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As clinical researchers interested in oral inflammatory disorders, we were gratified to read the January JADA article, "Xerostomia: Etiology, Recognition and Treatment," by Drs. James Guggenheimer and Paul Moore. Several points made in the article require clarification.

As stated, Sjögren’s syndrome is an autoimmune exocrinopathy, with involvement predominantly of salivary and lacrimal glands. But the primary disease is far from limited to those glands as stated in the article.

Altered secretory function of other organs, including sweating, hepatobiliary and pancreatic function, is well-established.¹ Extraglandular manifestations—including nonerosive synovitis, cutaneous and visceral vasculitis, interstitial pneumonitis, peripheral and central nervous system involvement (autonomic and peripheral neuropathy, myelopathy), distal renal tubular acidosis and interstitial nephritis—are frequent accompaniments.²

Readers also should be alerted to the potential pathogenic association of hepatitis C and the dramatically increased incidence of lymphoma.^3,4 In addition, the systemic nature of primary Sjögren’s syndrome is demonstrated by the systemic production of autoantibodies directed to the intracellular ribonucleoprotein molecules Ro/SSA and La/SSB, seen virtually exclusively in Sjögren’s syndrome and, to a lesser extent, in systemic lupus erythematosus.⁵

Although symptoms of Sjögren’s syndrome have been reported to occur with fibromyalgia and chronic fatigue syndrome, the article’s implication is that these represent autoimmune conditions of which Sjögren’s syndrome may represent a secondary manifestation. Our current understanding of these disorders is that they do not have a primary autoimmune etiology and have not been convincingly linked with the presence of autoantibodies, but that they have been known to accompany Sjögren’s syndrome.²

Other explanations for the loss of glandular function include antibodies against the M3 muscarinic receptor, inhibiting the neural stimulation of the functional glands.⁶ Apoptotic cell death also has been considered a potential mechanism for decreased glandular function, as seen in salivary ductal epithelial cells from patients with Sjögren’s syndrome.⁷

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2. Fox RI, Tornwall J, Michelson P. Current issues in the diagnosis and treatment of Sjögren’s syndrome. Curr Opin Rheumatol 1999;11(5):364–71.[Medline]
   
   
3. Ramos-Casals M, Garcia-Carrasco M, Cervera R, Font J. Sjögren’s syndrome and hepatitis C virus. Clin Rheumatol 1999;18(2):93–100.[Medline]
   
   
4. Mariette X. Lymphomas in patients with Sjögren’s syndrome: review of the literature and physiopathologic hypothesis. Leuk Lymphoma 1999;33(1–2):93–9.[Medline]
   
   
5. Mavragani CP, Tzioufas AG, Moutsopoulos HM. Sjögren’s syndrome: autoantibodies to cellular antigens—clinical and molecular aspects. Int Arch Allergy Immunol 2000;123(1):46–57.[Medline]
   
   
6. Humphreys-Beher MG, Brayer J, Yamachika S, Peck AB, Jonsson R. An alternative perspective to the immune response in autoimmune exocrinopathy: induction of functional quiescence rather than destructive autoaggression. Scand J Immunol 1999;49(1):7–10.[Medline]
   
   
7. Matsumura R, Umemiya K, Kagami M, et al. Glandular and extraglandular expression of the Fas-Fas ligand and apoptosis in patients with Sjögren’s syndrome. Clin Exp Rheumatol 1998;16(5):561–8.[Medline]
   
   

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Rosenstein, E. D. Articles by Kramer, N. Search for Related Content PubMed Articles by Rosenstein, E. D. Articles by Kramer, N.