COVID 19 and Wegener's - musings

[marta]

Hi y'all,

It's been a while. Ready for another LOOOONG Marta post? LOL
Well here it comes.

Needless to say, I'm sure we're all thinking about this new world order (C-19) and how it relates to OUR old world order (WG).
Man am I seeing a ton of parallels between the two, the more I hear about the symptoms (and post mortem) of Covid19 patients, the more I think that WG, and Covid 19 were designed together in some other worldly lab ;) and this also gives me some ideas on the management of the issues from our perspective.

I. Am. NOT. A. Doctor.
All of this is just me sitting at home and philosophizing in my pea brain.
What I write is not in any way intended as advice, or anything of the sort, just fodder for thought.

Point 1: The similarities

So C-19 attacks the lungs. We all know that. Same with WG. One of the symptoms they're telling people to watch out for, is loss of sense of smell and taste. I went through at least three years with that particular symptom. So we know C-19 is also hitting the sinuses. A lot of people who have passed from C-19 have also shown to have renal failure as one of the final symptoms, and found post mortem. Does this sound familiar to anyone on this forum? I'm sure the answer is yes.

Point 2: The actual killer

With WG, it is our immune system attacking healthy tissue that is the threat of killing us. In C-19, it's the immune system attacking the virus (who likes the same areas that our WG immune system has already had ample practice on). It's not he virus killing people, it's the immune response to the virus. That immune response is the same immune response that has threatened our lives in the past. The exact same immune response, in the exact same areas. It is the immune system creating extra phlegm and mucous and inflammation in the lungs that is keeping people from getting enough oxygen (I've been hanging at high 80's - low 90's oxygen saturation since diagnosis in 2010). It's the inflammation in the kidneys that make them shut down and not be able to filter.

Point 3: Precedent

How do we deal with the idea that our immune system can potentially kill us? We do that by dealing with the symptoms (pred) and trying to mellow out the immune response (the physiological equivalent to trying to flatten the curve socially). We take immune suppressants so that an overblown response by our immune system doesn't shut down the whole operation. By taking immune suppressants and steroids, we are essentially flattening the curve internally, and allowing the body not to get overburdened with the response. It makes me think about how my body has handled flus and colds in the last ten years while on immune suppressants. If I do catch something going around, it takes longer for my body to react, it takes longer for the viral infection to go through it's course, but it's not as harsh as it would be without immune suppressants. I see a parallel both socially and physiologically.

There isn't much we as humans can do about a viral infection. We haven't figured viruses out yet. All we can do, is let it run its course, and mitigate the symptoms keeping them from being deadly. In my mind, I've decided what I will do if I get hit (although I fear that this might be a nasty one to catch, I also in the back of my mind have a hope that we're actually trained and ready to go on this fight moreso than others... not sure which way to go, lol). If I get it, I will continue my Imuran, my Dapsone (PCP pneumonia deterrent) and I'll probably take some pred (I'm not on it now, but I think it would be a good one to take, as it decreases inflammation and it's inflammation that kills) I will (am) also supporting my immune system with Vitamin C, D, Oregano oil, Propolis, and Sambucol. That way (in my mind) I'm taking precautions (aside from social distancing - which I'm a pro at given the last ten years of WG) to keep any stray virus from taking hold in my body. Lots of snot rockets too - all you Weggies know the power of the snot rocket. Ha ha ha.

Point 4: We're number 1

In my usual Pollyanna fashion, I'd like to suggest we're the lucky ones. We've already gone through the panic, and fear that I see in people's faces on the news. We've done this for a while. We are the pros right now, despite being the vulnerable. This is our Olympics. Our exam time. We can help people who are truly panicked and give them peace of mind. I've gotten off social media (again) and I'm so glad I'm not on there as it's super gross right now, so maybe stay away from the negative nini platforms, but know that you've got this. Stay safe, do what you've been doing all along, and know that you're practiced in keeping safe and are miles ahead of the rest of the world.

Peace y'all.... thinking of you all, and sending you all 'safety jujus'.
;)
Marta

[woz]

Hi Marta,

Its good to hear what I have been thinking. The first time I read about the patients immune system attacking the lungs and other areas in the covid 19 cases, I thought wow!!! this is very similar to what a lot of us wegies have been through, hopefully we can all ride out this storm front, and all come out the other side.

Every day you wake up is a good day, some are just better than others.

Stay Safe.

Woz....

[marta]

I just got a great article sent to me by Geoff via Sam (thanks you two).
It talks about this very thing. Much much more articulate than my blabbing.

https://www.nytimes.com/2020/04/01/health/coronavirus-cytokine-storm-immune-system.html

So to bring it all back to us.... we've got this.
Stay safe everyone, and keep taking your meds.

m

[drz]

Is this drug ever used in treatment of GPA? tocilizumab

massive steroids are usually used but are there any other similarities in how Covid 19 and GPA flares are usually treated?

[richard052018]

I just got a great article sent to me by Geoff via Sam (thanks you two).
It talks about this very thing. Much much more articulate than my blabbing.

https://www.nytimes.com/2020/04/01/health/coronavirus-cytokine-storm-immune-system.html

So to bring it all back to us.... we've got this.
Stay safe everyone, and keep taking your meds.

m

Don't be so hard on your blabbering: it was quite entertaining (and informative)

[drz]

https://www.vasculitisfoundation.org/coronavirus-covid-19/vasculitiscovid19/

[marta]

Thanks drz, I just signed up.

Also, I found this pre-publication out for peer review which I imagine was the source for the article I linked above, but I sent it to my doc in Edmonton, and she ended up missing a meeting because she was so into the data and found it so fascinating.
He he... I made my doc miss a meeting.

http://www.sah.org.ar/pdf/covid-19/083-20_pre-publishing.pdf

As I said, I think we're the lucky ones in this particular scenario.
I've been more afraid of picking up well understood bacterial and viral infections than I am of this.
It's quite bizarre actually, how my brain is processing this.

Hope you're all faring well, and maybe this gives you a little extra peace of mind.
Stay well, stay healthy and don't forget to laugh. Find reasons to have full belly laughs - the most healing feeling ever.

Peace,
marta

[drz]

I just signed up for webinar on
What We Know and Don't Know: Vasculitis and COVID-19
Description Join our vasculitis experts in a discussion about vasculitis, COVID-19 and the immune-suppressed patient. Drs. Kevin Byram, Anisha Dua, Ulrich Specks, and Jason Springer will provide an overview and answer as many questions as possible from the attendees.

Time May 23, 2020 09:00 AM in Central Time (US and Canada)

Since I think this might have some useful info. I stopped going to see Specks for followup in their GPA study and wonder how COVID-19 and GPA treatment meds might interact or what special risks we have and treatment options that might help us.

[drz]

How many watched the webinar? Lot of info presented but consensus seemed to be we don't know enough yet about most of the issues. Use common sense to stay safe and stay sane.
I Liked Spechs statement that we know our body best and if some thing is off or different we should seek medical help. He did recommend taking your temp and O2 levels twice a day and to seek help if our O2 levels start dropping or if we get a higher temp since both are likely signs of COVID-19. I am going to order a no touch thermometer. We have an instant touch one in our lobby to screen visitors.

[Keith]

I watched the webinar and got the same impressions. Enjoyed it, more data needed.


Sent from my iPhone using Tapatalk

[drz]

"I question their conclusion. If we are no more likely to get it, I would think it due the fact that we are more fearful for good reason and therefore much more careful than other people."DRZ

Since the COVID-19 pandemic began, physicians who treat people with inflammatory or autoimmune conditions like lupus, Crohn’s disease, and rheumatoid arthritis have been trying to determine just how vulnerable these patients are to the virus. Because COVID is relatively new, many have largely based their predictions based on how this group has fared with other respiratory viruses, such as the flu. But now that it’s been eight months since coronavirus was first identified, more data about its impact is beginning to emerge.

A new research review, published in the journal Current Opinion in Rheumatology, has examined the best-available evidence to date and yields somewhat good news. The authors focused on several previously published peer-reviewed studies that specifically looked at COVID-19 incidence and outcomes in people with inflammatory-mediated immune disease (IMID). Some of these studies were in patients with rheumatic conditions (such as rheumatoid and psoriatic arthritis, axial spondyloarthritis, and lupus), some were in gastroenterology patients (such as Crohn’s disease and ulcerative colitis), and a small number were in psoriasis patients.

The authors concluded that “IMID patients are not at higher risk of developing COVID-19 than individuals without IMID and that most patients recover, including those on biologic therapies, which provides reassurance to both patients and providers.”

However, when patients with rheumatic disease do contract COVID-19, they’re more likely than people without these conditions to develop severe complications, including serious respiratory distress that requires being put on a ventilator.

Patients using glucocorticoids seem to have the highest risk of serious outcomes. As with the general population, advancing age and having a co-occurring condition like heart disease or diabetes are also extremely important risk factors.

This research review will not be the last word on how COVID-19 impacts people with inflammatory or autoimmune conditions, and the authors note that additional studies are “still urgently needed” since many of the studies they analyzed were small or otherwise limited in scope.

The authors did point out that biases in the way the studies are designed could limit overall knowledge about how patients with these conditions are affected by COVID-19. For example, if patients “have differential behavioral practices (i.e., be more likely to take preventive measures such as wearing masks, washing hands, and sheltering in place longer) than the general population due to awareness of being at higher risk of developing infections because of their disease or long-term medications, this could potentially lead to an underestimate of risk,” the authors explain.

The kind of studies that will provide such knowledge about differences between inflammatory and autoimmune patients and the general population will take more time (and require much bigger numbers of people) to collect. “Large-scale, population-based studies using nationwide registries, especially in countries with uniform COVID-19 reporting systems, may provide a better estimate of risk of COVID-19 in the IMID population, and whether differences in incidence and outcomes are present,” according to the authors.

In the meantime, most health experts recommend that IMID patients continue to pay extra attention to preventive measures such as wearing masks, avoiding extended in-person contact with people outside their household, and practicing hand hygiene.

If you develop any possible COVID-19 symptoms, contact your health care provider for guidance.
Get Free Coronavirus Support for Chronic Illness Patients

Join the Global Healthy Living Foundation’s free COVID-19 Support Program for chronic illness patients and their families. We will be providing updated information, community support, and other resources tailored specifically to your health and safety. Join now. The above is their latest mailing.

[vdub]

Fun reading this, but even more fun to see all my old friends still on the forum -- too many to list. I communicate with emails daily with Andrew and Geoff, but don't get on the forum much anymore. But, for a good reason.... I'm feeling quite well as long as I have the proper drugs. I'm still very dependent on pain pills, but mostly because of back issues and fibromyalgia. Wegs seems to be more of a hassle than a limitation. Fibromyalgia and, I suppose, arthritis seems to be the biggest source of pain, but its hard to say. I am in pain pretty much all the time, but it is well controlled with hydrocodone. Unfortunately, hydrocodone (and the other opioids) are the only pain meds I can take. All NSAIDS are off limits to me due to the pituitary (or lack there of) issues.

At any rate, so nice to see all of you up and active. My very best to all..... vw

[drz]

Glad to hear you feeling quite well. I wonder what projects or travels have occupied your time.I enjoyed hearing aboaut your travels and projects. Any new cars being restored. Keep on keeping on.

[vdub]

I'm not well enough to tackle in car restorations or even finish my MG. I now have to hire someone to do the work on the MG. It's really hard to find a mechanic who knows how to tune a carb, let alone twin carbs. Generators and regulators are also a thing of the past, so I bought an alternator which will replace both those items, but moves the car further away from being original. Of course, it could all be undone.

I can't do lawn work anymore and I had to hire someone to finish of our cabin. I have found that it is much easier to write a check to someone than it is to go through the pain of doing it myself.

My pain is pretty much controlled with drugs as long as I don't do anything strenuous to exacerbate it. So far, this year we haven't gone RV'ing, but we are thinking about it. Some days I think I could, but others days I'm not so sure about it. So, I'm enjoying life, but I've had to throttle back my activities quite a bit.

[Dirty Don]

Hated tuning the side draft dual carbs on the TRs, I feel your pain!!!!!! LOL Take care & enjoy!

[loisann11]

Love your thoughts on this. Background 1st I was diagnosed back in 2014 with GPA due to a bout of double pneumonia followed a couple months later with kidney failure. I have been getting Rituxin infusions every 6 months since and all has been good. I consider myself one of the lucky ones as i have no day to day issues. Just check labs every 3 months to make sure all is good. Last 2 infusions have been 11 months apart so lasting longer. No major flairs but last labs didn't look good so I just had my infusion last Friday.

End of May I had a symptom that wasn't "normal" for my GPA. I had "chills", so I thought I might as well get tested. It came back positive for Covid. I stayed home mostly in bed, no fever, none of the symptoms they all talk about. Just chills and and feeling of just wanting to lay around and do nothing. Didn't feel like eating much either.

Anyway I survived. I am about 70 years old and grew up in the farm country of Minnesota, so lots of "germs" etc. growing up. I think that may have helped me too.

I hope all stay safe and healthy out there.

[vdub]

I'm surprised with your double pneumonia issues that you had such a light time with covid. Really glad that you did, tho. I hope your theory of good farm germs is on target as I grew up on a farm, too, in Idaho. At least now you should have some antibodies. How long they will last depends who we want to believe. I have always told people that the extra weight I carry around is my surgery weight for when I get sick. Seems like a good idea. :-)

[loisann11]

they claim extra weight is good when older, I'm carrying mine too. I can be sick for awhile. I did lose 5 in the 2 weeks I was sick, unfortunately it has come back.

Hard to know what is true about virus. They change their minds everyday depending on the wind I think. County health contacted me when they were notified I was tested didn't even ask the proper questions in my opinion. No where do you think you got it, what symptoms did you have, just nothing really useful. Didn't care if I had other health issues. Should have all been helpful information.

Stay safe!

[drz]

But now, the Helsinki Airport is doing one better: It’s hiring (https://www.internationalairportreview.com/news/136484/helsinki-airport-covid-19-dogs/) a team of dogs, trained to sniff out COVID-19, to screen passengers.
Dogs have already proven their ability to sniff out diseases ranging from cancer (https://www.akc.org/expert-advice/news/meet-americas-cancer-sniffing-canines/) to malaria (https://www.wired.com/story/the-science-of-the-sniff-why-dogs-are-great-disease-detectors/). While we don’t always know exactly what they are detecting to ferret out specific illnesses, the clues are likely tied to a dog’s ability to smell volatile organic compounds (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919317/)—the metabolic junk our bodies produce all the time, which can vary with illness.
With 220 million scent receptors, versus the 5 million receptors that humans have, they have a sense of smell that’s 10,000 times more accurate than our own. They can sniff substances that are diluted to a point of just one part per trillion (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4919317/), or the equivalent of smelling one drop of liquid in the combined volume of 20 Olympic swimming pools.
Researchers at the Veterinary Faculty of the University of Helsinki have been training dogs to be able to detect COVID-19 since early 2020. In May, the research group reported (https://www.helsinki.fi/en/news/health-news/the-finnish-covid-dogs-nose-knows) that it had successfully trained dogs to detect COVID-19 in urine samples. But progress has happened fast. Now, the dogs have been trained to detect COVID-19 from sweat on our skin and have started trial testing at the Helsinki Airport.
According to International Airport Review (https://www.internationalairportreview.com/news/136484/helsinki-airport-covid-19-dogs/), these canines need as little as 10 molecules to detect COVID-19, while current test equipment requires 18,000,000. And there’s no comparison of speed. Abbot Labs has a 15-minute test that costs $5 to administer (https://www.fastcompany.com/90544507/abbotts-rapid-covid-19-test-heres-how-its-different-from-the-rest). Dogs can detect COVID-19 more or less instantly, and without an uncomfortable nasal swab (https://www.fastcompany.com/90539438/this-covid-swabbing-robot-is-terrifying-but-it-doesnt-need-to-be).
The screening process won’t be as simple as letting passengers walk by while a dog casually sniffs, however. Instead, passengers will be instructed to rub their skin with a wipe, then drop the wipe into a cup. The dog will sniff this cup inside an isolated booth. This arrangement allows for anonymous processing that protects a person’s privacy, while shielding the handler from direct contact with a potentially infected passenger. Any passenger who is suspected of having COVID-19 will be directed to the airport’s health information area.

The Helsinki program will soon employ four dogs but could expand to as many as 22 as enough canines are trained for the task. And while it’s unclear if the idea will scale beyond one airport—nursing homes (https://www.fastcompany.com/90484506/nursing-home-design-is-deadly-heres-how-to-change-it) would be another excellent use case of such dogs, according to researchers—it makes for a fascinating case study on how we don’t necessarily need more technology to screen for COVID-19 when 130,000 years of domesticated canine evolution is already on our side.

About the authorMark Wilson is a senior writer at Fast Company who has written about design, technology, and culture for almost 15 years. His work has appeared at Gizmodo, Kotaku, PopMech, PopSci, Esquire, American Photo and Lucky Peach
More (https://www.fastcompany.com/user/mark-wilson)

[vdub]

That's pretty amazing! Maybe we'll get back to flying and cruising again. This is really good news.

[woz]

Gives a new meaning to "Mans Best Friend"
Sorry to all the cat lovers!!

Regards Woz.....

[drz]

September 29, 2020



Self-collected saliva test could detect silent SARS-CoV-2 carriers





Self-collected saliva is a valuable specimen to detect severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in mass screening of asymptomatic persons, according to a study published in Clinical Infectious Diseases.
“Rapid detection of asymptomatic infected patients is critical for the prevention of outbreaks of coronavirus disease 2019 (COVID-19) in communities and hospitals,” wrote Isao Yokota, Hokkaido University Graduate School of Medicine, Sapporo, Japan, and colleagues.
The researchers conducted a mass-screening study to determine and compare the sensitivity and specificity of nucleic acid amplification using paired samples (nasopharyngeal swabs and self-collected saliva) for the detection of SARS-CoV-2 in 1,924 asymptomatic individuals from two cohorts (contact tracing and airport quarantine cohorts) in Japan, using reverse transcriptase-polymerase chain reaction (RT-PCR) and reverse transcriptase loop-mediated isothermal amplification (RT-LAMP) test.
The study showed that the sensitivity of nucleic acid amplification testing with nasopharyngeal and saliva specimens was 86% (90%CI: 77-93%) and 92% (90%CI: 83-97%), respectively, with specificities of 99.93% (90% CI: 99.77-99.99%) and 99.96% (90%CI: 99.85-100.00%), respectively. Further, the researchers found the viral loads were equivalent and highly correlated between nasopharyngeal and saliva samples of individuals testing positive and they said both specimens “may be useful in detecting viral RNA.”
In addition, the true concordance probability was estimated at 0.998 (90% CI: 0.996-0.999) in the airport quarantine cohort. The researchers noted that “true concordance probability with varying estimation constraints of sensitivity is shown to be very high, and therefore the RT-PCR results from saliva and nasopharyngeal [samples] appeared to be sufficiently consistent.”
“We report for the first time the accuracy of viral detection using natural clinical specimens of asymptomatic persons, that the sensitivity is higher than the 52% to 71% reported in symptomatic patients,” the authors wrote.
“The current study further extends that saliva may be a beneficial alternative to nasopharyngeal fluid in detecting SARS-CoV-2 in asymptomatic carriers. The comparison between paired samples have shown equivalent utility with similar sensitivity and specificity,” the authors said.
They added that “self-collected saliva has significant advantages over nasopharyngeal sampling especially in the setting of mass screening. For example, saliva collection is non-invasive and does not require specialized personnel nor the use of PPE.”
“It is unlikely that the sensitivity of RT-LAMP is significantly less than that of RT-PCR, and that tests by RT-LAMP had little impact on our conclusions. Our study suggests that RT-LAMP may be a useful alternative to RT-PCR for the diagnosis of SARSCoV-2, especially where diagnosis is required at the point of sample, ” the authors noted.
“Mass screening of the virus using self-collected saliva can be performed easily, noninvasively, and with minimal risk of viral transmission to health care workers,” the authors concluded.




Reference: https://academic.oup.com/cid/advance-article/doi/10.1093/cid/ciaa1388/5911780



SOURCE: Clinical Infectious Diseases

[drz]

This might be helpful for us? The big question is how a vaccine works and if it will be safe and effective for us people with a suppressed immune system.

September 30, 2020



Interim data show mRNA-1273 vaccine for COVID-19 triggered antibodies, had acceptable safety profile in older adults



Interim data from a Phase I study published in The New England Journal of Medicine showed that adverse events associated with the coronavirus disease 2019 (COVID-19) vaccine candidate mRNA-1273 were mainly mild or moderate among adults who were 56 years of age or older. In addition, the 100-μg dose of the vaccine, which encodes the prefusion-stabilized spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was found to induce higher binding- and neutralizing-antibody titers than the 25-μg dose.
The Phase I trial, initially conducted among participants between the ages of 18 and 55 years, was expanded to include 40 older healthy participants who were stratified into two subgroups: 20 adults between the ages of 56 and 70 years, and 20 who were 71 years of age or older. All participants were assigned sequentially to receive two doses of either 25 μg or 100 μg of vaccine administered 28 days apart. The trial was conducted at Kaiser Permanente Washington Health Research Institute in Seattle, the Emory University School of Medicine in Atlanta, and the National Institute of Allergy and Infectious Diseases (NIAID) Vaccine Research Center in Bethesda, Maryland.
The researchers reported that solicited adverse events were predominantly mild or moderate in severity and most frequently included fatigue, chills, headache, myalgia, and pain at the injection site. All 10 solicited local adverse events that were classified as moderate, and all but 2 moderate systemic events, occurred after the administration of the second dose. Symptoms typically occurred on the day of vaccination or 1 day afterward and "resolved quickly," researchers noted.
The study showed that binding-antibody responses increased rapidly after the first immunization. By day 57, among participants who received the 25-μg dose, the anti–S-2P geometric mean titer (GMT) was 323,945 (95% confidence interval [CI], 182,202 to 575,958) for those ages of 56 and 70 years, and 1,128,391 (95% CI, 636,087 to 2,001,717) among those 71 years or more. Meanwhile, for participants who received the 100-μg dose, GMTs in the two age subgroups were 1,183,066 (95% CI, 379,698 to 3,686,201) and 3,638,522 (95% CI, 1,316,233 to 10,058,130), respectively. Researchers noted that after the second immunization, serum neutralizing activity was detected in all the participants by multiple methods.
"Binding- and neutralizing-antibody responses appeared to be similar to those previously reported among vaccine recipients between the ages of 18 and 55 years and were above the median of a panel of controls who had donated convalescent serum," wrote Evan J. Anderson, MD, Emory University School of Medicine, Atlanta, Georgia, and colleagues. "These data also suggest that a second dose of vaccine is needed to achieve neutralizing antibodies in participants after the age of 56 years, and titers rapidly increased by 7 days after the booster vaccination," the authors noted.
Meanwhile, the study also showed that the vaccine elicited a strong CD4 cytokine response involving type 1 helper (Th1) T cells among participants in the two age subgroups who received the 100-μg dose and among participants between the ages of 56 and 70 years administered the 25-μg dose. The authors noted that response involving Th2 T cells (IL-4 and IL-13) was found to be "minimal" regardless of age or dose, while CD8 T-cell responses to S-2P were observed only at low levels after the second vaccination among participants in the two age subgroups given the 100-μg dose.
"Overall, these preliminary findings show that in a small group of participants, adverse events associated with the mRNA-1273 vaccine were mainly mild or moderate in older adults, a group that is particularly at risk for illness and death from COVID-19. The 100-μg dose induced higher binding- and neutralizing-antibody titers than the 25-μg dose, findings that support the continued evaluation of the 100-μg dose level and two-dose regimen in a large Phase III trial with a more diverse population to ascertain the safety and efficacy of the mRNA-1273 vaccine and to assess its level of protection against COVID-19," the authors concluded.
Important limitations of this study, according to the authors, include the small numbers of participants and the limited ethnic diversity. "In addition, at the time of this interim report, the long-term durability of immunogenicity could not be assessed, although the magnitude of antibody, cellular, and memory responses will be followed for 12 months after the second vaccination," the authors said. They also suggested that "the presence of chronic diseases (eg, diabetes) and frailty may be better predictors of poor immunologic responses than age alone."




Reference: https://www.nejm.org/doi/full/10.1056/NEJMoa2028436?query=featured_coronavirus



SOURCE: The New England Journal of Medicine

[drz]

October 15, 2020
Increased risk of COVID-19 in patients with autoimmune diseases, glucocorticoid use plays a role: Study

By Denise Baez

NEW YORK -- October 15, 2020 -- Patients with autoimmune diseases appear to have an increased risk of coronavirus disease 2019 (COVID-19), primarily attributed to glucocorticoid use, although their clinical outcomes were not considerably worse when compared with individuals without autoimmune diseases, according to a meta-analysis published in the Annals of the Rheumatic Diseases.

The study also found that monotherapy with biologic or targeted synthetic disease-modifying anti-rheumatic drugs (DMARDs) was associated with a lower risk of severe COVID-19, suggesting its safety in the COVID-19 pandemic.

Shintaro Akiyama, MD, University of Chicago Medicine, Chicago, Illinois, and colleagues scrutinised data from 62 observational studies including 319,025 patients with autoimmune diseases from 15 countries.

Rheumatic diseases included rheumatoid arthritis, lupus, psoriatic arthritis, spondyloarthritis, ankylosing spondylitis, vasculitis, polymyalgia rheumatica, Sjögren’s syndrome, systemic sclerosis, and other autoimmune-mediated diseases, including Behcet’s syndrome, sarcoidosis, and inflammatory myopathies.

Of the 319,025 patients, 878 tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), for an event rate of 0.011.

Patients with lupus, Sjögren’s syndrome, and systemic sclerosis had a higher prevalence of COVID-19 (58 of 1,641; event rate of 0.034) when compared with the other disease groups, which is likely due to a higher proportion of glucocorticoid use (60.3%). Patients with irritable bowel disease had the lowest prevalence (309 of 251,568; event rate of 0.003).

The researchers also analysed 7 case-controlled studies to compare the prevalence of COVID-19 in patients with and without autoimmune diseases. In this analysis, out of 30,771 patients with autoimmune diseases, 278 tested positive for COVID-19, compared with 144,283 out of 24,511,773 individuals without autoimmune diseases (odds ratio = 2.19; 95%  confidence interval [CI], 1.05-4.58; P = .038). These 7 studies only included individuals with psoriasis (OR = 3.43; 95% CI, 1.68-7.01; P = .001) and rheumatic diseases (OR = 1.60; 95% CI, 1.13-2.25; P = .008), both of which demonstrated an elevated risk of COVID-19 compared with controls.

The researchers also assessed 65 studies that included a total of 2,766 patients with autoimmune diseases who tested positive for COVID-19. Among this group, 1,102 patients were hospitalised for an event rate of 0.352, and 188 patients died, for a rate of 0.066.

“Patients with rheumatic diseases had the highest mortality rate, which was consistent with the analysis of the hospitalisation rate,” the authors noted.

Another meta-analysis of 6 case-controlled studies showed no differences in hospitalisations (OR = 1.05; 95% CI, 0.78-1.42; P = .73), death (OR = 0.55; 95% CI, 0.081-3.68; P = .53), admission to the intensive care unit ([ICU] OR = 1.22; 95% CI, 0.42-3.60: P = .72), or mechanical/non-invasive ventilation (OR = 1.03; 95% CI, 0.22-4.81; P = .97) when compared with the control population.

“Subgroup analyses according to comorbidities showed that patients age ≥64 years, male gender, hypertension, diabetes, body mass index ≥30, and at least 1 comorbidity had higher rates of hospitalisation, ICU admission, ventilation, and death due to COVID-19 when compared with those without these comorbidities,” the authors wrote. “Subgroup analyses according to medical therapies showed that patients treated with glucocorticosteroids, conventional synthetic DMARDs, or a combination of biologic/targeted synthetic DMARDs and conventional synthetic DMARDs had a 2 to 3 times higher event rate of each clinical outcome when compared with those treated with biologic or targeted synthetic DMARD monotherapy. Importantly, patients with anti-tumour necrosis factor (TNF) monotherapy use tended to have a lower rate of hospitalisation and mortality when compared with those with non-TNF-targeted monotherapy.”

“This study is the first comprehensive meta-analysis which determined the prevalence and clinical outcomes of COVID-19 in autoimmune diseases,” the authors concluded. “Our study suggests that glucocorticoid use increases the risk of SARS-CoV2 infection and might contribute to the higher prevalence of COVID-19 in [patients with] autoimmune disease.”
Reference: https://ard.bmj.com/content/early/2020/10/13/annrheumdis-2020-218946
SOURCE: Annals of the Rheumatic Diseases

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[drz]

OCTOBER 13, 2020
Patients with mild, moderate COVID-19 unlikely to be infectious after day 10 of symptom onset
By Denise Baez

NEW YORK -- October 13, 2020 -- Patients with mild to moderate coronavirus disease 2019 (COVID-19) are highly unlikely to be infectious after day 10 of symptom onset, however, patients with severe disease may shed the virus for a longer period of time, according to a study published in the Journal of Infection.

The findings come from a rapid review of 13 virus culture studies and 2 contact tracing studies conducted between January 1, 2020, and August 26, 2020. The studies were conducted in the United States, the United Kingdom, Taiwan, Germany, Switzerland, Australia, Canada, Spain, South Korea, Hong Kong, and the Netherlands.

Across all 13 virus culture studies, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) culture was attempted from samples collected from at least 808 patients, with SARS-CoV-2 isolated in at least 206 of these patients. A total of at least 1,652 samples had SARS-CoV-2 culture attempted and at least 413 of these were positive.

For 5 of the virus culture studies, the last day on which SARS-CoV-2 could be cultured occurred within the first 10 days since onset of symptoms. For the most part, the clinical severity of patients was mild to moderate in these 5 studies. For another 5 virus culture studies, SARS-CoV-2 was isolated beyond day 10 for approximately 3% of included patients. The remaining 3 virus culture studies included patients with severe or critical disease. In one of these studies, SARS-CoV-2 was isolated up to day 32, and in 2 studies that included immunocompromised patients, SARS-CoV-2 was isolated for up to 20 days.

The 2 large contact tracing studies reported that when close contacts were first exposed greater than 5 days after symptom onset in the index case, there was no evidence of laboratory-confirmed onward transmission of SARS-CoV-2.

“The evidence to date from virus culture studies would appear to suggest that patients with mild-to-moderate COVID-19 are highly unlikely to be infectious beyond 10 days from symptom onset,” wrote Kieran A. Walsh, MD, Health Information and Quality Authority, Cork, Ireland, and colleagues. “Evidence from large contact tracing studies appears to support this finding. However, evidence from a limited number of studies indicates that patients with severe or critical illness, and or those who are immunocompromised, may be infectious for a prolonged period, possibly for 20 days or more.”

There were 6 studies that examined the relationship between viral load and culture of SARS-CoV-2, and all 6 studies found an inverse correlation. One study that included 234 samples (Basile et al) concluded that any clinical sample with a cycle threshold (Ct) value of ≥37 was not indicative of replicative (or potentially transmissible) virus. Another study that included 90 samples (Bullard et al) estimated that for every 1 unit increase in Ct value, the odds of culturing SARS-CoV-2 decreased by 32%.

“The findings from our rapid review are largely in agreement with 4 previous reviews conducted in this general area,” the authors wrote. “All of these reviews concluded that infectiousness generally declines 7 to 10 days after symptom onset, and point to uncommon outlier cases where this duration is exceeded. Another common finding across 3 of these reviews was the prolonged duration of SARS-CoV-2 RNA detection, sometimes for 2-3 months after onset of symptoms, along with cases of repeat SARS-CoV-2 RNA detection after a patient has clinically recovered. Hence, patients are unlikely to be infectious for the entire duration of viral RNA detection as the presence of viral RNA may not represent transmissible or replication-competent virus. Our rapid review is the first to attempt to quantify the proportion of patients with COVID-19 that are potentially infectious beyond day 10 post symptom onset, and draws on more recent evidence, including both virus culture and contacting tracing studies.”

Reference: https://www.journalofinfection.com/article/S0163-4453(20)30651-4/fulltext
SOURCE: Journal of Infection

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October 7, 2020
Updated guidance on the management of COVID-19 from an American Thoracic Society/European Respiratory Society coordinated task force

An International Task Force convened by the American Thoracic Society (ATS) and European Respiratory Society (ERS) has updated its guidance on the pharmacological management of acute coronavirus disease 2019 (COVID-19), including remdesivir, hydroxychloroquine (HCQ) and dexamethasone.

“The changes to these consensus suggestions reflect the publication of several randomised trials since the prior guidance was issued, the Task Force noted.

The updated guidance was published in European Respiratory Review. The Task Force, composed of respiratory physicians, critical care physicians and infectious disease physicians, made seven consensus suggestions. Agreement was measured using the Convergence of Opinion on Recommendations and Evidence (CORE) process.

For hospitalised patients with COVID-19 pneumonia who require supplemental oxygen but are not mechanically ventilated or receiving extracorporeal membrane oxygenation (ECMO), the Task Force suggests remdesivir.
For hospitalised patients with COVID-19 pneumonia who are mechanically ventilated or receiving ECMO, the Task Force suggests remdesivir.
For hospitalised patients with COVID-19 pneumonia who require supplemental oxygen but are not mechanically ventilated or receiving ECMO, the Task Force suggests not using HCQ except within a clinical trial.
For hospitalised patients with COVID-19 pneumonia who are mechanically ventilated or receiving ECMO, the Task Force suggests not using HCQ except within a clinical trial.
For hospitalised patients with COVID-19 pneumonia who require supplemental oxygen but are not mechanically ventilated or receiving ECMO, the Task Force suggests dexamethasone.
For hospitalised patients with COVID-19 pneumonia who are mechanically ventilated or receiving ECMO, the Task Force suggests dexamethasone.
For adults who were hospitalised with COVID-19 pneumonia and had confirmed venous thromboembolism, the Task Force suggests therapeutic-dose anticoagulant therapy for 3 months to reduce the risk of recurrent venous thromboembolism.

“It is noteworthy that there was more agreement for remdesivir in less severely ill patients (ie conventional supplemental oxygen) than more severely ill patients (i.e. invasive mechanical ventilation or ECMO) and, conversely, there was more agreement for dexamethasone in more severely ill patients than less severely ill patients, reflecting the trends in beneficial outcomes across subgroups in the clinical trials and some Task Force members’ willingness to incorporate the subgroup analyses into their clinical decisions,” the Task Force noted.

The Task Force also urged caution in dexamethasone, particularly when administering to patients who require only a small amount of supplemental oxygen as these patients may not benefit as much as those who are more severely ill, are aged >70 years and mechanically ventilated, or are diabetic. “Alternative glucocorticoids are a reasonable choice (40 mg of solumedrol daily is equivalent) if dexamethasone is not available. Use of early dexamethasone in patients with COVID-19 pneumonia to avoid progression to ARDS and mechanical ventilation needs to be demonstrated, and delayed resolution of viral shedding needs further study,” the Task Force added.

Further, the Task Force made no suggestion for or against routine referral for pulmonary rehabilitation, pulmonary function testing, or mental health testing within 30–60 days after discharge.

“The clinical suggestions should never be considered mandates as no suggestion can incorporate all potential clinical circumstances. They are not intended to supplant physician judgment as it pertains to individual patients. The suggestions are interim guidance that should be re-evaluated as new evidence accumulates,” the Task Force cautioned.
Reference: https://err.ersjournals.com/content/29/157/200287
SOURCE: European Respiratory Review