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Relation of Sensory Peripheral Neuropathy in Sjögren Syndrome to Anti-Ro/SSA

Scofield, Amanda Kyle*; Radfar, Lida DDS; Ice, John A. MD*; Vista, Evan MD; Anaya, Juan-Manuel MD; Houston, Glen DDS; Lewis, David DDS; Stone, Donald U. MD¶#; Chodosh, James MD††; Hefner, Kimberly MD*; Lessard, Christopher J. PhD*; Moser, Kathy L. PhD*‡; Scofield, Robert Hal MD*†**

JCR: Journal of Clinical Rheumatology:
doi: 10.1097/RHU.0b013e3182675e4f
Original Articles
Abstract

Background: Sjögren syndrome is a common, chronic autoimmune disease that typically produces inflammation and poor function of the salivary and lacrimal glands. Other organs can be affected, including the nervous system. Sensory peripheral neuropathy is a common manifestation of the disease.

Methods: Eight-eight patients attending a dry eyes–dry mouth clinic were diagnosed to have primary Sjögren syndrome and underwent a neurological examination. Anti-Ro (or SSA) and anti-La (or SSB) were determined using immunodiffusion as well as Inno-Lia and BioPlex ANA screen. Serum vitamin B12 levels were determined using an enzyme-linked microtiter plate assay.

Results: Twenty-seven (31%) of the 88 patients had peripheral neuropathy as defined by loss of light touch, proprioception, or vibratory sensation. Anti-Ro and anti-La were found by immunodiffusion in 12 patients, and 8 of these 12 had neuropathy (χ2 = 8.46, P = 0.0036, odds ratio = 6.0 compared to those without precipitating anti-Ro and anti-La). Of the 27 patients with only anti-Ro by immunodiffusion, 13 (48.1%) had neuropathy (χ2 = 5.587, P = 0.018, compared to those without anti-Ro). There was no relationship of the other, more sensitive measures of anti-Ro and anti-La to neuropathy. In addition, we found no association of serum vitamin B12 levels to neuropathy among these patients with Sjögren syndrome.

Conclusions: Sensory peripheral neuropathy is common among patients with Sjögren syndrome and is associated with the presence of anti-Ro and anti-La when determined by immunodiffusion.

Author Information

From the *Arthritis & Clinical Immunology Program, Oklahoma Medical Research Foundation; †Department of Medicine, ‡Pathology, and ∥Ophthalmology, University of Oklahoma Health Sciences Center; ¶College ofDentistry, University of Oklahoma Health Sciences Center; the #DeanMcGee Eye Institute; and the **Department of Veterans Affairs Medical Center, Oklahoma City, OK; ††Massachusetts Eye & Ear Infirmary andHarvard Medical School, Boston, MA; ‡‡Center for Autoimmune Diseases Research, School of Medicine and Health Sciences, Universidad del Rosario, Bogotá, Columbia.

This work was supported in part by a Center of Research Translation award from the National Institute of Arthritis, Musculoskeletal, and Skin Diseases. D.U.S. and J.C. were supported by a Research to Prevent Blindness grant to the OUHSC Department of Ophthalmology and the Dean McGee Eye Institute.

The authors declare no conflict of interest.

Correspondence: Robert Hal Scofield, MD, 825 NE 13th St, MS24, Oklahoma City, OK 73104. E-mail: hal-scofield@omrf.ouhsc.edu.

© 2012 Lippincott Williams & Wilkins, Inc.