Mast Cell Activation Syndrome (MCAS) - discussion thread

[Jonathan Edwards]

What would expect to see if MCAS was implicated in decodeME? What in the current decodeME data is suggesting it’s not? Wanting to understand how decodeME could show a positive or negative correlation to the connection

If abnormal mast cell activation was genuinely associated with ME/CFS I think we could expect some sort of clue to turn up in terms of a linked gene involved in a mast cell specific pathway. It might be an IgE receptor gene or tryptase gene. The absence of any gene being found on DecodeME may not exclude mast cell involvement but it is another negative.

 

[Jonathan Edwards]

Naturally it isn't anybodies responsibility to do this.

I think if somone claims that a concept like MCAS has been 'repeatedly validated' or some such, and then can produce nothing to back that up at least has a responsibility to admit they had no basis for the original claim. We are dealing with what is almost certainly medical misinformation used by physicians for personal profit and kudos that affects people's lives - even inducing them to have dangerous neck operations. I think there is a very real responsibility here.

 

[Jonathan Edwards]

I am getting ever more angry about just how much of a mess the ME/CFS world is and how much that is contributed to by people who see themselves as advocates but are constantly bringing up make-believe memes from fringe physicians that ensure that nobody with ME/CFS gets treated seriously anywhere useful. I seem to be the only physician in the UK who sees the problem and wants to do something about it. Having spent another month trying to get over yet another Covid* bout myself I admit to being fairly grumpy.

*Which of course was also the fault of physicain colleagues playing with viruses, not to mention the concept of 'multidisciplinary teams' and the list goes on...

This post has been copied and following posts moved to:
Problems arising for pwME from additional diagnoses of MCAS, hEDS and POTS. Advocacy discussion.

 

[Clio]

Food intolerance/allergy-like symptoms can be a consequence of viral infections (like norovirus, not just covid), but whether it's part of the same thing as ME/CFS or something else remains to be shown (just like with POTS).

I don't think many patients are super dependent on a certain pathophysiology (besides a general urge of "see my illness is biological" which is caused by the prevalence of BPS ideology and thus is understandable to want to be believed).

It would be nice to know more but a temporary imperfect word to talk about it would also be nice (just like ME was imperfect), perhaps something like MCAS/CIS (Chronic Intolerance Syndrome)

I do not really care what the name ends up being but I would like something better than "covid induced cromolym sodium dependence". After my infection I became intolerant to every single food and not just with GI symptoms. And not just food but almost all fragrances as well. It got so bad I almost died of malnourished and was TPN dependent for half a year. Then I randomly tried cromolyn sodium (quite literally because of the MCAS overhyped pseudoscience) and it helped me eat enough food by myself to survive - and my then partner even helped me to single-blind test it, since cromolyn has no taste nor obvious effects on me. It was clear from the results that cromolyn sodium helps me (results for anyone else may vary).

 

[V.R.T.]

I have allergic type symptoms too since becoming severe/getting covid, and hands going bright red after I eat high histamine foods like curry. I decided to take it seriously after two occasions where I ate a heavily fermented food (kimchi on one occasion and yellow bean paste on another) and had intense symptoms.

After I was put on a low histamine diet a year ago I noticed a lot of symptoms decreased significantly, but the diet is utterly miserable and hard for my carers to stick to. I have tried H1 antihistamines twice, ceterzine made my brain fog worse and a recent trial of fexofenadine coincided with a period of frightening crashes. I have a backlog of famotidine I keep meaning to try.

I really want to reintroduce normal foods but every time I try I crash and feel unwell. This may be correlation not causation though, as it is miserably easy for me to trigger PEM.

I know someone with ME/LC who suffers terribly with MCAS/allergies, and have heard a lot of similar stories in support groups.

I do sometimes think the MCAS clincal category is too broad (Afrin claims it can cause everything under the sun), but imo there is definitely something happening here that sometimes accompanies ME/CFS and worsens with PEM.

Attached two more extreme examples of said swelling and redness in hands.

Edit: Since covid/becoming severe I also find that black pepper, which I used to love, now burns my mouth, and if a crumb of it stays on my tongue it almost has a numbing effect. so i had to stop eating it.

For the record the other week I ate a high histamine meal that wasn't spicy and the same thing happened.

But I've also had it happen a few times recently when Ive stuck to diet but am in PEM.

 

[Jonathan Edwards]

I don't think many patients are super dependent on a certain pathophysiology (besides a general urge of "see my illness is biological" which is caused by the prevalence of BPS ideology and thus is understandable to want to be believed).

It would be nice to know more but a temporary imperfect word to talk about it would also be nice (just like ME was imperfect), perhaps something like MCAS/CIS (Chronic Intolerance Syndrome)

The problem is that that very desire to have the illness seen as biological plays right into the hands of the BPS crowd. To the extent that EDS has now been adopted by gastroenterologists as an especially 'functional' disorder - in other words entirely imaginary but we must say it is real, or whatever double think they prefer.

MCAS may sound 'biological' but to a physician it just sounds pseudoscience. And people with ME/CFS are deliberately being excluded from a physician led service because they keep insisting they have these pseudo-diseases. As soon as a mouth is opened and MCAS and EDS are mentioned you are in the functional pigeonhole where feeding support is not good management.

If we think someone has food intolerance we can just call it food intolerance. Adding a special syndrome is where the make-believe comes in. And if it is part of ME/CFS it doesn't need another syndrome because it is already part of one with a meaningful definition. It is vanishingly unlikely that there are so many people with four unrelated syndromes together (MCAS/POTS/EDS/ME/CFS) when as far as we know there is no biological or epidemiological evidence for a link. Yet so many people have been told they have all these diagnoses.

I may be misguided but it seems that in the UK it is me that has the job of trying to persuade physicians to begin taking ME/CFS seriously again. I have managed to get lab researchers interested - that was remarkably easy. There was no hesitation. But persuading physicians is going to need a very persistent and well organised campaign. As long as advocacy groups keep talking in pseudo-biology terms I think I am probably scuppered.

ME/CFS is a real biological problem.
Food intolerance is a real problem. It probably involves mast cells somewhere along the line but then pretty much any tissue reaction does so calling it a mast cell problem just muddles things.
EDS is a real biological problem but hEDS is not - it has no useful meaning.

The patient community needs to dig itself out of this hole if we are to get any clinical service. To some degree it has, but judging by what I have heard in terms of responses to our Fact Sheet 3 there are still a lot of people out there who cannot see the wood for the trees.

This posts has been copied to:
Problems arising for pwME from additional diagnoses of MCAS, hEDS and POTS. Advocacy discussion.

 

[Jonathan Edwards]

I know someone with ME/LC who suffers terribly with MCAS/allergies, and have heard a lot of similar stories in support groups.

But if you look at the stories carefully it is all a muddle. Reacting to histamine in food is not the same as mast cells producing histamine. Curry produces vasoactive changes because of things like capsaicin. Normal guts react to curry, often with watering eyes and sweating as well.

And the only studies we have that looked at this without coming from a clinic already committed to believing in a link seem to show no particular relation with allergy, which is common enough anyway.

A relation to mast cell events could be tested very easily with double blind trials of inhibitors and other such things but these are never done. Personal observations are no good to the community. There is always gross reporting bias, particularly on social media.

 

[Jonathan Edwards]

there are a huge amount of pwME and LC with new onset allergy type symptoms triggered by a range of things.

But there are no data. Why not? Allergy-type symptoms can cover a vast range of things. Yes mast cells will be in there somewhere in all of them but that doesn't make them even allergy (and MCAS is supposed not be allergy just to confuse things further).

When I started learning about ME/CFS I accepted the common view that it was linked to allergy but everything I have seen over the ten years now indicates that there are no useful positive data and some quite reasonable negative data. Allergies tend to be very specific - nuts seem to be the best documented. A lot of other intolerances like milk, gluten, seafood are other things but can also be very specific. The broad spectrum intolerance commonly reported by people with ME/CFS does not sound like allergy or a primary mast cell thing at all to me. It sounds much more like part of a more general intolerance of stimuli that might have a basis in sensory neurons (where that CA10 gene sits).

 

[V.R.T.]

The broad spectrum intolerance commonly reported by people with ME/CFS does not sound like allergy or a primary mast cell thing at all to me. It sounds much more like part of a more general intolerance of stimuli that might have a basis in sensory neurons (where that CA10 gene sits).

That's an interesting idea.

 

[Nightsong]

I believe Afrin even claims it causes autism.

Afrin claims it is a likely cause of spontaneous human combustion:



The screenshots are from ch29 of Afrin's 2016 book "Never Bet Against Occam".

 

[Jonathan Edwards]

Afrin claims it causes spontaneous human combustion:

That is a truly remarkable find.

I keep thinking that I had given up giving a bit of the benefit of the doubt.
But I had not expected to see something quite as science fiction as that.
Even the writers of Death in Paradise could not think up something as implausible.
The invocation of mast cells is without credible basis.
It is worth a read. This is what patients are putting their faith in it seems.

 

[Trish]

Moderator note

Moderators have reviewed the recent discussion on this thread. We have removed comments that focused more on other posters than on the thread subject, and replies to those comments.

Where there are different views, discussion is more productive, and easier for others to follow and join in, if members focus on discussing the subject and giving reasons and evidence for their opinions.

We have copied or moved some posts to a new thread:
Problems arising for pwME from additional diagnoses of MCAS, hEDS and POTS. Advocacy discussion.

 

[Trish]

I thought it was time I tried to find out more about MCAS for myself, as this discussion is so active at present and clearly raising strong reactions.

Since I'm in the UK, I wanted to find out what is being advised for the NHS.

As far as I can see there is no NICE guideline for MCAS, but I did find this article in
BMJ best practice:

https://bestpractice.bmj.com/topics/en-gb/3000310#:~:text=21 Jun 2023-,Summary,MCAS may require cytoreductive therapy.

Mast Cell Activation Syndrome

Summary​

Mast cell activation syndrome (MCAS) is a rare condition that is characterised by recurrent sudden-onset episodes of severe systemic symptoms associated with the release of mast cell mediators. In many cases the recurrent episodes present as anaphylaxis.

Acute episodes of MCAS-associated anaphylaxis must be managed according to the usual emergency protocol, with immediate administration of intramuscular adrenaline (epinephrine) alongside an ABCDE approach to assess the need for supplemental oxygen, intravenous fluids, and airway management.

A diagnosis of MCAS is confirmed by evidence of a significant rise in a mast cell marker (e.g., serum tryptase) during acute episodes and a positive clinical response to a medication that targets a mast cell mediator. It is important to then evaluate the MCAS sub-type: primary (clonal), secondary (usually associated with IgE-dependent allergy), or idiopathic.

Treatment involves trigger identification and avoidance together with a stepwise approach to long-term pharmacotherapy, starting with an antihistamine (H1 antagonist) and H2 antagonist. Add-on options include a leukotriene receptor antagonist, sodium cromoglicate, and omalizumab. Patients with refractory primary (clonal) MCAS may require cytoreductive therapy. Lifelong immunotherapy is recommended for individuals with sensitivity to Hymenoptera venom.

Definition​

MCAS is a rare condition defined by severe, episodic reactions to mast cell-derived mediators.[1] For a diagnosis of MCAS to be confirmed:[2][3]

• There must be recurrent, acute episodes of symptoms/signs associated with secreted mast cell mediators that affect two or more organ systems at the same time
• A transient rise in a mast cell mediator (e.g., tryptase) must be confirmed during these acute episodes, and
• The symptoms must respond to drugs that either target released mast cell mediators or suppress mast cell activation (e.g., antihistamine, H2 antagonist, leukotriene receptor antagonist, sodium cromoglicate).

In most cases, MCAS presents with recurrent episodes of anaphylaxis.[4]

 

[Trish]

Having read the above summary of the article, I am curious to understand whether severe reactions usually presenting as anaphlaxis are more common in people with ME/CFS than in the general community.

Or is it some other version of MCAS that is being diagnosed. Can someone point me to the description of MCAS that Afrin and others are talking about?