October 23, 2008 at 8:24 pm

These last two days of postings have really been rich in knowledge and have gone a long way in answering many of the questions I’ve wrestled with in the last year. Thanks Threads for your help.

If I narrow our discussion to anti-MAG IgM MGUS, then I take it that there are really several subclasses of this disease:
– B cell sourced anti-MAG IgM MGUS
– Plasma cell with CD20 expression sourced anti-MAG IgM MGUS
– Plasma cell without CD20 expression sourced anti-MAG IgM MGUS
– a combination of the above?
I wonder first of all whether there is a way to test a patient to determine which type of anti-MAG IgM MGUS the patient has. This would help to direct the appropriate recommended course of treatment.
For example, theoretically of the above first 3 subclasses, the first two would likely respond to Rituxan whereas the third would not. And timing for detectable clinical change would be different for the first two because of the different half lives of the dysfunctional cells.
Conversely, without clinical improvement from Rituxan treatment, would the patient conclude that the anti-MAG is being produced by a plasma cell without the CD20 protein?
Also, does the disease progress from one type to another? If so, how fast does this generally happen? Is catching the disease early a critical factor in treatment (apart from being able to limit the damage to peripheral nerves)?
Maybe this is a bit of an over-simplification, but, hey, I’m only a chemical engineer looking for those engineering-type cause and effect answers!!!


October 23, 2008 at 1:01 pm

I am sorry about your son and the difficult times you had and still have to go through. I wasn’t aware that he has CIDP.

Thank you for your explanation and the abstract. Interesting material. I’ll try to get a copy through my DIL who has access.

We didn’t define what I meant by [U]short[/U] and you by [U]long[/U] half-life of Ig. Would you agree that this table is fairly representative?

[U]Isotype Biological half-life (days)[/U]
IgA1 5.9
IgA2 4.5
IgD 2-8
IgE 1-5
IgG1 21-24
IgG2 21-24
IgG3 7-8
IgG4 21-24
IgM 5-10


October 22, 2008 at 6:51 pm

Welcome back, Threads. I was quite surprised this morning when I saw your name pop up again after a long absence. How have you been?

I certainly missed your expert input these last two years since the forum went down and I hope you don’t mind if I have a few questions right away. If you’ve read this thread here, you probably noticed that I’m now undergoing Rituxan treatment every six-month since last fall. I’m currently in the middle of my third round. So far I have not seen any kind of improvement.

A few days ago I posted three graphs showing my antibody titres since I started treatment. What puzzles me is the fact that the titre for IgG and IgM is only going down slowly – and still is in normal range -given the short half-life of antibodies and plasma cells as well as the reduction in B-cells which should be significant. Some authors even state that B-cells are absent beyond detection after Rituxan treatment. Is it possible that this is because of the existence of some long-lived nonmalignant plasma cells similar to memory B-cells. I remember reading one article in which the author reports the presence of long-lived plasma cells – I believe it was in animal studies (I did save the report but I would have to dig it up again).

The other question I have is why doesn’t the anti-MAG protein go down at the same rate as the overall population of antibodies? Do you have any thoughts on that?

By the way, my Rituxan treatment officially is not for my anti-MAG IgM neuropathy but for an asymptomatic indolent B-cell lymphoma which my oncologist – on my insistence – diagnosed after a bone marrow biopsy. I hope the effort is not wasted but I do know that chances for success are not very great.

I hope you’re well, take care