Phase III Rituximab Trial - News

I think this was about something called Vh4 heavy chain usage, which came up as opposite. I have not heard more from Jo on this. It may not have proved consistent.

 

Responses in lupus are actually high (remember I introduced rituximab for lupus). The problem with rituximab in lupus is that the initial company sponsored trials excluded anyone with significant disease. The design shot itself in the foot. Rituximab is widely used lupus.

Failure to respond to rituximab does exclude autoimmunity. Scleroderma does not respond much. But this result really takes away the main reason for thinking that the illness is often autoimmune.

 

Yes, areas of research. And that is chiefly hoe F&M saw rituximab, rather than as an instant treatment. Things take time I am afraid.

 

Thanks.

General query, do you think the very original responders ( cancer patients) may actually have responded, but to something different in their chemotherapy ? Or any thoughts on this ?

It's unlikely placebo played a part in those patients I would say.

 

@Jonathan Edwards yet, there seems to be reasonable response to cyclophosphamide if they have moved onto stage B of the CycloME trial, giving it to the more severe patients. Would that not indicate autoimmunity for a subset?

 

Dear Jonathan,

Regarding the Cyclo drug trial by Fluge & Mella, does the results from rituximab have any implications for expectations for the effectiveness of Cyclo in ME?

Regards

 

A true placebo response is only one of several reasons why people get better following treatments. I think it most likely that the original responses do not tell us anything useful about ME. They may have had immune dysfunction associated with lymphoma. The time course of immune dysfunction does not alaways follow the lymphoma in an obvious way so may appear to be a separate illness.

 

The problem with cyclophosphamide is that you cannot blind it because of the side effects. So the cyclo studies alone are not solid evidence.

 

This sort of situation has been playing on my mind.

It's tough for us to take the news that the trial was negative but we have to accept the facts.

What bothers me is that there is going to be an admittedly very small percentage of pwME who have been misdiagnosed and confined to our little wastebasket without extensive testing. The adage "if you hear hoof beats, think horses" is all very well but if you don't actually take a look, you might miss the funny stripy creature disappearing over the horizon.

Do we need to push for more comprehensive investigation in the revised NICE guidelines?

How many times do we hear of someone formerly diagnosed with ME/CFS who finds out that something else was wrong all along and they are now getting treatment? It's tragic for everyone who has an ME/CFS diagnosis but how wasteful to lose years of your life on a misdiagnosis.

 

Isn't PEM exclusive to ME. If you don't get pem, you don't have ME. I don't understand confusion about who has or hasn't the disease. I could diagnose it and I ain't a doctor. No doctor diagnosed me until I diagnosed myself...the crashing was key plus the energy depletion. For people with ME, it is one disease with varying symptoms just like MS patients vary in their symptoms. The notion that ME is an umbrella over a number of different diseases makes no sense to me. I had acute onset, I hardly got struck down with a load of different illnesses at the same time. What we so need to find is what the hell is driving the illness. It always seemed to me that it was immune dysfunction as immune system never settled back after trigger.

 

Without getting into a prolonged discussion about various criteria, yes and no. ME/CFS (CCC) does, CFS/ME (NICE) does, ME (ICC) does, SEID (IOM - clinical only) does, CFS (Fukuda/CDC1994) doesn't, [CFS (Oxford) doesn't but who cares, it's nonsense and for research only].

There must be a lot of people out there diagnosed under Fukuda who don't have PEM.

Post Exertional Malaise and/or Fatigue is also something of a grey area (CCC and NICE).

 

Well if they don't have PEM....they don't have ME. PEM is the crucifying part of ME that restricts our lives so much. I know any researcher with any knowledge of ME would not be using Oxford Criteria, that should be binned long ago.

 

Over your last few posts you seem to be assuming that those with PEM must have ME, this may not be a valid assumption, especially given the confounding influence that some people seem to have been making the reverse assumption, when told they have ME.

PEM is, in one sense, just a series of words, who is to say it means the same to all.

 

Yes but the crucial thing is that even though I was careful to use ME, CFS, ME/CFS and CFS/ME appropriately in this instance, terms are commonly used interchangeably.

 

But could effectiveness be measured pre- and post-treatment using a CPET?

 

Ive spent time on Lupus, MS, thyroid and Lyme boards in an attempt to get to the bottom of my ilness and a lot of people with htose illnesses report something similar to PEM.

In terms of M.E and autoimmunity - of course quite a few of us have positive ANA titres, which have been brushed off by medical professionals. Im also keen to find out if the EDS/MCAS subset (group?) is different and if we actually have a different disease? Having said that my illness meets all criteria of M.E and looks like M.E and feels like M.E, without the severe pain symptoms some others have (i do get pain, its just not a major part of my illness).

 

Or could it be one disease which manifests differently according to people's genetic make up/environmental exposure/initiating infection?

 

Hi @Jenny TipsforME yes I agree with your good point about the delayed response in the Phase II trial,

Invest in ME Research commented on Facebook -

That Facebook post links to their statement: http://www.investinme.org/IIMER-Newslet-1711-03.shtml - extract below -