Sjogrens Syndrome and MS

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Sjogrens Syndrome and MS

Postby Alicia » Mon Nov 12, 2012 3:41 pm

I have a question. About 6 months ago I started to have a very dry mouth. It felt like I had cotton under my tongue. My saliva glands (I think they are called parotid glands) were noticeably larger than they usually are. I was seen by my dentist and he said that this was normal. Then all of a sudden I woke up one day, my glands were smaller than they have been in a long time and my mouth was no longer dry. I have had bouts of dry eyes as well on and off for several years. I have also seen an eye doctor for the eye problems who didn't have any awnsers for me except to use eye drops which only made a minimal difference. I have been dx with ms for 13 years now. I have been reading up on the Sjogrens website. Many of the Sjogrens symptoms are the same as MS symptoms. This whole salivary gland thing makes me wonder if I have Sjogrens instead of MS or maybe if I have both?? Does anyone here have Sjogrens or both MS and Sjogrens Syndrome?

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Re: Sjogrens Syndrome and MS

Postby LR1234 » Tue Jul 02, 2013 12:47 am

I am looking into this myself at the moment as I believe I might have both
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Re: Sjogrens Syndrome and MS

Postby jimmylegs » Tue Jul 02, 2013 5:00 am

I think the latest reply I posted for someone on this topic, indicated that comorbidity was rare. and that misdiagnosis of sjogren's was common. and that it is known to look like ms. i'll find that post and link it up here.
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Re: Sjogrens Syndrome and MS

Postby CureOrBust » Tue Jul 02, 2013 5:59 am

from memory (as I think Sjogrens was my first diagnosis) the test to confirm it is normally a CAT Scan of your chest.
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Re: Sjogrens Syndrome and MS

Postby jimmylegs » Tue Jul 02, 2013 9:31 am

here's the recent discussion undiagnosed-f54/topic22539.html#p211605
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Re: Sjogrens Syndrome and MS

Postby LR1234 » Tue Jul 02, 2013 1:26 pm

Thanks jimmylegs
Cureorbust are you thinking of sarcoidosis?
I had blood test today for ss antibodies so we shall see.
Esr high at the moment and have painful dry eyes hence me researching ss.

Has anyone got actual optic atrophy after optic neuritis attacks? I got told the other day my eye is showing quite a bit of atrophy:( that's what chronic optic neuritis does for you:(
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Re: Sjogrens Syndrome and MS

Postby Wrinkles » Tue Jul 02, 2013 5:59 pm

Sjogren's syndrome can be primary or it can be secondary to RA, lupus, or MS. A recent hypothesis article describes how they can be related:
http://www.frontiersin.org/Molecular_Innate_Immunity/10.3389/fimmu.2013.00091/abstract
You can download the whole article as a pdf since the abstract alone doesn't give enough explanation. It explains involvement of EBV in causing overly reactive lymphocytes in the autoimmune diseases. The particular symptoms (and disease classification) can depend on the tissue location(s) where the overly reactive lymphocytes accumulate or where autoantigen/autoantibody complexes accumulate.
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Re: Sjogrens Syndrome and MS

Postby jimmylegs » Tue Jul 02, 2013 6:14 pm

ah, i had only seen RA, lupus and SYSTEMIC sclerosis (scleroderma) linked to SS before. (not an expert by any stretch)
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
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info: www.whfoods.com, www.nutritiondata.com
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Re: Sjogrens Syndrome and MS

Postby lyndacarol » Tue Jul 02, 2013 6:49 pm

Wrinkles wrote:Sjogren's syndrome can be primary or it can be secondary to RA, lupus, or MS. A recent hypothesis article describes how they can be related:
http://www.frontiersin.org/Molecular_Innate_Immunity/10.3389/fimmu.2013.00091/abstract
You can download the whole article as a pdf since the abstract alone doesn't give enough explanation. It explains involvement of EBV in causing overly reactive lymphocytes in the autoimmune diseases. The particular symptoms (and disease classification) can depend on the tissue location(s) where the overly reactive lymphocytes accumulate or where autoantigen/autoantibody complexes accumulate.


Can this work (http://www.frontiersin.org/Molecular_In ... 1/abstract) be that of our very own BioDocFL (Wesley)?

http://www.springer.com/medicine/internal/journal/12016

He has his polyamine hypothesis. Do a search on the author BioDocFL and find his many postings, such post150256.html?hilit=Wesley#p150256!

Especially here: general-discussion-f1/topic14179.html?hilit=Wesley
My hypothesis: excess insulin (hyperinsulinemia) plays a major role in MS, as developed in my initial post: http://www.thisisms.com/forum/general-discussion-f1/topic1878.html "Insulin – Could This Be the Key?"
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Re: Sjogrens Syndrome and MS

Postby mmpetunia » Tue Jul 02, 2013 10:00 pm

i have wondered the same thing since my grandmother was dx'd with sjogrens. my neuro never did any differential dx on me, she just looked at my scans and told me there was nothing else that could cause the combination of my symptoms and lesions. i wondered if it was possible for me to have sjogrens instead of MS or possibly both because of the family history so i had my pcp run a sed rate and another autoimmune lab that i am blanking on the name of right now. both were 0 or very close to it. in other words--inflammation in my body was nil. that effectively ruled out sjogrens for me but it is possible to have both, although sjogrens is more commonly associated with lupus than MS.
Dx: 9/8/11 RRMS
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copaxone x3: let's hope the third time is the charm!
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Re: Sjogrens Syndrome and MS

Postby CureOrBust » Wed Jul 03, 2013 3:11 am

LR1234 wrote:Cureorbust are you thinking of sarcoidosis?
No. With that diagnosis my GP (who along wioth me also9 found it hard to accept) sent me to a very good immunologist, who ran more tests to confirm his disagreement with that diagnosis.
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Re: Sjogrens Syndrome and MS

Postby jimmylegs » Wed Jul 03, 2013 3:42 am

found this, fwiw
Sjögren's syndrome: a review of clinical features, diagnosis and treatments available (2010)
http://globalresearchonline.net/journal ... le-014.pdf
"The occurrence of central nervous system and spinal cord involvement in Sjogren syndrome is estimated by various studies at 8-40%, with manifestations including
myelopathy, optic neuropathy, seizures, cognitive dysfunction, and encephalopathy21,24,25.Attempts must be made to distinguish other causes of these symptoms,
including concomitant SLE, multiple sclerosis, cerebrovascular disease, and Alzheimer disease. "
READ ME key info on nutrient targets - www.thisisms.com/ftopict-2489.html
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info: www.whfoods.com, www.nutritiondata.com
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Re: Sjogrens Syndrome and MS

Postby Annesse » Wed Jul 03, 2013 9:28 pm

I believe that MS and Sjogren's are really just different symptom manifestations of one common underlying disease pathway, caused by missing enzymes called protease.

For instance, in the following study when fifty-eight Sjögren syndrome (SS) patients with neurologic manifestations associated with SS had magnetic resonance imaging (MRI) of the brain, the researchers found that 70% of the patients had white matter lesions and 40% met the radiologic criteria for MS.


Medicine (Baltimore). 2004 Sep;83(5):280-91.
Neurologic manifestations in primary Sjögren syndrome: a study of 82 patients.
Delalande S, de Seze J, Fauchais AL, Hachulla E, Stojkovic T, Ferriby D, Dubucquoi S, Pruvo JP, Vermersch P, Hatron PY.
Department of Neurology, CHRU Lille France
“…We retrospectively studied 82 patients (65 women and 17 men) with neurologic manifestations associated with primary SS, as defined by the 2002 American-European criteria…Thirty-three patients had brain involvement and 13 patients had optic neuropathy. The disease mimicked relapsing-remitting multiple sclerosis (MS) in 10 patients and primary progressive MS in 13 patients… Thirty percent of patients (all with CNS involvement) had oligoclonal bands… Fifty-eight patients had magnetic resonance imaging (MRI) of the brain. Of these, 70% presented white matter lesions and 40% met the radiologic criteria for MS…”

Protease control tumor necrosis factor. Both MS and Sjogren's also have elevated tumor necrosis factor. Tumor necrosis factor attacks both the salivary glands and the myelin producing cells, as the following studies show.


Sjögren's syndrome is “currently defined” as a chronic autoimmune disease in which a person’s white blood cells attack their moisture-producing glands. These include the lacrimal glands that produce tears and the salivary glands which produce saliva.The basic secretory units of salivary glands are clusters of cells called an acini. In the following study the researchers stated that TNF “causes destruction of acini”.


The future of biologic agents in the treatment of Sjögren’s syndrome.
Meijer, J.M., J. Pijpe, H. Bootsma, A. Vissink, C.G.M. Kallenberg. 2007. Clin Rev Allergy Immunol. 32(3): 292–297.

“The intraglandular synthesis of TNF-α causes destruction of acini by up-regulation of Fas at the surface of the glandular epithelial cells, stimulation of secretion of type 2 and 9 matrix metalloproteases by epithelial cells, and overexpression of different chemokines…”


In the next study the researchers concluded their results suggest a central role of TNF in the initiation and progression of autoimmune destruction of salivary glands.

Inhibition of submandibular and lacrimal gland infiltration in nonobese diabetic mice by transgenic expression of soluble TNF-receptor p55.
Hunger, R.E., S. Müller, J.A. Laissue, M.W. Hess, C. Carnaud, I. Garcia, and C. Mueller. 1996. J Clin Invest. 98(4): 954–961.

“Direct evidence for an instrumental role of TNF-alpha in initiation and progression of submandibular and lacrimal gland infiltration is provided …These data suggest a central role of TNF-alpha in the initiation and progression of autoimmune tissue destruction of salivary glands and indicate beneficial effects of soluble TNF receptors in the treatment of organ-specific autoimmune diseases.”

Here are some studies confirming the involvement of TNF in MS.


In the following study published in the New England Journal of Medicine the researchers concluded their results provided evidence of intrathecal synthesis of TNF in MS and that the level of TNF in cerebrospinal fluid correlated with the severity and progression of the disease.



N Engl J Med. 1991 Aug 15;325(7):467-72.
Association between tumor necrosis factor-alpha and disease progression in patients with multiple sclerosis.
Sharief MK, Hentges R.
“Tumor necrosis factor-alpha (TNF-alpha), is a principal mediator of the inflammatory response and may be important in the pathogenesis and progression of multiple sclerosis, an inflammatory disease of the central nervous system…These data provide evidence of intrathecal synthesis of TNF-alpha in multiple sclerosis and suggest that the level of TNF-alpha in cerebrospinal fluid correlates with the severity and progression of the disease…”


Brain. 2003 Jun;126(Pt 6):1358-70.
TNF-induced death of adult human oligodendrocytes is mediated by c-jun NH2-terminal kinase-3.
Jurewicz A, Matysiak M, Tybor K, Selmaj K.
Tumour necrosis factor (TNF) induces death of oligodendrocytes, the putative cell target in multiple sclerosis.


Research confirms the involvement of protease in both diseases.

In the following study from Mayo College of Medicine the researchers stated that an “array of studies” implicate protease in multiple sclerosis pathogenesis.


Curr Top Microbiol Immunol. 2008;318:133-75.
The multiple sclerosis degradome: enzymatic cascades in development and progression of central nervous system inflammatory disease.
Scarisbrick IA.
“An array of studies implicate different classes of protease and their endogenous inhibitors in multiple sclerosis (MS) pathogenesis based on expression patterns in MS lesions, sera, and/or cerebrospinal fluid (CSF). Growing evidence exists regarding their mechanistic roles in inflammatory and neurodegenerative aspects of this disease…”

Research has also found that the majority of Sjögren’s syndrome patients have
“subclinical” (having no noticeable clinical symptoms) exocrine pancreatic
insufficiency. Exocrine pancreatic insufficiency is the inability to properly
digest food due to a lack of digestive enzymes. The exocrine pancreas is where
protease originate.


In the following study the researchers identified subclinical exocrine pancreatic
insufficiency in not only Sjögren’s syndrome, but in rheumatoid arthritis (RA) patients as
well. In the Sjögren’s patients tested, 58.3% had a “significant decrease” in
pancreatic enzymes.



Pancreatic duct antibodies and subclinical insufficiency of the exocrine
pancreas in Sjögren’s syndrome.

D’Ambrosi, A., A. Verzola, P. Buldrini, C. Vavalle, S. Panareo, S. Gatto, R. La Corte, L.
Vicentini, A. Boccafogli, R. Scolozzi. 1998. Recenti Prog Med 89(10):504-9.


“In previous studies we reported evidence of subclinical exocrine
pancreatic insufficiency in primary or secondary Sjögren’s syndrome (SSI, SSII)
and rheumatoid arthritis (RA)…test results, compared to controls, showed
a statistically significant decrease in duodenal juice volumes, bicarbonates and
enzymes in 58.3% of SSI, and in 30% of RA…”


In an additional study entitled “Exocrine pancreatic function in Sjögren’s
syndrome” the researchers concluded, “Exocrine pancreatic impairment was
found to be present in 63% of the patients” (Coll, 1989).

So, just to tie this together even more. If RA patients are also deficient in these enzymes, then we would expect to find an association between MS and RA.

J Rheumatol. 2006 May;33(5):1027-8. Epub 2006 Mar 15.

Association of rheumatoid arthritis with multiple sclerosis: report of 14 cases and discussion of its significance.
Toussirot E, Pertuiset E, Martin A, Melac-Ducamp S, Alcalay M, Grardel B, Seror P, Perdriger A, Wendling D, Mulleman D, Beraneck L, Mariette X; Club Rheumatismes et Inflammation

“…Since a great proportion of our patients developed MS first and subsequently RA, the best explanation for these cases is a predisposition in MS patients to develop another autoimmune disease with common etiologic cofactors…”
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Re: Sjogrens Syndrome and MS

Postby Annesse » Wed Jul 03, 2013 9:54 pm

I also wanted to add some information on the association between polyamines and MS and Sjogrens. You can trace the elevated polyamines directly back to elevated prolactin. Here is a link where this was demonstrated.
general-discussion-f1/topic22466.html

Elevated prolactin would result from missing protease. Here are some studies on the elevated prolactin levels in these diseases.

Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 2004 May;97(5):579-83.
A comparison of the hormone levels in patients with Sjogren's syndrome and healthy controls.
Taiym S, Haghighat N, Al-Hashimi I.


RESULTS: Mann-Whitney U test revealed a significantly higher levels of prolactin among patients than controls (11.41 ng/ml vs. 6.74 ng/ml, p=0.003)...
CONCLUSION: Abnormal levels and relative ratios of hormones may play a role in the pathogenesis of Sjögren's syndrome.

Hyperprolactinemia in multiple sclerosis.
Kira, J., M. Harada, Y. Yamaguchi, N. Shida, I. Goto. 1991. Journal of the Neurological Sciences 102(1):61-6.
“…Serum prolactin levels were found to be significantly higher in MS patients than in healthy controls in both sexes…All relapsing-remitting patients with hyperprolactinemia showed a rise in prolactin levels in the acute stage of the relapse and a decrease during the recovering stage and the following remission phase…”

Patients with rheumatoid arthritis (RA) also have increased levels of prolactin. In the following study the researchers concluded that their findings of increased prolactin levels in patients with RA leads to the assumption that prolactin may play a role in disease severity and the process of joint damage in RA.

Elevated prolactin levels in patients with rheumatoid arthritis: association with disease activity and structural damage.
Fojtíková, M., J. Tomasová Studýnková, M. Filková, Z. Lacinová, J. Gatterová, K. Pavelka, J. Vencovský, L. Senolt. 2010. Clin Exp Rheumatol. 28(6):849-54. Epub 2011 Jan 3.

“Prolactin (PRL) is a hormone with cytokine-like activities that has been demonstrated to be involved in immune responses…The findings of increased prolactin levels in patients with RA lead to the assumption that prolactin may play a role in disease severity and the process of joint damage in RA.”
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