Dry eye syndrome and the subsequent risk of CFS - a prospective population-based study

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Oncotarget. 2018 Jul 17;9(55):30694-30703. doi: 10.18632/oncotarget.25544. eCollection 2018 Jul 17.
Dry eye syndrome and the subsequent risk of chronic fatigue syndrome-a prospective population-based study in Taiwan.
Chen CS1,2,3, Cheng HM4,5, Chen HJ6,7,8, Tsai SY9,10, Kao CH11,12,13, Lin HJ14,15, Wan L5,16,17,18, Yang TY19,20,21.
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Abstract

Background and Aim:
The clinical association between dry eye syndrome (DES) and chronic fatigue syndrome (CFS) remain unclear with less evidences. We aimed to investigate the relationship between CFS and DES using a national insurance and prospective cohort study.

Methods:
Data from the Longitudinal Health Insurance Database 2000 was applied to estimate the incidence of CFS among patients with DES, and their age- and sex-matched controls without DES over a long-term follow-up period. All participants were CFS free at baseline, before the interval (2005-2007), but were later diagnosed with CFS. DES patients and its relative matched controls were excluded prevalent CFS before the same interval.

Results:
We identified 884 patients with DES and 3,536 matched controls in baseline and estimated the hazard ratios for incident CFS in the follow-up period. Patients with DES had a 2.08-fold considerably increasing risk of developing CFS, compared to non-DES group. An elevated risk of developing CFS remained (1.61-fold risk) even after adjusting for age, sex, and comorbidities. There was a presence of increasing risk in DES-related CFS when CFS-related comorbidities existing (adjusted hazard ratio, 1.98, 95% confidence interval, 1.19-3.29; p < 0.01). The subsequent risk for CFS between DES and non-DES patients was significant increased with three or more annual medical visits, the adjusted risk for CFS was 4.88-fold risk (95% CI, 2.26-10.58, p < 0.001).

Conclusion:
We recommended that physicians should be aware of the increased risk of CFS among DES patients and adequately assess the health impacts among these patients.

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StarChild56

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Does this study relate to also having Sjogrens?
I did not read the full text, just what was posted here and did not find anything that suggests it is related to SS, but - some of the major symptoms of SS - pain, dysautonomia and fatigue - well you find that in CFS, too. So it is hard to tease out when multiple illnesses have overlapping symptoms, you know?
 

kangaSue

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There a few people around who have been diagnosed with ME/CFS initially then found that up to ten years down the track, they have Sjogren's and because of the latent time it can take for Sjogren's antibodies to appear, could have had Sjogren's all along.

Dry eyes can go along with having sudomotor dysfunction and this is common in a lot of autoimmune conditions where it's often down to Autonomic Neuropathy but this (AN) does occur just as an idiopathic thing as well. Either way, autonomic sweat tests of QSART and TST can shed some light on a reason as to why you might be suffering from DES.
 

Wonkmonk

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Cause or symptom? I have DES diagnosed by an ophtalmologist and I know it developed while I had developing CFS.

So in my case I think it is a symptom rather than a risk factor or precursor.

It might also be possible that DES is an early sign of already developing CFS that shows up before the more prominent signs like fatigue etc. show up (at least in a subset of patients).

So one might say those with DES are at higher risk of 'developing CFS' at a later point in time, but I think at least some of those - like me - are already having CFS without knowing it and the DES is an early symptom that appears before the other symptoms get severe enough to diagnose the patient with CFS.
 

used_to_race

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I developed dry eye syndrome in my left eye shortly after developing ME/CFS. Ophthalmologist didn't find any cause, swab was clean etc.

It never even occurred to me to link the two. Fascinating.

I'm almost a decade into having ME/CFS and so far no sign of other autoimmune conditions.
I've never had noticeably dry eyes or mouth, but tested positive for Salivary Protein IgM in an early Sjogren's panel recently. The idea that symptoms can show up prior to the presence of antibodies is something I've been thinking about a lot lately. It seems to imply that there's some core issue that is not being detected. Maybe it's a metabolic problem. Maybe it's a genetic/protein synthesis problem. To be honest, I've also heard the opposite, i.e. that in some cases the autoantibodies will appear years or decades before the onset of symptoms. It probably varies by disease, but it would seem that a generalized immune activation that causes symptoms is not necessarily present with some autoantibodies, and that the generalized immune activation itself can be independent of specific antibodies. But I guess people who get immunoadsorption + IVIg can really benefit in conditions like POTS, so there is probably some interplay.

Basically it seems like there is a huge (possibly even primary) component to a broad range of immune dysfunctions that just hasn't been identified yet.
 

Gingergrrl

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I wonder if patients with CFIDS (that is what my first primary care doc dx me with and our specialist) have an overall higher incidence of autoimmune disease(s) than the regular population...
I wonder this as well (both if many are misdiagnosed with ME/CFS who later actually have an autoimmune diagnosis, and if many have both as co-morbid diagnoses). I don't think enough people are being tested to really ever know.

There a few people around who have been diagnosed with ME/CFS initially then found that up to ten years down the track, they have Sjogren's and because of the latent time it can take for Sjogren's antibodies to appear, could have had Sjogren's all along.
That is really interesting but makes a lot of sense.

But I guess people who get immunoadsorption + IVIg can really benefit in conditions like POTS, so there is probably some interplay.
It is near impossible to get immunoadsorption (plasmapheresis) in the U.S. (I tried and was determined as hell to find a way but ultimately realized it was just not going to happen). IA or PP can be very helpful diagnostically for autoimmune conditions b/c you can get a quick remission of symptoms but then it goes away when the autoantibodies return. Vs. IVIG is a much longer commitment and while it improves the autoimmunity, it does not stop B-cells from producing new auto-antibodies like Rituxan does.

Basically it seems like there is a huge (possibly even primary) component to a broad range of immune dysfunctions that just hasn't been identified yet.
I totally agree.
 

Wishful

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The lipids in tears are critical for keeping eyes properly wetted, and are quite complex. It's quite reasonable to expect that metabolic dysfunction would affect those glands too. I don't quite have dry eye syndrome, but I'm borderline. The optometrist said she could see that I had diminished oil production. It's hard to know whether it started before or after my ME.
 

Crux

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It's estimated that 49% of the world's population is inefficient at converting pro-vitamin A, (beta-carotene), to active vitamin A, the retinoids. Xeropthalmia, dry eyes, is from a vitamin A deficiency. Also, if there isn't enough zinc, or if thyroid is low, then it's hard to convert vitamin A to active form.

Another possible cause of dry eyes is insufficient Lactoferrin. Lactoferrin is found in tears, saliva, body fluids, etc.

I've had this problem off and on for years. Now I eat foods with active vitamin A, like eggs, butter,cream, etc.

I take a small amount of Lactoferrin daily. 75mg.
 

Wonkmonk

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This may well apply to some patients, but I tried very high doses of both beta carotene (diet and supplements) and Vitamin A (both fat- and water soluble) for several weeks in very high doses (up to 100,000 iUs) without any effect on my dry eyes. An ophtalmologist found no cause and could recommend no other treatment.

I think for some patients including me, it really has to do with the CFS and it is not a vitamin deficiency.
 
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I tried vitamin A in supplement form, through the consumption of carrots and veal liver but but they didnt help at all. I'm convinced its some sort of persistent pathogen with inflammation driven by the immunological process causing the issue. The only thing I can put a finger on was a primary herpes infection and possible Lyme.

I had 3 eye exams and although no lesions were discovered I believe my case was sub acute even though the symptoms were horrible such as photophobia, burning itchy, redness and dryness. Now I have little to no corneal sensation and am concerned a form of retinal necrosis may be developing.

Different MMPs namely (mmp9) can be elevated during viral ocular infection and cyclosporine is said to reduce them so I'm hoping to give that a try also.
 
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Dry eyes can go along with having sudomotor dysfunction and this is common in a lot of autoimmune conditions where it's often down to Autonomic Neuropathy but this (AN) does occur just as an idiopathic thing as well. Either way, autonomic sweat tests of QSART and TST can shed some light on a reason as to why you might be suffering from DES.
@kangaSue
This is really interesting as I believe I have a form of Autonomic nueropahty. Lack of ability to sweat, severly depressed breathing, low heart rate variability, gastrointestinal dysmotility. I don't think symptoms of autonomic dysfunction can get clearer than that.

I got a diagnosis of "idiopathic hereditary neuropathy" which I think is absurd as it happend right after a viral infection.
(Modern medicines way of absolving themselves from the responsibility of identifying and treating root causes imo)

I also tested highly positive on one of the early sjogrens panel values. Getting to the root of the issue- is it not possible that a herpes virus which lives in the nerves is triggering an attack on them in turn causing the neuroapahty?

I read dry foot skin which I also seem to have developed rather suddenly is a symptom of nerve damage leading to sweating inability.

You mentioned the parasym supplement in another post and reviews mention it's helped people with dry eye and dry mouth as well which would also indicate nerve involvement as it's said to stimulate the vagus nerve. Have you tried the supplement yourself?
 
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StarChild56

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The lipids in tears are critical for keeping eyes properly wetted, and are quite complex.
In addition (and distinct from) to having Dry Eyes, my ophthalmologist said that not having enough oil in my tears can contribute to dry eyes - I believe that my glands not producing enough oil is due to my Posterior Blepharitis.
 

Judee

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My constant dry eye issues started about 2-3 years ago. I don't recall a problem before but now it is really bad and I get anisocoria--one pupil much larger than the other--that I never noticed before though I did get episodes of bad double vision going way back.

I also get very dry lips and have to use lip balm all the time. Blood antibody tests for Sjogren's came back negative.
 

used_to_race

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I also tested highly positive on one of the early sjogrens panel values. Getting to the root of the issue- is it not possible that a herpes virus which lives in the nerves is triggering an attack on them in turn causing the neuroapahty?
I totally get this, but we have to remember that most people who get EBV and other herpesviruses do not have immune dysfunction or neuropathy, at least after the acute phase of the infection. We have coevolved with these viruses for a long time and although they have shaped and certainly play a role in the peculiarities of our immune systems, there must be some further underlying issue that causes some of us to get chronic illnesses. In my opinion anyway. Many of us, myself included, have had isolated periods, perhaps hours or days, perhaps longer, of remission or near-remission since becoming ill. I would be interested to know what changes during these periods. I would bet it's got nothing to do with low-level viral populations or antibody titers to viruses. And furthermore, I would imagine there is some way to replicate these conditions and dramatically improve symptoms if we can understand the molecular basis for all these different conditions more generally.
 

kangaSue

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@Sidney That would be my idea of classic symptoms of autonomic dysfunction and other than the breathing issue, these are similar symptoms to what I had before being diagnosed with AN (Autonomic Neuropathy). There's some hypothesis that a vagus nerve infection can contribute to this sort of autonomic dysfunction so I guess it's possible for that to be of viral origin.

I tried Mestinon for this rather than Parasym Plus and, while it helped with improving my sweat response, I had to stop it because it was like most other meds (or supplements) and caused severe abdominal pain. I figured from that that I would be wasting my money in trying Parasym Plus.

I was tested for Sjogren's and a heap of other autoimmune things but nothing came up positive so AN was put down to idiopathic. I've since found I have a totally occluded left renal vein (Nutcracker Syndrome) though which is known to also cause autonomic dysfunction (including breathing problems and chest pain for some people) but the mechanism of how it occurs is not fully elucidated yet.