People with MS need to get up close and personal with their lymphocytes and lymphocyte counts and hence need to understand what the term lymphopaenia actually means.
I am a nurse practitioner and MS certified nurse. This blog post puts into layman's terms what I have been struggling to learn and remember for YEARS. Thank you!
Thanks for the explanation. Very clear and I really learned a lot reading it, specifically about some concepts that I did not understand well about B and T lymphocytes
I appreciate the level of detail. I only get lab work just prior to my infusion with Ocrevus so maybe once or twice a year. My GP does not believe in routine lab work so the Neuro is the only one that orders any lab work. I have no idea if my counts drop after my infusion. So clearly there is no standard which is why, I feel, we don’t like uncertainty. For example, I have never heard from my neurologist anything about maybe the Covid vaccine won’t work nor that maybe I should get an antibody test to see if it worked or not. Maybe I should not be seeking outside sources of information as this leads to said uncertainty.
There was no mention of dimethyl fumarate in your list of DMT’s. Dimethyl fumarate gave me lymphopaenia, <0.4 so I was moved to teriflunomide. My lymphopaenia now cycles between 0.5 and 0.9, but is usually 0.6 or 0.7 which is giving cause for concern. Currently had teriflunomide suspended for 8 weeks to see what happens. I’ll be pleased but very surprised if I make it to 1.0 or higher in 8 weeks. Not sure what the future holds, as I hate the idea of injectables, but GA seems the only thing that will not give me lymphopaenia.
I’m a pwMS and I’d like to know how does Ocrevus compares to Kesimpta in terms of safety and immunology? I read a few weeks ago a study that said that Kesimpta had a better safety profile than Ocrevus because B-Cell Repopulation was faster, but they never went into details to explain really why is safer because of that. I appreciate if you could explain it to me a little bit better.
P.S: I’ve been taking Kesimpta for 3 months including loading doses. All good so far.
Dear prof. G, could you help clarify something for me?
After 2 months of teriflunomide, my CD19 B cells have dropped from 120 to 73 (so about 40%).
After horrible experiences with DMF and chronic lymphopenia, and infections, I wonder how this drop in CD19 B cells can affect my infection risk.
Also in the long run. With DMF, chronic lymphopenia seemed to increase infections over time, even if ALC stayed 'stable' around 0.6.
I know DMF, teri, etc. are not depleting therapies, but I can't help wonder whether depleting en repopulating is sometimes less risky for infections, than years of continous significant suppression.
Thanks for the thorough explanation. I had my first Ocrevus 1 month after I had my second COVID vaccine. I had never been on an anti-CD20 before that date. Now I'm trying to figure out if that 1 Ocrevus treatment impacted my response to the vaccine. I am assuming not really, since I had all of my normal B cells when I got the vax. My next Ocrevus is in late October, and that would presumably impact my response to any boosters (I think).
I keep trying to do a risk assessment on myself - in my 40s with no other health concerns and vaccinated, I finally stopped masking in mid-June when my state dropped the mandate. Now trying to figure out if I'm a bit too lax.
I am due to start my 2nd course of Cladribine treatment and my lymphocytes have been stubbornly stuck at 0.6 for the last six months. I just hope to reach .8 in the next 1-2 months.
Any natural way to boost these, or is it just a waiting game?
hi there. Just wanted to feed back how clear this article was. Really landed the B cell T cell thing for me which after 9 years post diagnosis and avid reading of the Barts blog was still a bit woolly concept for me. Very timely as well as just stopped fingolimod to start cladribine (hooray). Waiting for those pesky lymphocytes to increase and fingers crossed for no rebound. Thanks for all the great info Prof you have been a massive boon in my quest to stay well and walking the Yorkshire hills xx
When you have completed the MS-Selfie Newsletters on each of the DMTs would ther be any possibility you could create an algorithm (diagram) for the best treatment at this point in time with the research we have, eg
1. start on ocrelizumab, ofatumumab or natalizumab (if alemtuzumab is not offered)
2. what next for those at risk of PML or failing, would you have different recommendations depending on age, activity level prior to starting treatment, MRI, risk of SPMS, likely benign course, ie how would you decide between cladribine, ocrelizumab, fingolimod, interferon etc for a patient
3. when would you stop treatment, if a patient doesn't turn progressive should they remain on a high efficacy DMD for life of drop to a lower with age.
I know this could be a large diagram with lots of parameters but I think it would be really useful for patients to have your view on this and understand what would give them the best chance!
Thank you doctor, that is exactly what we (patients) need. Even go deeper and get more details should be basic knowledge if we care about our health.
Dr. Giovanni,
I am a nurse practitioner and MS certified nurse. This blog post puts into layman's terms what I have been struggling to learn and remember for YEARS. Thank you!
Katy Clark, FNP-BC, MSCN
Thanks for the explanation. Very clear and I really learned a lot reading it, specifically about some concepts that I did not understand well about B and T lymphocytes
I appreciate the level of detail. I only get lab work just prior to my infusion with Ocrevus so maybe once or twice a year. My GP does not believe in routine lab work so the Neuro is the only one that orders any lab work. I have no idea if my counts drop after my infusion. So clearly there is no standard which is why, I feel, we don’t like uncertainty. For example, I have never heard from my neurologist anything about maybe the Covid vaccine won’t work nor that maybe I should get an antibody test to see if it worked or not. Maybe I should not be seeking outside sources of information as this leads to said uncertainty.
There was no mention of dimethyl fumarate in your list of DMT’s. Dimethyl fumarate gave me lymphopaenia, <0.4 so I was moved to teriflunomide. My lymphopaenia now cycles between 0.5 and 0.9, but is usually 0.6 or 0.7 which is giving cause for concern. Currently had teriflunomide suspended for 8 weeks to see what happens. I’ll be pleased but very surprised if I make it to 1.0 or higher in 8 weeks. Not sure what the future holds, as I hate the idea of injectables, but GA seems the only thing that will not give me lymphopaenia.
Hi Dr. Giovannoni. Hope you are doing well.
I’m a pwMS and I’d like to know how does Ocrevus compares to Kesimpta in terms of safety and immunology? I read a few weeks ago a study that said that Kesimpta had a better safety profile than Ocrevus because B-Cell Repopulation was faster, but they never went into details to explain really why is safer because of that. I appreciate if you could explain it to me a little bit better.
P.S: I’ve been taking Kesimpta for 3 months including loading doses. All good so far.
Dear prof. G, could you help clarify something for me?
After 2 months of teriflunomide, my CD19 B cells have dropped from 120 to 73 (so about 40%).
After horrible experiences with DMF and chronic lymphopenia, and infections, I wonder how this drop in CD19 B cells can affect my infection risk.
Also in the long run. With DMF, chronic lymphopenia seemed to increase infections over time, even if ALC stayed 'stable' around 0.6.
I know DMF, teri, etc. are not depleting therapies, but I can't help wonder whether depleting en repopulating is sometimes less risky for infections, than years of continous significant suppression.
Any thoughts would be very helpfull!
Thanks for the thorough explanation. I had my first Ocrevus 1 month after I had my second COVID vaccine. I had never been on an anti-CD20 before that date. Now I'm trying to figure out if that 1 Ocrevus treatment impacted my response to the vaccine. I am assuming not really, since I had all of my normal B cells when I got the vax. My next Ocrevus is in late October, and that would presumably impact my response to any boosters (I think).
I keep trying to do a risk assessment on myself - in my 40s with no other health concerns and vaccinated, I finally stopped masking in mid-June when my state dropped the mandate. Now trying to figure out if I'm a bit too lax.
Hello Dr. Giovanni,
I am due to start my 2nd course of Cladribine treatment and my lymphocytes have been stubbornly stuck at 0.6 for the last six months. I just hope to reach .8 in the next 1-2 months.
Any natural way to boost these, or is it just a waiting game?
I am fully cov vaccinated.
hi there. Just wanted to feed back how clear this article was. Really landed the B cell T cell thing for me which after 9 years post diagnosis and avid reading of the Barts blog was still a bit woolly concept for me. Very timely as well as just stopped fingolimod to start cladribine (hooray). Waiting for those pesky lymphocytes to increase and fingers crossed for no rebound. Thanks for all the great info Prof you have been a massive boon in my quest to stay well and walking the Yorkshire hills xx
Wonderful x10. Thank you Prof GG
Dear Prof. G,
When you have completed the MS-Selfie Newsletters on each of the DMTs would ther be any possibility you could create an algorithm (diagram) for the best treatment at this point in time with the research we have, eg
1. start on ocrelizumab, ofatumumab or natalizumab (if alemtuzumab is not offered)
2. what next for those at risk of PML or failing, would you have different recommendations depending on age, activity level prior to starting treatment, MRI, risk of SPMS, likely benign course, ie how would you decide between cladribine, ocrelizumab, fingolimod, interferon etc for a patient
3. when would you stop treatment, if a patient doesn't turn progressive should they remain on a high efficacy DMD for life of drop to a lower with age.
I know this could be a large diagram with lots of parameters but I think it would be really useful for patients to have your view on this and understand what would give them the best chance!