Phase III Rituximab Trial - News

arewenearlythereyet said:
So there appears to be a difference in how I respond to something new vs how well I respond to antigens my immune system already recognises. Again this might be nothing to do with the immune system itself, but more about metabolic energy deficit or even poor circulation/poor wound healing. It just feels immune related in some way. (Feelings are not very scientific...so I do tell myself off periodically). Sorry if that rambled a bit.
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But poor wound healing doesn't mean a poor immune response at the injury site. If that were the case you'd have an infected wound, not one that just took ages to heal.

Or am I reading something wrong?
 
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Woolie said:
But poor wound healing doesn't mean a poor immune response at the injury site. If that were teh case you'd have an nfeccted wound, not one that just took ages to heal.

Or am I reading something wrong?
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I take the oozing yellow stuff at the wound site to be an infection ( sorry). It could be chicken and egg though slow wound healing increases the liklihood of infection etc.
 
I just have slow healing, still got holes and cuts on my feet from about 4 months ago which haven't completely healed yet - one from a dropped drill and a series of 4 small holes on my other foot from my cat using it as a springboard, which happened on the same day, bad foot day lol. They aren't open or anything, but can still be clearly seen.

Always have had slow wound healing, but it's definitely getting slower, even with my rate I would have expected the claw ones to be completely healed within a month, but nope, still there ;)

The trick is not to worry about it until it the stink drives the maggots away ;)
 
Wonko said:
PEM is, in one sense, just a series of words, who is to say it means the same to all.
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Yes, I would like to see some evidence to show that using PEM actually excludes certain individuals from the pool - in a meaningful way.

We have always been eager to accuse those meeting only Oxford-style CFS criteria of having some other disease (probably depression). I now think of it the other way around - many of those with depression probably have something that overlaps with ME.
 
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I'm fairly sure, although not certain, that I haven't accused those only meeting .......

I don't actually care what I have, I just want it to stop.

To the limits of my knowledge, and apparently (although it's not saying much), my doctor and a couple of consultants, I have ME.

But if someone told me I have Random Nasty Symptom Syndrome (RNSS), it's caused by eating all your vegetables when young, as well as burnt toast, here's a pill, you'll be fine tomorrow - then as long as I was, I 'd be less grumpy, for a while.

I don't care what anyone calls it, what causes it etc. - I just want it fixed ;)
 
Justy said:
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).
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I wonder if some clear groups are starting to form here?

autoimmunity
EDS/MCAS
autoinflammation (at least one case, me)

Others are endocrine, mitochondrial (but maybe not exacerbated by exertion?)
 
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Gingergrrl said:
Alvin, I am still thinking it is the people with auto-antibodies who are the potential responders but I have always wondered what is the overlap between autoimmunity and those with MCAS and/or toxic mold exposure?
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+1
Gingergrrl said:
Maybe they did not find the answer for ME/CFS, but they might have found an answer for something, even if we don't know what it is yet
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i hope they pursue this, their patients that responded leading them in this direction obviously improved, your improving, something is responsible for that.

Joh said:
On the bright side, this guy made me laugh:
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I love it. However they would spin it to look even worse because they have already decided it can only be psychosomatic
 
Jenny TipsforME said:
Oh that’s actually a lot more positive than I had interpreted from the news. I’d consider being able to treat a third of pwme (or people previously misdiagnosed) a substantial advance.
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That's what I keep thinking, too, and am not sure (yet) why 30% response rate is so bad? (Unless the 30% was from the placebo group).

Jenny TipsforME said:
I can’t think of what I’m thinking of right now, but isn’t there some evidence already that the POTS subgroup are the likely rituximab responders?
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My understanding is that (even though still very little is known about POTS by the average doctor), there are several sub-types of POTS and one of them is "Autoimmune POTS" and I would assume that this is the sub-type that could be potential responders to Rituximab and that I am in this sub-type.

Jonathan Edwards said:
Failure to respond to rituximab does exclude autoimmunity.
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I am not sure if I understand this? Aren't there proven autoimmune diseases, like RA or Lupus, in which Rituximab is tried but only a certain percentage of those patients are responders? If someone with RA did not respond to Rituximab, they would still have RA and it would not exclude autoimmunity vs. that they need a different drug.

Scarecrow said:
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.
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I agree on all counts. When I first got sick in 2013, I had "post mono fatigue" (real fatigue following real mono at that time) plus very high EBV IgM+ antibodies, and symptoms like nausea, tachycardia, very low BP, etc, that were vague and unexplained and I got a "CFS" diagnosis which made sense to me at that time. It was only as my symptoms greatly morphed in the following years, and I fought to receive very thorough testing, that we figured out that something else was likely going on. So I think many illnesses (Hashimoto's, POTS, MCAS, EDS, Lyme, Autoimmune Diseases, etc) may start out very similar to "CFS" but if followed closely, the symptoms and test results become more specific. I hope that made sense!

Wonko said:
I don't care what anyone calls it, what causes it etc. - I just want it fixed ;)
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@Wonko, I cannot tell you how much I have struggled with this issue and waver between wanting to know the EXACT name and cause of my diagnosis versus not caring about those things at all as long as something is making me better like now.

Alvin said:
i hope they pursue this, their patients that responded leading them in this direction obviously improved, your improving, something is responsible for that.
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I agree that something is responsible and even if only 15-30 patients (I am making up the numbers) had a long-term remission, I would want to study the hell out of that group to figure out why.
 
Gingergrrl said:
I agree on all counts. When I first got sick in 2013, I had "post mono fatigue" (real fatigue following real mono at that time) plus very high EBV IgM+ antibodies, and symptoms like nausea, tachycardia, very low BP, etc, that were vague and unexplained and I got a "CFS" diagnosis which made sense to me at that time. It was only as my symptoms greatly morphed in the following years, and I fought to receive very thorough testing, that we figured out that something else was likely going on. So I think many illnesses (Hashimoto's, POTS, MCAS, EDS, Lyme, Autoimmune Diseases, etc) may start out very similar to "CFS" but if followed closely, the symptoms and test results become more specific. I hope that made sense!
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That made an incredible amount of sense to me. And my pathway was similar - more detectable abnormalities in my blood as things progressed.

I think the idea of ME/CFS as having multiple causes is seriously back on the table.
 
Gingergrrl said:
That's what I keep thinking, too, and am not sure (yet) why 30% response rate is so bad? (Unless the 30% was from the placebo group).
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Apparently there were noe statistically significant difference between those who received Rituximab and the placebo-group. (But I've only read bits and pieces here and there and no proper summarisations (yet) of Mella's lecture)
 
Scarecrow said:
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).
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There are a few other conditions that are known to cause PEM. I believe Primary Biliary Cirrhosis is one them.

I 100% have PEM and meet all the "respected" criteria for ME/CFS and was diagnosed by Dr. Chheda earlier this year. However doctors now suspect I could have a rare autoimmune disease called "Relapsing Polychondritis" (RP). If I do have RP then only time will tell if my PEM improves once I am put on medication for the RP. If the PEM does improve or go away then perhaps I never had ME/CFS and the RP was the cause of my PEM? The worst case scenario would be that I have RP and ME/CFS. (Btw...there is no biomarker for Relapsing Polychondritis so that coupled with the fact it is very rare results in delay of diagnosis)

I was also just diagnosed with a rare genetic partial Complement C3 deficiency (my C3 is only 30% of normal) and partial C3 deficiency can in some instances cause a "Lupus-like illness". If I am not diagnosed with RP then doctors want me to take Plaquenil to see if my symptoms improve. If that ends up being what happens than it will also be interesting to see what happens with my PEM.
 
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Gingergrrl said:
I am not sure if I understand this? Aren't there proven autoimmune diseases, like RA or Lupus, in which Rituximab is tried but only a certain percentage of those patients are responders? If someone with RA did not respond to Rituximab, they would still have RA and it would not exclude autoimmunity vs. that they need a different dru
...

I agree that something is responsible and even if only 15-30 patients (I am making up the numbers) had a long-term remission, I would want to study the hell out of that group to figure out why.
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Sorry Ggl, there was a 'not' missing from that sentence. I am using an iPad and it plays tricks.

Something is responsible for people getting better equally often with placebo, so it was not the rituximab.
 
arewenearlythereyet said:
I also think that PEM means different things to different people and that this probably varies from person to person in terms of how it manifests itself.
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I'm sure you're right, and I also imagine it will scale in some way according the severity of a person's ME. So just because someone with mild ME does not experience PEM the same way someone with severe ME does, would not automatically mean they do not get PEM. I'm certain my wife experiences PEM, commensurate with her ME severity, which I think is mild/moderate.

Using the battery analogy. A battery stores chemical energy that can be rapidly converted into electrical energy, immediately it is needed; if rechargeable then its chemical energy can be replenished from externally provided energy. As I understand it (very sketchily!), the ATP cycle manages the storage of chemical energy within our mitochondria, ready for rapid conversion to usable energy immediately the host cells need it; the lost energy being replenished from energy external to the cells. The neat bit being the stored energy is in a form it can be converted rapidly on demand as our bodies need it ... until it runs out.

Observing my wife, I think the battery analogy works, but needs a bit of improvement. Yes, it is as if the battery only gets partly charged, so she has much less stored energy in reserve than if she was healthy; I'd guess 50% at best in my wife's case, but often lower. But I also believe it is as if the battery (and/or maybe its charger) is damaged. So the battery not only fails to reach full charge, but crucially, takes much longer to recharge, even to its lower charge level. This much extended recharge time, and the notion of a damaged recharging mechanism, is what to me characterises her PEM. Not only does she have negligible energy available during this time, but feels dreadful during it also.

So a healthy (albeit possibly sedentary) person exercises, and reduces their stored energy to a still not that low a level, then takes a normal time for their energy to recharge to normal levels. But it is as if someone with ME exercises, reducing their energy to complete depletion level, and to compound things recharges much more slowly to a lower charge level.

Needless to say I have to highlight that these are just my idle ponderings; I have no medical expertise at all.
 
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