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.
“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
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 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…”