HTLV-I associated Sjögren's syndrome is aetiologically distinct from anti-centromere antibodies positive Sjögren's syndrome.
OBJECTIVE
To investigate whether Sjögren's syndrome (SS) with anti-HTLV-I antibodies is aetiopathologically distinguishable from SS without these antibodies, the study compared prevalence of autoantibodies in serum samples of SS patients with or without anti-HTLV-I antibodies.


METHODS
The test group included 135 patients with primary SS and 97 patients with secondary SS. Serum samples of the patients were examined for the presence of anti-nuclear antibodies (ANA), anti-SS-A/Ro antibodies, anti-SS-B/La antibodies, anti-centromere antibodies (ACA), and anti-HTLV-I antibodies.


RESULTS
Anti-HTLV-I antibodies were detected in 25.0% of primary SS patients and in 29.2% of secondary SS patients. There were no significant differences in the mean age, sex, values of asparate aminotransferase, alanine aminotransferase, alkaline phosphatase, serum complements and IgG between HTLV-I seropositive and seronegative SS patients. The rheumatoid factor, ANA, anti-SS-A/Ro, and anti-SS-B/La antibodies in serum samples of SS patients were detected in 60.0%, 84.0%, 51.9%, and 12.0%, respectively. There was no significant difference in the prevalence of these antibodies between HTLV-I seropositive and seronegative SS patients. Using the indirect immunofluorescence test, 14.2% showed a discrete speckled staining pattern. All serum samples contained significant amounts of ACA determined by enzyme linked immunosorbent assay. These antibodies were detected in only 4% of HTLV-I seropositive SS patients but were present in 19.9% of HTLV-I seronegative SS patients. Furthermore, the prevalences of anti-SS-A/Ro and anti-SS-B/La antibodies in serum samples of ACA positive patients were significantly lower than those in ACA negative SS patients.


CONCLUSIONS
These results suggest that SS patients with anti-SS-A/Ro or anti-SS-B/La antibodies, or both, might be aetiopathologically distinct from SS patients with ACA. HTLV-I might be involved in the pathogenesis of SS in a subset of patients with anti-SS-A/Ro or anti-SS-B/La antibodies, or both, but not SS patients with ACA.
Hida
A
A
The First Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
Kawabe
Y
Y
Kawakami
A
A
Migita
K
K
Tominaga
M
M
Nakamura
H
H
Eguchi
K
K
D000368:Aged; D000914:Antibodies, Viral / Q000097:blood; D001323:Autoantibodies / Q000276:immunology*; D001324:Autoantigens / Q000097:blood; D002503:Centromere / Q000276:immunology*; D016009:Chi-Square Distribution; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D015490:HTLV-I Infections / Q000150:complications*; D006801:Humans; D008297:Male; D008875:Middle Aged; D020733:RNA, Small Cytoplasmic; D012261:Ribonucleoproteins / Q000097:blood; D012859:Sjogren's Syndrome / Q000209:etiology* / Q000276:immunology / Q000821:virology; D000097585:SS-B Antigen; D000099207:SS-A Antigen
D000914:Antibodies, Viral; D001323:Autoantibodies; D001324:Autoantigens; D020733:RNA, Small Cytoplasmic; D012261:Ribonucleoproteins; D000097585:SS-B Antigen; D000099207:SS-A Antigen; C116006:RO60 protein, human