Poll - Have you been tested for Sjogren's Syndrome?

[Pibee]

Sorry but I have to laugh at this, so everything is unscientific, adding SFN to the SjD criteria, the diagnosis of SFN too, everything is unscientific except the strict arbitrary verbal definition of what MECFS is, worded in English language. (with the additional problems of translating it to any other language). That same word definition /salad is a thing that even MECFS patients among themselves have hard time agreeing on.
But S4ME claims that IS science but everything else isn't.

Just like almost everyone else who commented in this thread, it looks like you have no true interest to get informed what SjD is, instead you pasted some AI summary and nonsense about Ro antibodies even tho theyre not in the criteria for SjD diagnosis even and it is well documented that 60% patients are Ro negative and they found 30 new antibodies in SjD in seronegative group (by they I mean EULAR not retired rhuematologists who have a hobby of posting about it online, I mean the teams currently focusing on research in SjD).

Since you don't accept biopsy for SFN; we can apply strict scientific criteria for SFN (the one you use for the ME diagnosis) and define it through symptoms: burning or numbness or dizziness or pain etc (add 100), and then we can act like it's a real disease ? I guess this would be acceptable to you.


Also , it is concerning that you dont even accept the formal position of EULAR -European Alliance of Associations for Rheumatology, AND of American Academy of Neurology (AAN) who 1) agree on what SFN is and how it is diagnoed 2) clearly list SFN as a possible complication of SjD. You think you know better than them what SjD is or you're just repeating what someone else said in this thread before and trusting that post over formal organization?

intermediate connections to POT

The connection of ME with anything else has to be via intermediate variable becasue ME cant be defined, measured etc. it exists only as a group of words that anyone can repeat and nobody can actually disprove I don't or I do have ME.
So not sure what do you expect, a real science related to ME? Have you not checked any of the neurology conferences in the last 10 or 20 years? how many have actually addressed MECFS? does that mean it's not a neurological condition ? because you expect some big data on ME and SjD.
ME is not recognized, officially yes but in practice it is not and there is absolute no science about it in any neuro research circles.


For myself, I got SFN and MECFS, and POTS in 2005, I tested for years, negative on ANA, Ro, La. I tested since 2022 positive for Ro, La. Also not always. it is a disease of eldery, the way they recorded it and when I am old, if I don't get LLPC treatment, I'll be increasingly positive. But it still took 20 yrs . I match all other criteria and have bad dryness, with onset in 2019, so 14 yrs delay. And 14yrs untreated, if I was treated with LLPC meds it would prob be postponed or never happen.
The description of SjD came from ophtalmologist who first observed it, it shows just one disease manifestation

 

[EndME]

Sorry but I have to laugh at this, so everything is unscientific, adding SFN to the SjD criteria, the diagnosis of SFN too, everything is unscientific except the strict arbitrary verbal definition of what MECFS is, worded in English language. (with the additional problems of translating it to any other language). That same word definition /salad is a thing that even MECFS patients among themselves have hard time agreeing on.
But S4ME claims that IS science but everything else isn't.

Just like almost everyone else who commented in this thread, it looks like you have no true interest to get informed what SjD is, instead you pasted some AI summary and nonsense about Ro antibodies even tho theyre not in the criteria for SjD diagnosis even and it is well documented that 60% patients are Ro negative and they found 30 new antibodies in SjD in seronegative group (by they I mean EULAR not retired rhuematologists who have a hobby of posting about it online, I mean the teams currently focusing on research in SjD).

IF we apply strict scientific criteria for SFN from the ME diagnosis can we define it through symptoms: burning or numbness or dizziness or pain etc (add 100), and then we can act like it's a real disease ? I guess this would be acceptable to you, because the next level of biopsies etc isn't lol


Also , it is concerning that you dont even accept the formal position of EULAR -European Alliance of Associations for Rheumatology, AND of American Academy of Neurology (AAN) who 1) agree on what SFN is and how it is diagnoed 2) clearly list SFN as a possible complication of SjD. You think you know better than them what SjD is or you're just repeating what someone else said in this thread before and trusting that post over formal organization?





The connection of ME with anything else has to be via intermediate variable becasue ME cant be defined, measured etc. it exists only as a group of words that anyone can repeat and nobody can actually disprove I don't or I do have ME.
So not sure what do you expect, a real science related to ME? Have you not checked any of the neurology conferences in the last 10 or 20 years? how many have actually addressed MECFS? does that mean it's not a neurological condition ? because you expect some big data on ME and SjD.
ME is not recognized, officially yes but in practice it is not and there is absolute no science about it in any neuro research circles.


For myself, I got SFN and MECFS, and POTS in 2005, I tested for years, negative on ANA, Ro, La. I tested since 2022 positive for Ro, La. Also not always. it is a disease of eldery, the way they recorded it and when I am old, if I don't get LLPC treatment, I'll be increasingly positive. But it still took 20 yrs . I match all other criteria and have bad dryness, with onset in 2019, so 14 yrs delay. And 14yrs untreated, if I was treated with LLPC meds it would prob be postponed or never happen.
The description of SjD came from ophtalmologist who first observed it, it shows just one disease manifestation

I would strongly recommend to actually read what others write, before laughing and making accusations.

You indicated a connection between ME/CFS and Sjörgens based on SFN prevalence. There is however no good research to indicate that SFN is more prevalent in ME/CFS than in the general popoluation as you will not find studies with controls and SFN assessments are known for their false positives as research has repeatedly shown. This is documented in studies! Please provide one serious study of SFN in ME/CFS with HCs that would show the opposite. The negative results have already been commented on in that the prevalence is not higher in Fibromyalgia. I would recommend looking at the Fibromyalgia study. If you have good SFN studies for Sjögrens feel free to post them. It would be nice to see the research quality in other fields not being as poor as it is in ME/CFS and see if some of those methods can translated to ME/CFS.

Your comment on antibodies pretty much misses the point. If 60% of Sjögrens people are Ro negative that means 40% are positive. That is not the case for ME/CFS. For ME/CFS there isn't evidence that the rate is even higher than in in healthy people. That's what people are telling you, but you seem to be missing this.

I'm guessing you would also prefer to not comment on the genetic data if it doesn't fit your beliefs or can a meaningful conversation be had there, how would you explain a lack of obvious signal correlation if there is supposedly a big overlap?

I tried to engage in a conversation, but it seems you have no such interests and instead prefer making unjustified claims about AI comments. I will not comment further and am sceptical about whether a conversation can even be had. I would strongly recommend looking at @Evergreen 's post.

 

[Pibee]

Nobody is saying everyone with MECFS has SjD, thus, of course not 40% of ME pts will have Ro, and also, among neurological SjD it is higher prevalence of seronegative, as well as among younger SjD which is MECFS / SFN group anyway.

From what I see, some people don't want to know the truth and don't want to truly be helped. I am not new in this, I was on these fourms 8 years ago too. I know how it is before I knew I had SjD and before I heard of SFN and POTS and when I thought I have only MECFS, and I know how it is to be gaslighted and I know how would I likely react if someone compares me to rheumatic diseases. I'd think, it is a trivial comparison because my level of fatigue (and sleep disorder, and cognitive impairment) absolutely can not be compared to RA or SLE as these patients are functional. I have not known of this type of SjD. My family members have SLE and SjD and they're funcitonal without neurological disabilities.
So i understand the resistance.


You were arguign against including SFN in SjD criteria , this is from very old American Associatin of Neurologist website: About 50% of the people with neuropathy had diabetes, compared to 22% of those without neuropathy. The people with neuropathy were also more likely to have insomnia, at 86% compared to 54% for those without neuropathy. They were also more likely to have heart attacks, at 46% compared to 27%. “Based on these findings, people with small fiber neuropathy should be screened for heart problems and their blood glucose should be monitored for signs of diabetes,” Klein said. The people with neuropathy were also more likely to take opioids for pain. For 67 of the people with neuropathy, no cause could be determined, called idiopathic neuropathy. For 14 people, the neuropathy was caused by diabetes. Other causes included Sjögren syndrome and lupus. A total of 36% of the people developed large fiber neuropathy during the study, an average of five years after they developed the small fiber version.

Seems like both, neurologist and rheumatologist societies are very clear that SjD can cause SFN, CIDP, .. the only place this is refuted is S4ME. It i sconcerning


Talking about no data on the connection of SFN and ME makes little sense cos it is underfunded disease, I believe oyu there might not be hard evidence but that is not proving anything, there is no funds , science, for ME in general. Except OMF which is an organization based on the case of Whitney Dafoe and if he doesnt have SFN they will show very little interest in it (which they have).

This is all very harmful for the patients.

P.S. this Poll is missing the most common group.: I have dry eyes or dry mouth and I tested negative.

I just checket the link you posted (see the discussion here: https://www.s4me.info/threads/long-...limitation-2025-jothi-et-al.45990/post-638833), , wow, so you're linking discussion on FMS? that is not MECFS. This sounds like the argument you were going against when I mentioned SFN or POTS as an itermediate variables for connection with ME and SjD.

why is this actually wrong data: One-third of patients with ME/CFS are definitively diagnosed with SFN according to results of protein gene product 9.5-immunolabeled lower-leg epidermal biopsy,7 a prevalence similar to that observed in fibromyalgia and postural orthostatic tachycardia syndrome (POTS).37 link

 

[EndME]

Seems like both, neurologist and rheumatologist societies are very clear that SjD can cause SFN, CIDP, .. the only place this is refuted is S4ME. It i sconcerning

Nothing is concerning. I never claimed anything about the role of SFN in SjD nor did I ever claim it should not be included in SjD. It is hard to have a discussion when the opposite person prefers to invent statements about what other people are supposed to have said instead of actually having a discussion. I made statements about SFN and SFN within ME/CFS and was asking whether there is good research in SjD for SFN that could show those in ME/CFS how things are done to put an end to the beliefs of some with negative or positive results.

Talking about no data on the connection of SFN and ME makes little sense cos it is underfunded disease, I believe oyu there might not be hard evidence but that is not proving anything, there is no funds , science, for ME in general.

Maybe, but it isn't very fruitful to have purely speculative discussions without any data useful either. And as you will be very aware every single neurologist and rheumatologist asscociation, which you cite which much endeavour, prefer to not draw these connections that haven't been witnessed by anybody.

But it seems this whole discussion seems to be about neglecting data anyways. Luckily we have different ways forward as well, using genetic data for example. Some will continue to neglect that and instead prefer their belief to actual data. If there are people that are serious about Sjögrens and ME/CFS connections it will be interesting to see how they can explain that lack of genetic connection as well as the missing other connections.

PS: The linked post is to illustrate that talking about SFN prevalance in ME/CFS without controls is meaningless when a test is known for false positive and low reproducibility rates and high heterogenetiy amonst the different test prodecures. I thought my post made that clear. Perhaps it was not.

 

[Trish]

@Pibee, I don’t think it's helpful to discussion to say that there is an S4ME opinion on this or any topic. Forum threads are discussions and people with different levels of knowledge and views on evidence are welcome to join in. Nor is helpful to accuse forum members of not wanting to be helped. Maybe stick to discussing the topic.

 

[Pibee]

I was only expressing my opinion, not trying to be useful with every word I say (although I was trying to be useful with most of them)

 

[EndME]

why is this actually wrong data: One-third of patients with ME/CFS are definitively diagnosed with SFN according to results of protein gene product 9.5-immunolabeled lower-leg epidermal biopsy,7 a prevalence similar to that observed in fibromyalgia and postural orthostatic tachycardia syndrome (POTS).37 link

These are type of results why one needs high quality SFN research in ME/CFS not this low quality research. A high quality study would have the skin biopsy analysis blinded to the participant group, since counting intraepidermal fibers involves a large amount of subjective judgment. This is all well-documented in the literature including that IEFND results can be driven by the observer in setups as the one used in the ME/CFS study (see for instance https://pmc.ncbi.nlm.nih.gov/articles/PMC2672925).

Additionally, the ME/CFS paper’s healthy controls (HCs) all had normal IENFDs, which is statistically improbable. In well-controlled reference studies that is not the case, see the literature.

I strongly suspect this is the kind of stuff why SFN connections to ME/CFS are not taken seriously, including by any of the associations you've been citing. We have to get serious. Not just cite whatever fits our beliefs.

 

[Pibee]

I cited only OMF, and they dont acknowledge SFN only because Whitney doesn't have it, how is that relevant. Anyway, as I said if ME can be diagnosed from a set of symptoms, SFN should be too (we're just grateful it doesnt have to be), but it can, and certainly over 50% of MECFS patients complain of symptoms that fit SFN. Burning tingling etc. And what about the study with severe ME patients having OI from just 10% tilt, of course there could be other causes of OI, but the SFN is certainly the most recognized cause.

The study you posted actually doesnt show drastic interobserver variability.

I'd call this acceptable, r=0,92? what do you expect? it is a visual method like many other in diagnostics.

 

[EndME]

It isn't because I was never talking about the OMF. You've been talking about other societies, neurologists and rheumatologists. That was the reference (with many of their recommendations not being fulfilled in the ME/CFS study you cited.)

 

[Pibee]

It isn't because I was never talking about the OMF. You've been talking about other societies, neurologists and rheumatologists. That was the reference (with many of their recommendations not being fulfilled in the ME/CFS study you cited.)

Those societies acknowledge IENFD and biopsy as a valid method to diagnose SFN. That was my argument and not sure what your counter-argument is. No testing method is perfect. You can test SLE in 2 labs and you get differences. EMG can vary a lot based on who is performing it too, they will still keep using it.

 

[Jonathan Edwards]

Those societies acknowledge IENFD and biopsy as a valid method to diagnose SFN. That was my argument and not sure what your counter-argument is. No testing method is perfect. You can test SLE in 2 labs and you get differences. EMG can vary a lot based on who is performing it too, they will still keep using it.

The counterargument is that the medical world is rife with unreliable opinions, especially when it comes to societies dealing with slightly uncertain diagnostic groupings, like Sjogren's and ME/CFS of course. One of the things I have learnt being on these forums is just how accepting people are of medical pronouncements and dogma.

Everyone nows that you get different titres for ANA from different labs but the difference between a lupus and a healthy population is cast iron reproducible. EMG can be done badly and there is some operator influence but again everyone takes that into account and if a median nerve potential is undetectable (like mine), but the level of unreliability is not comparable if what I hear and read is anything to go by. Skin biopsy for SFN is the sort of test that labs can set up and produce systematically misleading reports.

I may be being oversceptical but in this area of ill-defined chronic illness I am constantly finding that if anything I have not been sceptical enough - even last week.

 

[Verity]

Nobody is saying everyone with MECFS has SjD, thus, of course not 40% of ME pts will have Ro, and also, among neurological SjD it is higher prevalence of seronegative, as well as among younger SjD which is MECFS / SFN group anyway.

We know you’re not saying that. The issue is that if there’s even a significant subset of ME patients who have Sjogren’s, the rate of relevant antibodies should still be higher in ME/CFS than in the general population—unless you’re trying to say that “neurosjogren’s” and young Sjogren’s patients have the same levels of antibodies as the general population. Even then, there are plenty of older ME patients.

As far as we know, it’s not elevated at all. And that’s a big problem for the claim that Sjogren’s has something to do with ME.

 

[Binkie4]

I voted " no - I have never been tested".

However, when I was 29, I had a positive Shirmer's test at an eye hospital and was prescribed artificial tears which I still use at 78. My dentist says I have a dry mouth. Some years later I had anti SSB antibodies diagnosed and a positive ANA.
I don't have a diagnosis of Sjogren's syndrome. My rheumatologist wrote it in my notes with a question mark "just as a reminder. " So I may well have Sjogren's but none of my doctors have thought it necessary to test specifically. Would it have made any difference to anything?

 

[Pibee]

We know you’re not saying that. The issue is that if there’s even a significant subset of ME patients who have Sjogren’s, the rate of relevant antibodies should still be higher in ME/CFS than in the general population—unless you’re trying to say that “neurosjogren’s” and young Sjogren’s patients have the same levels of antibodies as the general population. Even then, there are plenty of older ME patients.

As far as we know, it’s not elevated at all. And that’s a big problem for the claim that Sjogren’s has something to do with ME.

The rate is probably higher indeed. Any study proving the opposite? They never took big enough number of ME patients to even demonstrate this.
It is a strange observation without providing numbers. You need 1000 MECFS blood samples for SSA - Both Ro60 and Ro52 to demonstrate that perhaps 20% of people have SjD out of which 20% would maybe score positive (because seronegative group is significant in younger and neurological), which is 40 patients..

Because you don't have the data for 1000 patients but 100 (maybe?) you can find 4 testing for Sjogrens positive

I can help with this I know a few SSA positive ones by name I MEAN NICKNAME on Twitter or this Forum or Discord.

So thanks for asking.

Just remembered that girl on Twitter who is 10-20 yrs bedbound with MECFS but then randomly checked dsDNA after decades, it is through the roof, she has a treatable condition and MECFS label would continue to direct her in the wrong direction.


We should note that most studies and SjD data is on patients 50-70 years old on average and their immunological profile look significantly different than average MECFS age. These women tend to have SjD going 40-50 yrs back but until it progressed to be diagnosable it took very long and their antibodies kept going up over the decades. Most people 60+ with SjD have way worse typical SjD parameters than me - higher Ro, La, ANA higher total IgG, simply because they're older.
However they are often more functional because no POTS and they tend to have NOH which is usually low symptoms, sometimes without complaints.
It is considered slow progressing disease.

So you shouldn't take studies done on 60 year old women and try to fit average MECFS (30s?) into that too. (like Scheibenbogen did)
We need a reference criteria for young onset.
And of course, I'm not speaking about % of MECFS who do have SjD; dysautonomia is more common certainly but people often fall on the spectrum between dysautonomia and SjD and it is often blurry simply because SSA marker is insufficient for this version of SjD and this age group.

The criteria for saliva for example is not corrected for the agr group - young men in 30s have even up to 5x more Saliva than men in 60s so a young man with SjD might score normal on saliva when he is barely able to spit (happened to my friend and to me as a female, I couldn't believe they said normal saliva I almost fell off chair because it melted all my enamel and I have constant pains in salivary glands , swelling and couldn't talk because not enough saliva to talk os swallow food, the reference range can be ridiculous). But, luckily we don't have to fit all criteria because once your glands really stop working , it might take more decades than 20 yrs in my case, and you fulfil the criteria that is just advanced disease, you did have it 20-30-40 years earlier when you didn't fulfill the criteria).