Can MDG and/or ocular surface inflammation lead to aqueous deficiency?

[hopeful_hiker]

We all know aqueous deficiency as the hallmark symptom of Sjogren’s as well as aging, surgeries or menopause.

However, it appears to me from reading on this forum and looking at studies (and my own signs) that aqueous deficiency can develop from other causes.

Rosacea studies:

https://www.nature.com/articles/eye2015277#t1
https://www.ncbi.nlm.nih.gov/m/pubmed/1532401/


They both have ocular rosacea patients with low TMH and Schirmer’s. Do you have any ideas or research material similar to this?

I have ocular rosacea (not visible) which manifests itself as meibomian gland clogging and MMP9 inflammation. I also have unstable tear volume production. Once I came to my doc and he said that I have extremely low tear meniscus height (TMH). Other times it was a bit low or normal. I’ve done Sjogren’s lip biopsy and full autoimmune bloodwork this past spring so most likely that is not the cause for my fluctuations.

[ebi1368]

I also have rosacea with low tear. Of course that could be because of Lasik.

Do you have plug?

[Meibum Ian]

I have been diagnosed with MGD with secondary aqueous deficiency. So whether true or not in my case, it does imply that it can happen.

[Guest]

I agree with Ian, once you get inflamed, whatever the cause, all of the systems are under attack. That includes the lacrimal gland. That’s why I believe controlling inflammation is probably the single most important part of dealing with dry eye.

[MGD1701]

Inflammation
is most critical but sadly some/most doctors still do not treat it (based on my experience too).
Dr Toyos mentioned it too in his recent article.
I know most experts in USA still treat it even with negative MMP-9 - I like such approach.
I think not all doctors are capable to detect inflammation. My doctor said MMP-9 can detect more things.

[Guest]

Inflammation
is most critical but sadly some/most doctors still do not treat it (based on my experience too).
Dr Toyos mentioned it too in his recent article.
I know most experts in USA still treat it even with negative MMP-9 - I like such approach.
I think not all doctors are capable to detect inflammation. My doctor said MMP-9 can detect more things.

I agree in treating even when MMP9 is negative. There may be inflammation that the test cannot pick up due to lack of sensitivity. I think the MMP9 test indicates weather treatment is effective or not in my humble opinion. I don’t think our testing is currently good enough to give us exact quantitative data, but I’m sure it will be.

[hopeful_hiker]

I have been diagnosed with MGD with secondary aqueous deficiency. So whether true or not in my case, it does imply that it can happen.

Thanks for chiming in! So did you first have normal aqueous production and MDG?

Did you rule out autoimmune and hormonal conditions?

[hopeful_hiker]

I agree with Ian, once you get inflamed, whatever the cause, all of the systems are under attack. That includes the lacrimal gland. That’s why I believe controlling inflammation is probably the single most important part of dealing with dry eye.

I am curious how that works. T-cells are on the eye surface, I wonder how the lacrimal gland gets into the cycle. Assuming it is not originally inflamed from Sjogren’s.

update: this study induced desiccating stress in mice* resulting in Sjogren-like symptoms though T-cell activity. Lots of medical jargon but the example they have mentioned is people with medically induced dryness who do not get better after stopping the medication. You could expand it to MDG, same idea.




*Side note

I absolutely hate experiments on animals. Science and all is not worth it for me personally. Knowing how painful/uncomfortable DED can be, I feel so sorry for these poor creatures. Born to be ok for a few weeks and miserable until the day experimenters kill them. I get they want to control their variables, but I think it would be just as appropriate to recruit people who are already on drying meds and observe them after they quit. Harder, yes. More expensive, yes. Exponentially more ethical, absolutely yes. Plus humans and other animals do not have identical lacrimal units.

[Guest]

I am curious how that works. T-cells are on the eye surface, I wonder how the lacrimal gland....[/I]

You and every dry eye doc in the world wants to know how this works lol. What I’m saying is, even the professionals have very little to work with in regards to how this is happening. That’s why the doctor I see now took a bunch of tears from me to look at T cells, cytokines, chemokines, and he took another vial I totally forgot what for. But I think they’re tracking these inflammatory markers to see how the disease and the treatment effect inflammation and vice versa. There are so many inflammatory markers other than T cells, my god where do you begin. Way over my head. I just hope someone figures this out soon.

The new reports on Lacritin sound promising. My hope is we get more new drugs/drops coming out the mimic the tear film and reduce inflammation safely AND effectively. I would love prescription artificial tears that mimicked our own tears. I think someone provided a study that showed over 200 components in human tears. The Australians did the analysis I believe. Would love to see that drop come out.

[Meibum Ian]

Thanks for chiming in! So did you first have normal aqueous production and MDG?

Did you rule out autoimmune and hormonal conditions?

Hi,

Hard to know how long aqueous production was ok for.. certainly by 3 months in it was poor. The first optometrist I saw a few weeks into the condition said I had plenty of tears, but of the wrong kind (low oil). That was subjective and based on slit lamp only..

RF, ANA, SS-A & SS-B blood tests all ok. hormonal not yet done.

[Meibum Ian]

I am curious how that works. T-cells are on the eye surface, I wonder how the lacrimal gland gets into the cycle. Assuming it is not originally inflamed from Sjogren’s.

This may go some way to help explain: https://bjo.bmj.com/content/100/3/300

[hopeful_hiker]

I also have rosacea with low tear. Of course that could be because of Lasik.

Do you have plug?

I did. One was inside the puncta and one was mushroom shaped (control flow). They kept 50%-60% and 90% respectively. One fell out, the mushroom shaped one got taken out after 3 months because I did not feel that different with one gone.

They did help to make the downs not as bad. I have weird symptoms so it is still trial and error for me. I want to try temporary ones. Perhaps, I could have them inserted when I feel worse.

[MGD1701]

Just read this, from DryEyeCoach, 11/23/2018
''Just like inflammation in a knee, the lungs, or liver,
a chronic inflammation of the eye can permanently damage the tear gland tissue
to the point that treatment becomes ineffective.''

[Milo007]

I am curious how that works. T-cells are on the eye surface, I wonder how the lacrimal gland gets into the cycle. Assuming it is not originally inflamed from Sjogren’s.

update: this study induced desiccating stress in mice* resulting in Sjogren-like symptoms though T-cell activity. Lots of medical jargon but the example they have mentioned is people with medically induced dryness who do not get better after stopping the medication. You could expand it to MDG, same idea.




*Side note

I absolutely hate experiments on animals. Science and all is not worth it for me personally. Knowing how painful/uncomfortable DED can be, I feel so sorry for these poor creatures. Born to be ok for a few weeks and miserable until the day experimenters kill them. I get they want to control their variables, but I think it would be just as appropriate to recruit people who are already on drying meds and observe them after they quit. Harder, yes. More expensive, yes. Exponentially more ethical, absolutely yes. Plus humans and other animals do not have identical lacrimal units.

hopeful_hiker

Inflammtory mediators can reach the lacrimal gland through the same channels as as drugs like restasis or xiidra or steroids do. How do you think a drop of restasis or xiidra instilled on the ocular surface is supposed to reduce the inflammation of the lacrimal glands if they don't reach the glands?

The inflammatory markers can flow with the residual tear to the lacrimal glands causing inflammation there. Remember punctal plugs are contradictory to the use of restatis or xiidra? In the website of restasis it's mentioned that restasis didn't work on those who had punctal plugs inserted. This indicates the tear ducts might have a channel to the lacrimal glands and blocking the tear ducts prevents the delivery of restasis, xiidra or steroids to the lacrimal glands.

I agree with Dowork123 that inflammation damages all parts of the system and left untreated MGD will translate to lacrimal dysfunction or vice versa.

[Milo007]

You and every dry eye doc in the world wants to know how this works lol. What I’m saying is, even the professionals have very little to work with in regards to how this is happening. That’s why the doctor I see now took a bunch of tears from me to look at T cells, cytokines, chemokines, and he took another vial I totally forgot what for. But I think they’re tracking these inflammatory markers to see how the disease and the treatment effect inflammation and vice versa. There are so many inflammatory markers other than T cells, my god where do you begin. Way over my head. I just hope someone figures this out soon.

The new reports on Lacritin sound promising. My hope is we get more new drugs/drops coming out the mimic the tear film and reduce inflammation safely AND effectively. I would love prescription artificial tears that mimicked our own tears. I think someone provided a study that showed over 200 components in human tears. The Australians did the analysis I believe. Would love to see that drop come out.

Dowork123

I am afraid even if we can synthesize a perfect substitute of our natural tears it won't be of use since the mechanical action of spreading the lipid layer over aqueous layer of the tear film needs continous and controlled delivery of lipids onto the lid margins that won't be the case with artificial instillation of tear drops even if it had ALL the components of natural tears including meibum. Such a tear drop would be drained away within minutes through the tear ducts and you would need to keep on instilling artificial tears every 10-15 minutes to be asymptomatic.

FURTHER more an artificial tear drop replicating the exact composition of natural tears would be hopelessly expensive to produce that won't be a feasible solution at all.

This is the reason why Dr. Korb says the incredible role of the meibomian glands can NEVER be substituted by any means let alone artifical tear drops.

For me the only hope is meibomian gland regeneration or tissue engineering to reproduce meibomian glands somehow and then transplant them. I would like to mention that a group of scientists had already reproduced a fully functional lacrimal gland using tissue engineering under laboratory conditions. Sounds fascinating?