Are there instances when you can't have Rituximab?

[lemonworld]

I'm sorry if this is asked somewhere else, but I'm wondering if there are instances when you can't have Rituximab? if you have any other health issues or conditions?

 

[minkeygirl]

I'm no authority on this by any means, probably dumber than most, but I remember some discussions that there are certain subsets that should not take this. I don't know if they've pinned that down exactly but I think there were some with immune issues that maybe shouldn't.

Again, I am just repeating what I think I saw in some other threads about this. And there are many. I don't blame you for not wanting to wade through them all.

 

[Jonathan Edwards]

I'm sorry if this is asked somewhere else, but I'm wondering if there are instances when you can't have Rituximab? if you have any other health issues or conditions?

Not often. If you have very low immunoglobulins it would potentially be a problem (maybe below 6gm/L). If you have severe chest disease it may be unwise. There is no information on subsets being suitable or not so far, except that very severe housebound patients do not seem to get the best response on average. But that may just be that they need repeated treatments.

 

[alex3619]

My understanding is that some active infections preclude its use till they are resolved. If we can identify responder and non-responder subsets using a biomarker, one of the things they are hoping to discover in the phase 3 trial, then some may not be offered treatment at all.

The active infection issue is not unique to Rituximab. Many medical procedures are postponed for the duration of acute illness.

One of the intriguing things, as yet unproven but with theoretical justification, is that the number of treatments may have impact over time. Non responders might in some cases be late responders. We already have evidence of that. Many respond at six months, but some who have responded so far have had to be treated for a year. I think this is also seen in other autoimmune diseases. We need better data on this because there is bound to be a cut-off point beyond which continued treatment is not warranted if a patient has not responded.

When I am in a pessimistic mood I consider that only about half of us will respond, and only some of those go into full remission. That is because of the one third or more non responders combined with the contra-indicated patients. Some have a severe allergic reaction, too severe to control, and are stopped from further treatment.

On the other hand we may wind up with response biomarkers, and alternative treatments, so this story is far from done. The phase 3 trial might tell us much of this, and other trials with other agents offer hope. Rituximab wont be for everyone, but the first treatment for a disease is rarely effective on everyone.

 

[A.B.]

One of the intriguing things, as yet unproven but with theoretical justification, is that the number of treatments may have impact over time. Non responders might in some cases be late responders. We already have evidence of that. Many respond at six months, but some who have responded so far have had to be treated for a year. I think this is also seen in other autoimmune diseases. We need better data on this because there is bound to be a cut-off point beyond which continued treatment is not warranted if a patient has not responded.

The mean response time for major responders in the open label study was 23 weeks (8-66 weeks). Different antibody washout times seem to suggest that a variety of different antibodies can be found in this patient cohort.

 

[Lynne B]

I'm interested in this discussion, of course, but I don't understand 'different antibodies.' Can someone enlighten me please?

Cheers.

 

[alex3619]

Its the non-major responders and non-responders that matter with this theory.

I am not sure different antibody types make sense. It might if the target is a very different tissue type. For example, if one tissue recovers fast but another recovers slowly this might make a difference. An example would be if someone had primarily an endothelial target, with rapid repair, versus a neurological target, with slow repair.

Currently I suspect that a single treatment does not eliminate enough antibody producing cells. I have not studied immunology recently enough to go beyond this without rampantly speculating. My knowledge is out of date.

Or alternatively it might be time to rewrite the history books because ME might have a different mechanism.

Or some combination in subsets, etc.

 

[alex3619]

I'm interested in this discussion, of course, but I don't understand 'different antibodies.' Can someone enlighten me please?

The human body has the potential to make millions (if not more) different antibodies, though one individual at one time probably does not have that many options. Each responds to a very different physical target, called an epitope. Its almost random, except that if the immune system has been previously triggered and presents an antibody to the right cell type, then oodles of antibody producing cells of that type are made. That is why we have better resistance to infections we have had before.

Epitopes can be little bits of amino acids or protein or protein combined with something else, from viruses or bacteria, or other pathogens, or even from ourselves if something goes wrong.

There are several different types of antibodies too.

I have tried to avoid technical jargon here, though in part that is because I only just got up and my brain is ppttthhh. There is lots to read in immunology, and its a deep well. It depends on how far you want to go.