Phase III Rituximab Trial - News

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?

 

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.

 

No, PEM occurs in some other immune diseases too. So it isn't "exclusive" to ME.

 

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

 

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.

 

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

 

Yeah, we really need to have that 'What is depression' discussion sometime but I can't find a suitable place for it. Maybe we should just put it in the members only ME/CFS forum.

 

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?)

 

+1

i hope they pursue this, their patients that responded leading them in this direction obviously improved, your improving, something is responsible for that.

I love it. However they would spin it to look even worse because they have already decided it can only be psychosomatic

 

I started the ball rolling here: https://www.s4me.info/index.php?thr...imab-for-treatment-resistant-depression.1027/

And there was also some discussion here: https://www.s4me.info/index.php?thr...ot-work-in-patients-with-chronic-illness.819/

 

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).

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.

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.

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, 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.

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.

 

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.

 

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)

 

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.

 

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.

 

Ohh, I see! Hehe! Can someone correct that in the original post? I almost forwarded that statement to about a dozen people.

 

And here I am just eating my lunchtime sandwich, with egg mayonnaise oozing out of it!

 

Does it exclude b cell involvement? Or could they still be part of this.

 

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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