#COVIDMS COVID ADVICE?-SCANDI STYLE with a US Twist?

#

To our friends like Swedish Sara, apparently here is the apparent advice from the Swedish Neuroscience Institute, Seattle, Washington, USA. However, this came as a blog comment from an unsubstantiated source and not from a website that links to the reported source so be warned.

ProfG may not be able to comment as he may be not near the internet of is at a Birthday Party

The people who wrote below have rather different viewes from the views posted by the ABN (Association for British Neurologists). This shows how difficult the decision is when there is no real evidence. This perhaps explains the flip-flopping of ProfG. You make your opinions based on science, but the science isn’t really there. In addition the infection landscape that you are in will influence your decisions.

I can’t verifty this is true advice but what is below walks you through some of the reasoning. I have removed the advice.

Multiple sclerosis medications and coronavirus Having multiple sclerosis would not increase the risk of coronavirus disease (COVID19) in most patients. People with MS generally have more robust immune systems, so robust that the immune system attacks their nervous system, causing the MS. The disease, MS, does not cause suppression of the immune system. Some people with disabilities may be at increased risk of complications of COVID19. This includes people with weakness of their breathing muscles, or decreased ability to cough. Very few people with MS are affected in this way. In general, people on disease-modifying therapies should continue these therapies. Specific information about each medication follows:

Interferons (Avonex, Betaseron, Extavia, Plegridy, Rebif): These are not immunosuppressive medications and there is no increase in infection risk. Some have suggested that the body does not produce enough interferon to combat COVID19 virus infection early in disease, and that this increases the risk of lung damage with COVID19. If this is true, then interferons for MS would potentially be beneficial. This remains unproven.

Glatiramer acetate (Copaxone, Glatopa, Mylan): These are not immunosuppressive medications and there is no increase in infection risk.

Fumarates (Tecfidera, Vumerity): Effects on lymphocytes: These medications can cause a decrease in the lymphocyte count. In most patients, this decrease is slight, but in about 5% of the patients it can be significant (and is part of the standard monitoring). Risk of respiratory infections: There have been rare reports of some viral infections on fumarates. However, there is no increase in upper respiratory infections seen with fumarates thus far. How long do immune effects last: Should fumarates be discontinued, the immunologic effects slowly return to normal over 2 or more months.

S1P receptor modulators (Gilenya, Mayzent, Zeposia): Effects on lymphocytes: These medications cause a marked decrease in lymphocyte counts, but this does not correlate with infections. However, the effector lymphocytes (the ones that fight viruses) are not altered by these medications. Risk of respiratory infections: There is an increase in upper respiratory infections with these medications. For example, bronchitis was seen in 8% of patients treated with Gilenya compared to 4% for those treated with placebo. Influenza was seen in 13% of patients treated with Gilenya compared to 10% for those treated with placebo. However, there is some suggestion that S1P receptor modulators might be helpful in decreasing the lung damage from COVID19, and a clinical trial is underway to determine whether treatment with S1P receptor modulators helps patients with COVID19 infections. How long do immune effects last: Should these medications be discontinued, the immunologic effects slowly return to normal over 2 or more months.

Teriflunomide (Aubagio): Effects on lymphocytes: This medication can cause a slight decrease in the lymphocyte count. Risk of respiratory infections: There have been rare reports of some viral infections on teriflunomide. There is an increase in upper respiratory infections with teriflunomide. For example, bronchitis was seen in 8% of patients treated with teriflunomide compared to 6% for those treated with placebo. Upper respiratory infections were seen in 9% of those treated with teriflunomide compared to 7% treated with placebo. Influenza was seen in 12% of patients treated with teriflunomide compared to 10% for those treated with placebo. There are several types of bacterial infections of the lungs reported with teriflunomide. How long do immune effects last: If teriflunomide is discontinued it must be actively removed from the body with cholestyramine or activated charcoal for 11 days. The immune effects last for a few months after removal of the teriflunomide.

Cladribine (Mavenclad): This medication is taken for one week. A second week of medication is given one month later. This is repeated 1 year later. There are no treatments in years 3 or 4. Effects on lymphocytes: Following these doses, there is a mild decrease in the lymphocyte count. There are long lasting effects on the immune system. Risk of respiratory infections: Upper respiratory infections were seen in 38% of those treated with cladribine and 32% in those treated with placebo. How long do immune effects last: If cladribine is discontinued, the immune effects last for several years.

Natalizumab (Tysabri): This medication is given intravenously once a month. Effects on lymphocytes: This medication blocks lymphocytes from being able to get out of the bloodstream and into the tissues. It prevents lymphocytes from getting into the brain in people with MS. It also blocks lymphocytes from getting into other body tissues. In the presence of an infection, these blood vessels get much more leaky and the lymphocytes are able to partially get into the tissue. Risk of respiratory infections: The risk of respiratory infections was 17% with natalizumab and 16% with placebo. There are rare lung infections from some bacteria or fungi. How long do immune effects last: If natalizumab is discontinued, the immune effects last about 3 months.

Anti-CD20 medications (Ocrevus, Rituxan): The medication is given intravenously every 6 months. Effects on lymphocytes: Anti-CD20 medications cause B cells to be removed from the body. These cells function as amplifiers of the immune response. T cells, which fight virus infections, can be activated if they detect a virus. In the presence of a B cell, the activation of the T cell is much greater. Risk of respiratory infections: Upper respiratory infections were seen in 40% of patients treated with Ocrevus and 33% of patients treated with Rebif. Lower respiratory infections (pneumonia) were seen in 8% of patients treated with Ocrevus and 5% of those treated with Rebif. In a separate study, 49% of patients treated with Ocrevus had an upper respiratory infection compared to 43% of patients on placebo. Lower respiratory infections were seen in 10% of patients treated with Ocrevus and 9% of patients on placebo. How long do immune effects last: If anti-CD20 medications are discontinued, the immune effects last about 8-12 months.

Alemtuzumab (Lemtrada): Alemtuzumab causes many types of white blood cells to be removed from the body. Effects on lymphocytes: Alemtuzumab causes a decrease in many types of lymphocytes. Risk of respiratory infections: Infections occurred in 71% of patients treated with Lemtrada and 53% of patients treated with Rebif. Upper respiratory infections were seen in 16% of those treated with Lemtrada and 13% of those treated with Rebif. How long do immune effects last: If Alemtuzumab is discontinued, lymphocyte numbers increase over about 12 months. However, other immune effects last for several years.

SPOILER ALERT

I went on the Swedish Institute website and did not find this document, but as it comes with no branding, be very cautious when you read it. It could be Fake News, but I can follow the logic Here are the signs from the Swedish Institute Website

This image has an empty alt attribute; its file name is respiratory%20symptoms.jpg

From the stance you can see that also a few people get the Diarrhea  🙂

About the author

MouseDoctor

5 comments

  • “Having multiple sclerosis would not increase the risk of coronavirus disease (COVID19) in most patients. People with MS generally have more robust immune systems, so robust that the immune system attacks their nervous system, causing the MS.”

    From what I read the severe complications from COVID-19 arise in the later stage of the disease, when the reaction of the immune system is exaggerated and attacks the lungs, causing ARDS. Hence the apparently succesful use of tocilizumab in Italy for grave COVID-19 complications, an anti-IL-6 drug used against rheumatoid arthritis (strangely while it’s been prominently featured in the news in Italian media for the last few days it hasn’t had much of an echo outside Italy).

    So isn’t a propension to autoimmunity a factor that would increase risk?

    I am a MS Patient treated by rituximab first, ocrelizumab second. While the treatment has been 100% succesful from a neurology point of view I have developed recurrent upper and lower respiratory bacterial infections (I just had a first round of IVIG to bolster my defenses against them) as well as an of yet unexplained arthritis (either a second primary autoimmune disease, or a reactional arthritis due to infections unchecked because of the immunosupression) which suggests again a capacity to have exaggerated inflammatory reactions.

    I was very reassured to read your detailed and thoughtful posts (thank you very much) about the risks related to each DMT and to learn that the capacity to fight a virus remains solid (this corresponds to the advice I received from one of my doctors but given the prevailing uncertainty a concurring opinion is welcome). But at this stage I wonder more about the risk of complications due to autoimmunity. Does this make sense?

    And is it accurate to say that an autoimmune disease like MS does not increase the risk of COVID-19?

    • I dont know you could argue MS can fight the infection better so you wont get to the ARDS stage. Sorry not more help

  • “People with MS generally have more robust immune systems, so robust that the immune system attacks their nervous system, causing the MS.”

    That is a very odd statement. Never heard anything like it before. As though one’s immune system knocking lumps out of the nervous system would be any sort of indication of ability to fend off viruses etc. It is more an indication of an “insane” immune system which wastes “effort” on pointless, damaging things.

  • Hello!

    Where did you get the information about the clinical trial of S1P1 receptor agonists for COVID19 infections? I actually came to that same idea a month ago as I was researching cytokine storms/ARDS and I emailed a scientist in Maryland who is doing trials with this coronavirus. I followed the development of one particular drug developed by Receptos and then bought by Celgene, now Bristol Meyers. At that time, it said Zeposia is up for FDA approval next week (3/25). It seemed so promising and finding your post got me excited. I just read a 34 year old from California died this morning two weeks after visiting Disney World. He had a history of childhood asthma and bronchitis and it was ARDS that eventually took his life. A S1PI receptor agonist may have made the difference.

    Jenny

    • Sadly therre are many people dying and obviously having a lung condition is less than ideal. The drug is ozanimod that you are taking about,
      and the fingolimod trial is on clinical trials.gov. There are also numerous studies on anti-interleukin 6 receptor as a licenced therapy for cytokine release sydrome

By MouseDoctor

Translate

Categories

Recent Posts

Recent Comments

Archives