Preliminary analysis of mortality associated with rituximab use in autoimmune diseases.

Strike me lucky

Well-Known Member
Scary thought when it seems most of the deaths are from infections . Used in cfsme they would want to be sure of no infections somehow. Most do have infections so probably limits most from being able to be prescribed it.
 

weyland

Well-Known Member
Scary thought when it seems most of the deaths are from infections . Used in cfsme they would want to be sure of no infections somehow.
For whatever reason this hasn't been a problem so far, which actually surprises me.

As they pointed out, this may be a factor in that:
Use of systemic corticosteroids and immunosuppressive agents as concomitant therapy with rituximab enhanced immunosuppression.
 

weyland

Well-Known Member
Did you know that rituximab is "more specifically is a human–mouse chimeric monoclonal antibody?"
Yes, that's what the 'xi' means in the name. All monoclonal antibody drugs that end in 'ximab' are chimeric mouse/human antibodies. The antibodies are created using mice, however a pure mouse antibody can't be used because our immune system will react to the antibody itself, so they have to introduce certain 'human' properties so the antibody will look human to our immune system and won't be destroyed.
 

weyland

Well-Known Member
This is the main takeaway in my eyes:
These preliminary data suggests that physicians using rituximab to treat autoimmune diseases should monitor their patients closely, especially their B-cell levels until they return to normal, be vigilant for possible sources of infection, and be aware of potential fatal outcomes.
I hope that this is something that the Norwegians and OMI are doing with their patients that they give rituximab to. The consequences of not doing so are shown in a recent paper that Lipkin was an author on. A girl developed hypogammaglobulinemia a bit after rituximab treatment (not for ME mind you), nobody caught it in time, and she died from a simple coxsackie B3 infection.
 

Strike me lucky

Well-Known Member
This is the main takeaway in my eyes:

I hope that this is something that the Norwegians and OMI are doing with their patients that they give rituximab to. The consequences of not doing so are shown in a recent paper that Lipkin was an author on. A girl developed hypogammaglobulinemia a bit after rituximab treatment (not for ME mind you), nobody caught it in time, and she died from a simple coxsackie B3 infection.

Thats a worry for many mecfsers if enteroviruses are implicated?
 

Strike me lucky

Well-Known Member
I think only if you end up with hypogammaglobulinemia which hopefully is pretty rare and I don't think has happened to any ME patients on rituximab yet.
My concern is that medicine cant seem to diagnose chronic low level infections that are common in cfsme. I was told after blood work that i had good immunity to varicella. Within a few days of going off avs i had a shingles outbreak. My gp said the blood work was probably really indicating chronic varicella not just antibodies.

I think it shows that when drs see an infection like ebv and its igg positive many immediately say its an old infection. They have know idea if these old infections are active or not. I think research needs to be in diagnosing chronic active infections accurately.

Also as many have low nk function, this marker shows we have a greater risk of infections. Im interested to see if Norwegian rtx study as before and after nk testing and other immune markers. I have heard that depleting b cells may increase nk function, but haven't seen any evidence of it yet. 2018 i guess we will find out.
 

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