reinfecting my vocal cords and so on..

I should also mention that I have several underlying conditions, I have psoriasis and I've struggled with fatigue, cold body and ADHD like symptoms all my life. I've been diagnosed with hypothyroidism one and was on t4 by a general practitioner for three months but then I went to a specialist who decided to discontinue, this was years ago btw. I don't get sick that often but when I do it is usually more severe than my GF or family members. For example last year I got the flu from my GF and had to go to the hospital and was off work for a whole week while she just took one day off work and was back on her feet after two days rest. My diet has been horrible these past few weeks because my GF usually does the cooking. I've been eating crappy microwave soup and pasta and fruits and chese puffs and chips!:meh:

Stay healthy folks.
 
Joined
Dec 18, 2018
Messages
2,206
Update III : so I went back to the hospital for my persistent chest pain. Huge mistake as the hospital was completely overrun this time. I had to wait for three hours to be examined, this is way beyond the norm in here, last time I was examined within 15 minutes. They had no beds with those big hospital ventilators next to them, last time they immediately put me on one of those beds, instead, they had a bunch of bi-pap machines that looked like home devices next to newly made beds.

There wasn't a special wing designed for corona patients like last time, the entire hospital had become a huge corona wing, with beds everywhere. There was one guy that was really bad and his situation was just horrible, he was very young too, younger than me for sure(I'm in my 30s). He was jumping up and down on his bed gasping for air and waving his hands frantically, fighting invisible enemies and asking for help. It looked really really horrible. I have no idea how these doctors and nurses stay sane and keep coming back to work. They couldn't do anything for him as he was able to still "breath" on his own, he wasn't hooked to a machine just oxygen.

I couldn't wait there for long and went outside to a special area they have designed with open-air that's for patients that are better, I would check back every ten minutes or so to see if the doctor had become available.

Anyway, the doctor finally came and took my bp and listened to my breathing and wrote another chest ct from my lungs and heart. The ct showed medium lung involvement but no heart enlargement. He asked whether I want to start treatment with chloroquine and be admitted or can I go home. I just wanted to gtho of there asap so I refused. He said I should immediately get back and start treatment if I get even slightly worse. He also reviewed the other doctor's recommendations and said I should stop taking vitamins c, d and e because they put a strain on my body. There was no time to ask him about other things I've started taking like reishi and b complex.

Yesterday I didn't take any vitamins but instead took around 10-15 grams of dried reishi mushroom about 5 hours before bed. Last night was the first night in two weeks that I didn't wake up gasping for air several times. Very glad about that. Also, my chest pain has become more centralized and is no longer located on the left side.

Today I had shortness of breath all day long but it wasn't as bad as say, five or six days ago. This is by far the longest I have been sick and it's definitely the strongest bug I have ever had. It is incredible that more than two weeks after the start of my symptoms I sometimes feel like the disease is making a comeback, like it's moving to another part of my body or reinfecting my vocal cords and so on..

I should also mention that I have several underlying conditions, I have psoriasis and I've struggled with fatigue, cold body and ADHD like symptoms all my life. I've been diagnosed with hypothyroidism one and was on t4 by a general practitioner for three months but then I went to a specialist who decided to discontinue, this was years ago btw. I don't get sick that often but when I do it is usually more severe than my GF or family members. For example last year I got the flu from my GF and had to go to the hospital and was off work for a whole week while she just took one day off work and was back on her feet after two days rest. My diet has been horrible these past few weeks because my GF usually does the cooking. I've been eating crappy microwave soup and pasta and fruits and chese puffs and chips!:meh:

Stay healthy folks.

Try your best to eat clean like meat and potatoes.
Vitamin C E and Bs are fine.
Bad Dieting is prolonging the process.
Take care.
 

Goobz

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Mar 2, 2019
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Australia
I am glad that this strategy works for you. I think that it may be best to make sure that you get more lysine than arginine in your diet. You may find that you do not need to supplement everyday.

It is the ratio of the two amino acids that counts. Supplementation with lysine can change the ratio and that is one way to keep the level of the viruses low. The other way is to keep arginine low. Chronometer can show you how much of lysine and arginine is in your diet. Here is a pdf if you want to plan ahead to insure that your ratio for the day will be desirable.
http://eiwellness.com/wp-content/uploads/2017/04/Lysine-and-Arginine-Food-Guide.pdf

I wonder about this though - despite negative sides of arginine, isn't it necessary for the immune system, especially in preventing pneumonia? There's a thread a while back from a well known poster, maybe was vinero, who was taking lysine and kept getting pneumonia and believed he induced an arginine deficiency. I don't know much about this personally, just remembered the thread....

I've also read a primary way cornoviruses are contained is via nitric oxide, which is boosted by l-arginine and many of the things that seem to "work" against these viruses.
 

David PS

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I wonder about this though - despite negative sides of arginine, isn't it necessary for the immune system, especially in preventing pneumonia?

I concur. It is all about the balance of lysine and arginine. As I said above, "I think that it may be best to make sure that you get more lysine than arginine in your diet. You may find that you do not need to supplement everyday. " There is no magic ratio but a ratio of 1.1 might be a good place to start. That can be achieved with diet.

As per Ray Peat, Ray Peat Email Exchanges - Ray Peat Forum Wiki

I've also read a primary way cornoviruses are contained is via nitric oxide, which is boosted by l-arginine and many of the things that seem to "work" against these viruses.

Nitric Oxide has a "dark side". In a 2015 interview with Haidut entitled "Nitric Oxide and Methylene Blue [Generative Energy #11]" , Danny Roddy left the following time stamps:

05:00 - Ray Peat’s Nitric Oxide Interviews (link: http://bit.ly/rayinterviews)
05:45 - Mainstream views of nitric oxide
06:25 - Can be thought of as an emergency substitute for carbon dioxide to dilate blood vessels (CO2)
07:14 - Nitric oxide can influence intracellular calcium levels
07:51 - Local vs. systemic release of nitric oxide
08:50 - Nitric oxide and lactate stimulate angiogenesis
09:20 - Nitric oxide irreversibly binds cytochrome c oxidase
10:28 - Infections acutely increase nitric oxide
11:05 - Good thyroid function for low levels of nitric oxide
11:30 - Caffeine, niacinamide, zinc, and magnesium can help lower nitric oxide
12:00 - The amino acid lysine can lower nitric oxide
12:27 - Health problems associated with nitric oxide (and testing it)
13:23 - Nitric oxide theory of aging (link: http://bit.ly/1WrgZuS)
14:19 - Chronic disease is associated with elevated levels of nitric oxide and contributes to the problem
15:39 - Activating cytochrome c oxidase to lower nitric oxide
16:10 - Red light and methylene blue lower nitric oxide
16:55 - Nitric oxide can lower the core temperature

In summary:

Drug-Side-Effects-Cartoon.jpg
 

Goobz

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Location
Australia
I concur. It is all about the balance of lysine and arginine. As I said above, "I think that it may be best to make sure that you get more lysine than arginine in your diet. You may find that you do not need to supplement everyday. " There is no magic ratio but a ratio of 1.1 might be a good place to start. That can be achieved with diet.

As per Ray Peat, Ray Peat Email Exchanges - Ray Peat Forum Wiki



Nitric Oxide has a "dark side". In a 2015 interview with Haidut entitled "Nitric Oxide and Methylene Blue [Generative Energy #11]" , Danny Roddy left the following time stamps:

05:00 - Ray Peat’s Nitric Oxide Interviews (link: http://bit.ly/rayinterviews)
05:45 - Mainstream views of nitric oxide
06:25 - Can be thought of as an emergency substitute for carbon dioxide to dilate blood vessels (CO2)
07:14 - Nitric oxide can influence intracellular calcium levels
07:51 - Local vs. systemic release of nitric oxide
08:50 - Nitric oxide and lactate stimulate angiogenesis
09:20 - Nitric oxide irreversibly binds cytochrome c oxidase
10:28 - Infections acutely increase nitric oxide
11:05 - Good thyroid function for low levels of nitric oxide
11:30 - Caffeine, niacinamide, zinc, and magnesium can help lower nitric oxide
12:00 - The amino acid lysine can lower nitric oxide
12:27 - Health problems associated with nitric oxide (and testing it)
13:23 - Nitric oxide theory of aging (link: http://bit.ly/1WrgZuS)
14:19 - Chronic disease is associated with elevated levels of nitric oxide and contributes to the problem
15:39 - Activating cytochrome c oxidase to lower nitric oxide
16:10 - Red light and methylene blue lower nitric oxide
16:55 - Nitric oxide can lower the core temperature

In summary:

Drug-Side-Effects-Cartoon.jpg

Thanks! Im aware of the dark side of nitric oxide, and Ray's views on it, but hadn't seen it all laid out so well like that.

But this is just my opinion, but... it may be worth temporarily not worrying about the long terms effects of nitric oxide, if this covid virus is sweeping through your region and that's something that concerns you. A few weeks of not worrying about lowering nitric oxide won't do anything to your long term risk of disease IMO, but who knows, may help you survive the virus if you're old, susceptible to lung problems, overweight, etc.

But really the thing that concerned me more, was that thread about the guy who kept getting pneumonia with supplementing lysine, and believed it was a arginine deficiency. Not a good thing, if the virus is indeed causing pneumonia. Seems kind of unlikely to me, that lysine would do that though.

Still, maybe a good idea to supplement some gelatin along with lysine (pretty sure that has a fair bit of arginine in it).
 

Kunstruct

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Messages
902
Still, maybe a good idea to supplement some gelatin along with lysine (pretty sure that has a fair bit of arginine in it).
Yeah, it has arginine in it, but what does it matter?
For example you can eat foods high in arginine and then take some MB to lower the nitric oxide.
I can see the anti-nitric oxide effects of Lysine and MB even with grams or arginine supplemented.
I am sure this will be different on everyone depending on so many other factors.
 
Joined
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Messages
2,206
RealNeat said: ↑

Do you have a really good study or proof of vitamin D in supplement form actually benefitting this thing or any other pneumonia related condition?



Im dumping abstracts to this important question,you and me want to know if supplemental D works,
it will be about that and about natural occurence D.





Relationship between vitamin D levels and outcome of pneumonia in children
AO Oduwole, JK Renner, E Disu, E Ibitoye, E Emokpae
West African journal of medicine 29 (6), 2010
ABSTRACT BACKGROUND: Pneumonia, a common childhood infection in Nigerian children with a number of debilitating complications such as empyema thoracis, has been linked to vitamin D deficiency due to its ability to modulate the T lymphocyte of the immune system.
OBJECTIVE: To determine the relationship between vitamin D and outcome of pneumonia in children. METHODS: This was a case-control study involving 24 children, admitted for pneumonia as subjects and 10 children without pneumonia as controls. Pre-formatted questionnaire was utilized to obtain background information, anthropometric measurements were made to determine nutritional status and estimation of 25-hydroxy cholecalciferol (25OHD) done for all those studied. RESULTS: The mean (SD) serum 25OHD concentration was 104 (59) nmol/L and 130 (107) nmol/L for subjects and controls respectively. Amongst the subjects 15 (54%) had serum 25OHD less than 70nmol/L and 11 (46%) serum 25OHD greater than70nmol/L. Hypocalcaemia was present in 15 (54%) of the subjects. Further analysis of hypocalcaemia with regards to the concentration of serum 25OHD showed that 2 (13%) had levels below 40nmol/L, 10 (67%) had levels below 70nmol/L and 3 (20%) above 70nmol/L. Hypocalcaemia was more frequent among subjects with 25OHD below 70nmol/L compared with those above70nmol/L,(p= 0.01). Empyema thoracis and death occurred amongst the two subjects with 25OHD between 27.5 and 40nmol/L. Anaemia was more frequent among subjects with 25OHD below 70nmol/L compared with those above70nmol/L (p= 0.03). CONCLUSION: The study showed that Vitamin D insufficiency, and not solely its deficiency, may have an important role to play in the immune and haemopoetic system. It may therefore affect the response of a child to infections especially pneumonia. WAJM 2010; 29 (6): 373–378.






Effects of vitamin D supplementation to children diagnosed with pneumonia in Kabul: a randomised controlled trial
Semira Manaseki‐Holland, Ghulam Qader, Mohammad Isaq Masher, Jane Bruce, M Zulf Mughal, Daniel Chandramohan, Gijs Walraven
Tropical Medicine & International Health 15 (10), 1148-1155, 2010
Objectives  To determine whether (i) supplementation of oral 100 000 iu of vitamin D3 (cholecalciferol) along with antibiotics will reduce the duration of illness in children with pneumonia; (ii) supplementation will reduce the risk of repeat episodes.
Methods  Double‐blind individually randomised placebo‐controlled trial in an inner‐city hospital in Kabul, of 453 children aged 1–36 months, diagnosed with non‐severe or severe pneumonia at the outpatient clinic. Children with rickets, other concurrent severe diseases, very severe pneumonia or wheeze, were excluded. Children were given vitamin D3 or placebo drops additional to routine pneumonia treatment.
Results  Two hundred and twenty‐four children received vitamin D3; and 229 received placebo. There was no significant difference in the mean number of days to recovery between the vitamin D3 (4.74 days; SD 2.22) and placebo arms (4.98 days; SD 2.89; P  = 0.17). The risk of a repeat episode of pneumonia within 90 days of supplementation was lower in the intervention (92/204; 45%) than the placebo group [122/211; (58%; relative risk 0.78; 95% CI 0.64, 0.94; P = 0.01]. Children in the vitamin D3 group survived longer without experiencing a repeat episode (72 days vs. 59 days; HR 0.71; 95% CI 0.53–0.95; P = 0.02).
Conclusion  A single high‐dose oral vitamin D3 supplementation to young children along with antibiotic treatment for pneumonia could reduce the occurrence of repeat episodes of pneumonia.





Is ventilator-associated pneumonia in trauma patients an epiphenomenon or a cause of death?
Louis J Magnotti, Martin A Croce, Timothy C Fabian
Surgical infections 5 (3), 237-242, 2004
Background: Ventilator-associated pneumonia (VAP) is a common infection among patients in trauma intensive care units (ICUs). It has been suggested by different investigators that VAP is an indicator of injury severity and not necessarily associated with mortality. Crude mortality rates approximating 20% have been reported for trauma patients with VAP. Most studies have involved the most severely injured patients, making it difficult to determine the relative contribution of either VAP or injury severity to death. If VAP is independently associated with mortality, this relationship should be most evident in less severely injured patients. We studied patients with less severe injuries (Injury Severity Score, ISS < 25) to determine the impact of VAP on outcomes.
Methods: Patients admitted to the trauma ICU with ISS < 25 were identified from the trauma registry of a level I trauma center. Patients with penetrating injuries and those who died within 48 h of injury were excluded. Pneumonia was diagnosed using quantitative cultures of bronchoalveolar lavage effluent (≥ 105 colony forming units/mL). Risk factors for VAP, including age, transfusions with 24 h of admission, brain injury, and chest injury severity were analyzed. Logistic regression analysis was then performed to determine independent factors for death.Results: There were 15,492 blunt admissions over a 5.5 year study period who survived >48 h. Of these, 5,860 (38%) were admitted to the ICU, and 4,111 (70% of ICU admissions) had ISS < 25. The incidence of VAP in this group was 8%. Patients with VAP were older (47 vs 39 years), had more transfusions within 24 h (2.5 vs 0.9 units of red blood cell concentrates) and had greater injury severity by ISS (16.7 vs 12.6 points), GCS (Glasgow Coma Scale) score (11.8 vs. 13.7 points) and chest AIS (Abbreviated Injury Scale) (1.7 vs 0.9 points; all p < 0.001). Overall mortality was 4%. Mortality was 16% in patients with VAP compared to 3% in those without VAP (p < 0.0001). Logistic regression analysis identified transfusions, age, and VAP as independent predictors of mortality. Other descriptors of injury severity (ISS, GCS, or chest AIS) were not associated with death.
Results: There were 15,492 blunt admissions over a 5.5 year study period who survived . 48 h. Of these, 5,860 (38%) were admitted to the ICU, and 4,111 (70% of ICU admissions) had ISS , 25. The incidence of VAP in this group was 8%. Patients with VAP were older (47 vs 39 years), had more transfusions within 24 h (2.5 vs 0.9 units of red blood cell concentrates) and had greater injury severity by ISS (16.7 vs 12.6 points), GCS (Glasgow Coma Scale) score (11.8 vs. 13.7 points) and chest AIS (Abbreviated Injury Scale) (1.7 vs 0.9 points; all p , 0.001). Overall mortality was 4%. Mortality was 16% in patients with VAP compared to 3% in those without VAP (p , 0.0001). Logistic regression analysis identified transfusions, age, and VAP as independent predictors of mortality. Other descriptors of injury severity (ISS, GCS, or chest AIS) were not associated with death.
Conclusions: Ventilator-associated pneumonia is independently associated with death in less severely injured trauma patients. This demonstrates the need for effective diagnostic techniques so that adequate therapy may be initiated. Prevention of VAP in less severely injured trauma patients should increase survival.






Vitamin D Status and Community-Acquired Pneumonia: Results from the Third National Health and Nutrition Examination Survey
Abstract
Objective
To investigate the association between serum 25-hydroxyvitamin D [25(OH)D] level and history of community-acquired pneumonia (CAP).

Patients and Methods
We identified 16,975 individuals (≥17 years) from the third National Health and Nutrition Examination Survey (NHANES III) with documented 25(OH)D levels. To investigate the association of 25(OH)D with history of CAP in these participants, we developed a multivariable logistic regression model, adjusting for demographic factors (age, sex, race, poverty-to-income ratio, and geographic location), clinical data (body mass index, smoking status, asthma, chronic obstructive pulmonary disease, congestive heart failure, diabetes mellitus, stroke, chronic kidney disease, neutropenia, and alcohol consumption), and season. Locally weighted scatterplot smoothing (LOWESS) was used to depict the relationship between increasing 25(OH)D levels and the cumulative frequency of CAP in the study cohort.

Results
The median [interquartile range (IQR)] serum 25(OH)D level was 24 (IQR 18–32) ng/mL. 2.1% [95% confidence interval (CI): 1.9–2.3] of participants reported experiencing a CAP within one year of their participation in the national survey. After adjusting for demographic factors, clinical data, and season, 25(OH)D levels <30 ng/mL were associated with 56% higher odds of CAP [odds ratio 1.56; 95% confidence interval: 1.17–2.07] compared to levels ≥30 ng/mL. LOWESS analysis revealed a near linear relationship between vitamin D status and the cumulative frequency of CAP up to 25(OH)D levels around 30 ng/mL.

Conclusion
Among 16,975 participants in NHANES III, 25(OH)D levels were inversely associated with history of CAP. Randomized controlled trials are warranted to determine the effect of optimizing vitamin D status on the risk of CAP.






Vitamin D Status and Acute Respiratory Infection: Cross Sectional Results From the United States National Health and Nutrition Examination Survey, 2001-2006
Dominique J Monlezun 1 2 , Edward A Bittner 3 4 , Kenneth B Christopher 5 6 , Carlos A Camargo 7 8 9 , Sadeq A Quraishi 10 11
Affiliations

Abstract
Vitamin D is a promising, though under-explored, potential modifiable risk factor for acute respiratory infections (ARIs). We sought to investigate the association of vitamin D status with ARI in a large, nationally-representative sample of non-institutionalized individuals from the United States. We analyzed 14,108 individuals over 16 years of age in the National Health and Nutrition Survey (NHANES) 2001-2006 in this cross-sectional study. We used locally weighted scatterplot smoothing (LOWESS) to depict the relationship between increasing 25-hydroxyvitamin D (25OHD) levels and ARI. We then performed a multivariable regression analysis to investigate the association of 25OHD levels with ARI, while adjusting for known confounders. The median serum 25OHD level was 21 (IQR 15-27) ng/mL. Overall, 4.8% (95% CI: 4.5-5.2) of participants reported an ARI within 30 days before their participation in the national survey. LOWESS analysis revealed a near-linear relationship between vitamin D status and the cumulative frequency of ARI up to 25OHD levels around 30 ng/mL. After adjusting for season, demographic factors, and clinical data, 25OHD levels <30 ng/mL were associated with 58% higher odds of ARI (OR 1.58; 95% CI: 1.07-2.33) compared to levels ≥30 ng/mL. Among the 14,108 participants in NHANES 2001-2006, 25OHD levels were inversely associated with ARI. Carefully designed, randomized, controlled trials are warranted to determine the effect of optimizing vitamin D status on the risk of ARI






Effect of Vitamin D Supplementation on Procalcitonin as Prognostic Biomarker in Patients with Ventilator Associated Pneumonia Complicated with Vitamin D Deficiency
Abstract
Ventilator-associated pneumonia (VAP) is a common and serious problem that develops after more than 48 h of mechanical ventilation. Improving the activity of immune system with vitamin D, and its consequent impact on prognostic biomarkers of VAP was studied in the current study.

A randomized double blind placebo controlled clinical trial was designed. A total of 46 patients with VAP, who were suffering from vitamin D deficiency, were randomly allocated into the study groups of placebo (n=22) and treatment (n=24) The treatment group received 300,000 units of intramuscular vitamin D. Serum levels of procalcitonin and vitamin D along with SOFA and CPIS scores were determined at baseline and on day 7 after intervention. The mortality rate of patients was also monitored for the succeeding 28 days after the injection.

The administration of vitamin D significantly enhanced its levels (P<0.0001) in the treated patients (12.28 ± 8.26) in comparison to placebo group (1.15 ± 1.50). The levels of PCT were significantly decreased (p=0.001) in the treatment group (– 0.02 ± 0.59 ng/mL) compared to that of placebo group (0.68 ± 1.03 ng/mL). However, changes in (SOFA) and CPIS scores were not significantly different between study groups (p=0.63 and p=0.32, respectively). Interestingly, the mortality rate of patients in the treatment group (5/24) was significantly lower (p=0.04) than that of the placebo group (11/22).

In conclusion, our results indicate that vitamin D supplementation can significantly reduce the procalcitonin in (VAP) patients, and must be considered as a preventive and/or therapeutic strategy.

Key Words: Procalcitonin, VAP, CPIS score, SOFA score, Vitamin D






Vitamin D Level Is Associated With Mortality Predictors in Ventilator-Associated Pneumonia Caused by Acinetobacter Baumannii
Murat Haliloglu 1 , Beliz Bilgili, Ozlem Haliloglu, Dilek Gogas Yavuz, Ismail Cinel
Affiliations

Abstract
Introduction: Vitamin D plays a role in host defense and is known to be associated with mortality in patients in the intensive care unit (ICU). We aimed to evaluate the relationships between vitamin D levels and predictors of mortality in patients with ventilator-associated pneumonia (VAP) caused by extensively drug-resistant Acinetobacter baumanii (XDR A. baumanii).

Methodology: A retrospective single-center study was conducted in an 18-bed adult ICU of a teaching hospital, including all patients with VAP due to XDR A. baumanii. Levels of 25(OH)D, procalcitonin (PCT), C-reactive protein (CRP), n-terminal pro-BNP (NT-proBNP), as well as clinical scores (Sequential Organ Failure Assessment [SOFA], Acute Physiology And Chronic Health Evaluation [APACHE II], Clinical Pulmonary Infection Score [CPIS) were recorded.

Results: Forty-for patients were studied over six months. All patients had vitamin D deficiency. The 28-day mortality in patients with 25(OH)D levels ≤ 10 ng/mL was higher than in patients with 25(OH)D > 10ng/mL (p = 0.001). The fourth- and seventh-day SOFA scores (p= 0.04 and p= 0.001) and first- and fourth-day procalcitonin levels (p = 0.03 and p = 0.004) were higher in patients with 25(OH)D levels ≤ 10 ng/mL. The clinical scores (SOFA, CPIS, and CEPPIS) and biomarkers (NT-proBNP, PCT) were negatively correlated with 25(OH)D levels in all study groups.

Conclusions: Severe vitamin D deficiency was associated with adverse outcome in VAP due to XDR A. baumanii. Vitamin D levels may be a prognostic predictor of VAP. It is also important to evaluate the effect of rapid vitamin D replacement on mortality






Vitamin D status in South Korean military personnel with acute eosinophilic pneumonia: a pilot study
Byung Woo Jhun, Se Jin Kim, Kang Kim, Ji Eun Lee, Duck Jin Hong
Tuberculosis and respiratory diseases 78 (3), 232-238, 2015
Background
A relationship between low vitamin D levels and the development or outcomes of respiratory diseases has been identified. However, there is no data on the vitamin D status in patients with acute eosinophilic pneumonia (AEP). We evaluated the vitamin D status in patients with AEP among South Korean military personnel.
Methods
We prospectively compared the serum levels of total 25-hydroxyvitamin D [25 (OH) D], 25 (OH) D3, and 25 (OH) D2 among patients with AEP, pulmonary tuberculosis (PTB), and community-acquired pneumonia (CAP).
Results
In total, 65 patients with respiratory diseases, including AEP (n= 24), PTB (n= 19), and CAP (n= 22), were identified. Of the 24 patients with AEP, 2 (8%) had deficient total 25 (OH) D levels (< 10 ng/mL), 17 (71%) had insufficient total 25 (OH) D levels (≥ 10 to< 30 ng/mL), and only 5 (21%) had sufficient total 25 (OH) D levels (≥ 30 to< 100 ng/mL). The difference in the total 25 (OH) D levels among patients with AEP, PTB, and CAP was not statistically significant (p= 0.230). The median levels of total 25 (OH) D, 25 (OH) D3, and 25 (OH) D2 were 22.84, 22.84, and 0.00 ng/mL, respectively, and no differences in the 25 (OH) D level were present among patients with AEP, PTB, and CAP with the exception of the total 25 (OH) D level between patients with AEP and PTB (p= 0.042).
Conclusion
We have shown that low vitamin D levels are frequently found in patients with AEP and are comparable with those in patients with PTB and CAP.






Vitamin D deficiency does not result in a breach of host defense in murine models of pneumonia
Julia Niederstrasser, Christian Herr, Lisa Wolf, Claus M Lehr, Christoph Beisswenger, Robert Bals
Infection and immunity 84 (11), 3097-3104, 2016
Vitamin D (VitD) has a role in the regulation of calcium and phosphate metabolism and in addition impacts the activity of the immune system. VitD deficiency might be linked to increased susceptibility to respiratory tract infection. The aim of the present study was to characterize the impact of VitD deficiency on the susceptibility to bacterial infection in murine models. C57BL/6N mice were fed a diet with or without VitD for 10 weeks. The VitD-deficient or -sufficient mice were infected with Pseudomonas aeruginosa or Streptococcus pneumoniae. The colonization and inflammatory response in the lung were analyzed at defined time points. The serum 25-hydroxy-VitD concentration was significantly lower in mice on the VitD-deficient diet. In infection experiments with Pseudomonas aeruginosa or Streptococcus pneumoniae, no differences could be observed in the numbers of viable bacteria or in differential cell counts in the bronchoalveolar lavage fluids. Measurements of inflammatory cytokines (KC and interleukin-1β [IL-1β]) did not show significant differences between the groups. In conclusion, VitD-deficient animals did not show significantly increased susceptibility to infection or an altered course of infection. The immune systems of humans and mice likely respond differently to VitD. Murine models are likely not appropriate for drawing conclusions on the role of VitD in human pulmonary host defense.






Pulmonary activation of vitamin D3 and preventive effect against interstitial pneumonia
Ichiro Tsujino, Ryoko Ushikoshi-Nakayama, Tomoe Yamazaki, Naoyuki Matsumoto, Ichiro Saito
Journal of clinical biochemistry and nutrition 65 (3), 245-251, 2019
Calcitriol [1, 25 (OH) 2 D 3] is usually investigated in studies on the preventive effect of activated vitamin D against interstitial pneumonia. Although cholecalciferol (vitamin D 3) can be easily obtained in the diet and has a longer half-life than calcitriol, there have been few investigations of its effect on interstitial pneumonia. We used human pulmonary fibroblast cell lines (HPFCs) and a mouse model of bleomycin-induced pulmonary fibrosis to evaluate whether vitamin D 3 was activated in the lungs and had a preventive effect against interstitial pneumonia. Expression of the vitamin D receptor gene and genes for enzymes metabolizing vitamin D was evaluated in two HPFCs, and the suppressive effect of vitamin D 3 on induction of inflammatory cytokines was also assessed. Gene expression of the vitamin D receptor and vitamin D-metabolizing enzymes was observed in both human pulmonary fibroblast cell lines. Vitamin D 3 suppressed bleomycin-induced expression of inflammatory cytokines and fibrosis markers by the HPFCs. In mice, symptoms of bleomycin-induced pulmonary fibrosis were improved and expression of fibrosis markers/fibrosis inducers was decreased by a high vitamin D 3 diet. Vitamin D 3 is activated locally in lung tissues, suggesting that high dietary intake of vitamin D 3 may have a preventive effect against interstitial pneumonia.






Prevention effect of thymosin-alpha1 aganist early ventilator-associated pneumonia in patients with mechanical ventilation
SS Zhang, K Li, YH Wang, BN Ye, Y Pan, XQ Shi
Sichuan da xue xue bao. Yi xue ban= Journal of Sichuan University. Medical science edition 46 (6), 957-959, 2015
To investigate the preventive effects of thymosin-alpha1 against early ventilator-associated pneumonia (VAP) in the patients with mechanical ventilation. Fifty two patients with expectancy of mechanical ventilation over 48 h were divided into routine therapy group (n= 26) and thymosin therapy group (n= 26) in random. The patients in routine therapy group were given intensive care unit (ICU) conventional treatment, and the patients in thymosin therapy group were given thymosin treatment additionally (1.6 mg subcutaneous injection, qd X 7 d). The incidence and occurrence time of VAP were observed, and the time of mechanical ventilation and ICU stay were recorded. The levels of CD3+, CD4+, CD4+/CD8+ T lymphocyte, CD14+ mononuclear cell human leukocyte antigens-DR (CD14+ HLA-DR) and procalcitonin (PCT) were detected before mechanical ventilation and at the 3d and 7th d after mechanical ventilation. The base line including the level of immunologic function had no difference between the two groups (P> 0.05). The incidence of VAP in thymosin therapy group was lower than that in routine therapy group, but it was not significant difference (P> 0.05). The durations of machine ventilation and ICU stay in thymosin therapy group were shorter than those in routine therapy group (P< 0.05). The occurrence time of VAP in thymosin therapy group was significantly later than that in routine therapy group (P< 0.05). At the 3rd and 7th d after mechanical ventilation, thymosin therapy group achived higher levels of CD3+, CD4+, CD4+/CD8+ T lymphocyte and CD14+ HLA-DR than routine therapy group did (P< 0.05). Thymosinal may be able to improve immunologic function and prevent the incidence of early VAP in the patients with mechanical ventilation.






Cholecalciferol, Ergosterol, and Cholesterol Enhance the Antibiotic Activity of Drugs
Jacqueline C Andrade, Maria Flaviana B Morais Braga, Gláucia Morgana M Guedes, Saulo R Tintino, Maria A Freitas, Lucindo J Quintans Jr, Irwin RA Menezes, Henrique DM Coutinho
International Journal for Vitamin and Nutrition Research, 2019
Background:
This is the first report demonstrating the antibiotic-modifying activity of cholecalciferol.
Aim:
In this study, cholecalciferol was evaluated against multiresistant strains of Staphylococcus aureus, Pseudomonas aeruginosa, and Escherichia coli.
Methods:
The antibacterial and modulatory effects of cholecalciferol, ergosterol, and cholesterol (8–512 μg/mL) were evaluated by microdilution assay against multiresistant bacterial strains.
Results:
Cholecalciferol, when combined with aminoglycosides, was more effective against P. aeruginosa, reducing the concentration of amikacin and gentamicin necessary to inhibit bacterial growth from 156.25 to 39.06 μg/mL and from 39.06 to 9.76 μg/mL, respectively. It is possible that cholecalciferol, due to its lipid-soluble nature, had a lipophilic interaction with the cell membrane, enhancing antibiotic uptake. Cholesterol and ergosterol were used to see if the mechanism of action of cholecalciferol was similar to that of these lipid compounds. Ergosterol and cholesterol increased aminoglycoside activity, where the effect was greater with higher subinhibitory concentration of sterol.
Conclusions:
There is no reported study on the use of cholesterol and ergosterol as modulators of antibiotics or any other drug, making this the first study in this area highlighting the interaction between cholesterol, ergosterol, and cholecalciferol with regard to modifying aminoglycoside activity.





Vitamin D status is associated with treatment failure and duration of illness in Nepalese children with severe pneumonia
Johanne Haugen, Sudha Basnet, Ingrid M Hardang, Arun Sharma, Maria Mathisen, Prakash Shrestha, Palle Valentiner-Branth, Tor A Strand
Pediatric research 82 (6), 986-993, 2017
Background
There is no consensus on optimal Vitamin D status. The objective of this study was to estimate the extent to which vitamin D status predicts illness duration and treatment failure in children with severe pneumonia by using different cutoffs for vitamin D concentration.
Methods
We measured the plasma concentration of 25 (OH) D in 568 children hospitalized with World Health Organization-defined severe pneumonia. The associations between vitamin D status, using the most frequently used cutoffs for vitamin D insufficiency (25 (OH) D< 50 and< 75 nmol/l), and risk for treatment failure and time until recovery were analyzed in multiple logistic regression and Cox proportional hazards models, respectively.
Results
Of the 568 children, 322 (56.7%) had plasma 25 (OH) D levels≥ 75 nmol/l, 179 (31.5%) had levels of 50–74.9 nmol/l, and 67 (%) had levels< 50 nmol/l. Plasma 25 (OH) D< 50 nmol/l was associated with increased risk for treatment failure and longer time until recovery.
Conclusion
Our findings indicate that low vitamin D status (25 (OH) D< 50 nmol/l) is an independent risk factor for treatment failure and delayed recovery from severe lower respiratory infections in children.
 
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