Dr Bieger and Dr Mikovits discuss treating ME patients with Rituximab

[A.B.]

This lowered my opinion of Mikovits considerably. We don't need Rituximab to become a fiasco like XMRV. Wrong information and poorly supported claims is a good way to get just that.

Rituximab hasn't been working for Dr Bieger so far. None of the 10 patients had any benefit, and 2 suffered as a result from it.

 

[heapsreal]

I think its good mikovits is starting up conversation on who is appropriate for rituximab and who isn't.

horrified to be the patient the german doctor treated or I think treated by someone else with rituximab, who is now in his care, who is now much worse than he started off with bedridden etc for last 18months since this treatment.

we need various experts to voice opinions and promote this type of discussion and provide research from varied researchers. This reduces tunnel visioned approaches and helps promote a wider view of issues.

mikovits has voiced her view its up to her to continue proving it and for other researchers to question it and back up their own views with research.

 

[nandixon]

This lowered my opinion of Mikovits considerably. We don't need Rituximab to become a fiasco like XMRV. Wrong information and poorly supported claims is a good way to get just that.

Rituximab hasn't been working for Dr Bieger so far. None of the 10 patients had any benefit, and 2 suffered as a result from it.

I didn't get the impression that those 10 patients were Dr. Bieger's, as he seemed to talk about them abstractly. Perhaps they were though.

Either way, Dr. Mikovits would probably say that the rituximab didn't work because the patients weren't correctly selected as to having increased CD20+ B cells (under her theory), and additionally that they were probably given too high a dose.

 

[heapsreal]

I didn't get the impression that those 10 patients were Dr. Bieger's, as he seemed to talk about them abstractly. Perhaps they were though.

Either way, Dr. Mikovits would probably say that the rituximab didn't work because the patients weren't correctly selected as to having increased CD20+ B cells (under her theory), and additionally that they were probably given too high a dose.

The person treated with rituximab who got very ill from it and became bedridden I gathered they were treated by someone else then after this went into care with the Dr in the video.

I gathered though that they may have used rituximab on other cfsers.

I didn't gather the video was anti rituximab, as some seem threatened by it, but I think they were concerned about using it for the correct cfs patients.

 

[Sidereal]

Rituximab hasn't been working for Dr Bieger so far. None of the 10 patients had any benefit, and 2 suffered as a result from it.

I got the impression these cases were treated by other doctor(s) in Germany. I understand that Dr K has also been using rituximab for some patients in the States. I think if this treatment worked for ME/CFS (in the real world outside of clinical trial mysteries) we'd have heard about all these remissions if there were any. The problem is we don't know what this disease is and until we find out more about it and its possible subsets, jumping to radical treatments is bound to lead to some tragic outcomes like the German patient.

 

[nandixon]

@Jonathan Edwards
Sorry to bother you again, but would you mind reading just the paragraph on page 101 of her book that I mentioned?

I think this link here will give you a direct download of the one chapter:
https://www.novapublishers.com/catalog/downloadOA.php?order=1&access=true

(The section on p.101 actually starts on the prior page with the header, The Percentage of CD19+ B Cells Is Reduced In SFFV Env Antibody Positive CFS Patients.)

Does what they've written there make sense?

I've been debating about trying rituximab and I match up well with the low CD19+ (and low NK cell function) being described. (I don't have any CD20+ or CD23+ numbers to look at, though.)

Thank you again!

 

[Sidereal]

@Jonathan Edwards
Sorry to bother you again, but would you mind reading just the paragraph on page 101 of her book that I mentioned?

I think this link here will give you a direct download of the one chapter:
https://www.novapublishers.com/catalog/downloadOA.php?order=1&access=true

(The section on p.101 actually starts on the prior page with the header, The Percentage of CD19+ B Cells Is Reduced In SFFV Env Antibody Positive CFS Patients.)

Does what they've written there make sense?

I've been debating about trying rituximab and I match up well with the low CD19+ (and low NK cell function) being described. (I don't have any CD20+ or CD23+ numbers to look at, though.)

Thank you again!

This thread may interest you:

http://forums.phoenixrising.me/inde...immune-changes-in-the-peripheral-blood.33019/

 

[nandixon]

@Sidereal
Well, that's doubly discouraging.

@Jonathan Edwards
Never mind.

 

[Marky90]

This was annoying as i just bough her book "Plague", which apparantly isnt very trustworthy

 

[Marky90]

Btw does an(t)ybody have an idea of why we get so fatigued in relation to the proposed autoimmunity? Any thoughts @Jonathan Edwards ?

 

[rebar]

thank you Jonathan Edwards. Disappointed but thankful for your imput on this forum.

 

[Jonathan Edwards]

@Jonathan Edwards
Sorry to bother you again, but would you mind reading just the paragraph on page 101 of her book that I mentioned?

I think this link here will give you a direct download of the one chapter:
https://www.novapublishers.com/catalog/downloadOA.php?order=1&access=true

(The section on p.101 actually starts on the prior page with the header, The Percentage of CD19+ B Cells Is Reduced In SFFV Env Antibody Positive CFS Patients.)

Does what they've written there make sense?

I've been debating about trying rituximab and I match up well with the low CD19+ (and low NK cell function) being described. (I don't have any CD20+ or CD23+ numbers to look at, though.)

Thank you again!

To be honest, the errors Dr Mikovits makes in the video are so basic that I would not know what to make of results from her lab. Anybody can put cells through a sorting machine but it takes months to learn how to get reliable findings and that presumes at least you know the basic markers. Dr Mikovits talks of plasma cells having CD19 and B cells having CD20 but more or less all B cells have CD20 and CD19 and plasma cells lose both.

What I think is important to realise is that these are just markers of how mature the B cells are. They are not markers of separate subsets like CD4 and CD8 T cells.

I am sorry to disappoint people but I think I have some sort of responsibility to point it out when someone who appears not to have a grasp of the subject is giving clinical advice. Clinical decisions on rituximab usage have nothing to do with numbers of CD19 or CD20 positive cells. I would personally advise Dr Bieger to withdraw this video because I think it could potentially lead to inappropriate use of a drug that is not without significant risk

 

[Joolz]

@Jonathan Edwards: I remember that some researchers looked into the FCGR3A receptor gene variants for predicting response to RTX in RA - and found quite some differences. Why don't they do that for CFS patients?
Here's the paper: http://www.ncbi.nlm.nih.gov/pubmed/23002160

What would be your best guess concerning NK cytotoxicity - would CFS patients with low NK function be good or bad candidates for RTX? Or is it a lot more complicated than that? Would it just predict the risk for side effects, but not the response to RTX?

EDIT: I haven't watched the video - yet.

 

[Jonathan Edwards]

@Jonathan Edwards: I remember that some researchers looked into the FCGR3A receptor gene variants for predicting response to RTX in RA - and found quite some differences. Why don't they do that for CFS patients?

What would be your best guess concerning NK cytotoxicity - would CFS patients with low NK function be good or bad candidates for RTX? Or is it a lot more complicated than that?

EDIT: I haven't watched the video - yet.

Variations in FcR3A just alter the potential killing efficiency of the drug and might alter the dose required. However, it seems that the dose response curve is pretty flat and is not affected much by FcR3 variation. We looked at that right at the beginning.

I cannot see what NK function has to do with using rituximab to be honest. I am not even convinced that people are agreed on what NK defect there may be in ME/CFS. I am afraid that to me as an immunologist most of this stuff is fairy tales. Real immunology does not work like that.

 

[Joolz]

I cannot see what NK function has to do with using rituximab to be honest.

At least this is good news for those with low NK cytotoxicity!

I got the impression these cases were treated by other doctor(s) in Germany.

As far as I know, no one has received RTX treatment from Dr Bieger. I'm quite surprised to read that dosage was too high for the ten German patients who received RTX. Olaf Bodden received it from Prof Scheibenbogen, as he revealed to the press. I was and am under the impression that she was in close contact with Fluge/Mella.

I understand that Dr K has also been using rituximab for some patients in the States. I think if this treatment worked for ME/CFS (in the real world outside of clinical trial mysteries) we'd have heard about all these remissions if there were any.

From what I've heard, some of Dr K's patients have become a lot better, but I haven't heard any remission stories either. Unfortunately, that is. Apart from one in the Norwegian press - but the girl received RTX, Valcyte AND (later on) immunoglobulins.

 

[heapsreal]

I didnt think it was about promoting use of these treatments but more to do with what they had previously done and results found. Definately didnt come across as a how to do type video.

I think it raised really good points especially on safety. They were really after information or stimulate the topic of what treatments are best for what patients. It was mentioned that it is unknow who should be getting the rituximab and who shouldnt. If someone has a few theories on how to select the right patient for the right drug, i would think it would be very advantageous. The soccer player who is now bedridden from rituximab probably now wishes there was some type of immune profile used to match patients to treatments.

@Jootz im sure she says low nk function would rule one out of rituximab??

 

[heapsreal]

My understanding is that rituximab knocks out our antibodies, so to clean up any infections the nk cells job it is to do so. But if you have low nk function and also have reduced antibodies than your immune function would be very low and open to infections and reactivations. I think its a risk factor or contraindication fpr rituximab in immune suppressed.

 

[Joolz]

My understanding is that rituximab knocks out our antibodies, so to clean up any infections the nk cells job it is to do so. But if you have low nk function and also have reduced antibodies than your immune function would be very low and open to infections and reactivations. I think its a risk factor or contraindication fpr rituximab in immune suppressed.

That's what I was thinking. But many CFS patients with low NK function AND reduced antibodies don't seem to be prone to infections at all - more the opposite.

What about the Norwegian RTX trial(s) - were low NK function and/or hypogammaglobulinemia exclusion criteria? @deleder2k, do you know?

 

[DanME]

To be honest, I think, this video is a total mess. Prof. Edwards has already informed us about all the mistakes Judy Mikovits made about immunology and RTX. Some mistakes are so basic, that even I recognised them. Also she is all over the place. Her main theory seems to be ME is caused by a retrovirus, but XMRV could never be replicated and she has absolutely no evidence for her claims. Then she switches, and at one point ME is a slow burning form of cancer, then an autoimmune disease, then chronic EBV plays a role and ultimately it is an immuno deficiency. A lot of confusing claims without any serious evidence. What makes her claims even more disturbing, that she didn't realise, that there is no form of oral RTX.

Olaf Bodden, the soccer player, who is mentioned, was treated with RTX a by Prof. Scheibenbogen, who has a lot of collaboration going on with Haukeland in Bergen. She stopped treating patients with RTX after the incident and wants to wait for further results from Norway, which is wise, I think. At this stage, RTX should be carefully tested in ME patients by doctors, who have a lot of experience with the drug and the disease. Like Fluge and Mella have.

 

[Sidereal]

I don't think Mr Bodden's case is an isolated example of ME deterioration following rituximab. Some of our forum members have reported adverse reactions.

http://forums.phoenixrising.me/inde...osis-glandular-fever.35059/page-3#post-563186

I would have been the exception if the study expanded to year 14 for me. Mild relapse at year 8 (misdiagnosed as depression), moderate at year 14 (cut work back to 32 hours) . Had substantial debilitating relapse year 15 1/2 (had to quit work) then in year 20 developed into progressive decline until present, 95% bedbound similar to when I originally got sick at age 15. Year 24, I found follicular b cell non-hodgkins lymphoma in nasolabial area (aka lower tear duct gland) and throat lymph nodes ( many anecdotal reports of cancers in these areas for % of ME patients). Rituximab temporarily got rid of cancer, ME symptoms worsened due to chronic multiple viral infections acquired during Rituximab treatment.