OBJECTIVE: To investigate the prevalence of alpha-fodrin autoantibodies in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) with and without secondary SS, using an in vitro transcription and translation assay (ITT). METHODS: cDNA encoding JS-1, the amino-terminal portion of alpha-fodrin, was used for ITT. Immunoprecipitation was performed with sera from 56 primary SS patients and 67 SLE patients, 14 with and 53 without secondary SS. Correlations to RF, ANA, anti-dsDNA, anti-SS-A and anti-SS-B antibodies, hypergammaglobulinemia, labial salivary gland biopsy grade, extraglandular manifestations and a modified SLE disease activity index (mSLEDAI) were made. RESULTS: Autoantibodies against alpha-fodrin were detected in 16/56 (29%) of primary SS patients and in 25/53 (47%) of sera from SLE patients without secondary SS. In SLE patients with secondary SS the prevalence was 3/14 (21%). None of the blood donors showed alpha-fodrin reactivity. Correlations were found to RF, ANA, anti-dsDNA antibodies and a positive mSLEDAI score. CONCLUSION: The frequency of alpha-fodrin autoantibodies detected by this method is similar in sera from primary SS patients and SLE patients with or without secondary SS. The presence of alpha-fodrin autoantibodies seems to reflect non-organ-specific autoimmunity in primary SS and SLE and to be of limited discriminating value.
OBJECTIVE: To investigate the prevalence of alpha-fodrin autoantibodies in primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE) with and without secondary SS, using an in vitro transcription and translation assay (ITT). METHODS: cDNA encoding JS-1, the amino-terminal portion of alpha-fodrin, was used for ITT. Immunoprecipitation was performed with sera from 56 primary SS patients and 67 SLEpatients, 14 with and 53 without secondary SS. Correlations to RF, ANA, anti-dsDNA, anti-SS-A and anti-SS-B antibodies, hypergammaglobulinemia, labial salivary gland biopsy grade, extraglandular manifestations and a modified SLE disease activity index (mSLEDAI) were made. RESULTS: Autoantibodies against alpha-fodrin were detected in 16/56 (29%) of primary SS patients and in 25/53 (47%) of sera from SLEpatients without secondary SS. In SLEpatients with secondary SS the prevalence was 3/14 (21%). None of the blood donors showed alpha-fodrin reactivity. Correlations were found to RF, ANA, anti-dsDNA antibodies and a positive mSLEDAI score. CONCLUSION: The frequency of alpha-fodrin autoantibodies detected by this method is similar in sera from primary SS patients and SLEpatients with or without secondary SS. The presence of alpha-fodrin autoantibodies seems to reflect non-organ-specific autoimmunity in primary SS and SLE and to be of limited discriminating value.