Serum levels of n-3 and n-6 polyunsaturated fatty acids in patients with systemic lupus erythematosus and their association with disease activity: a pilot study.

OBJECTIVE: Polyunsaturated fatty acids (PUFAs) may modulate the inflammatory process in systemic autoimmune diseases, including systemic lupus erythematosus (SLE). The aim of this study was to assess the serum concentrations of essential 18-carbon PUFAs and their long-chain derivatives in patients with SLE and healthy controls, and to analyse their associations with laboratory and clinical features of the disease. METHOD: n-6 and n-3 PUFA composition was assessed in the sera of 30 SLE patients and 20 healthy controls using gas chromatography-mass spectrometry. We investigated the associations between PUFAs and disease activity measured with Systemic Lupus Erythematosus Activity Index (SLEDAI) scores, erythrocyte sedimentation rate, C-reactive protein, complement C3 and C4 concentrations, anti-nuclear antibody (ANA) titre, anti-double-stranded DNA (anti-dsDNA) antibody concentration, and medications. RESULTS: Serum linoleic acid (LA) and α-linolenic acid concentrations were significantly higher in SLE patients compared with healthy controls. LA concentration correlated positively with the ANA titre and corticosteroid doses; eicosapentaenoic acid (EPA) and docosahexaenoic acid correlated inversely with anti-dsDNA antibody concentration. Patients treated with immunosuppressants had significantly lower concentrations of LA, arachidonic acid, and EPA. CONCLUSION: Both n-6 and n-3 PUFA precursors can participate in the inflammatory process in SLE patients. The mechanism of the PUFA metabolism disturbance needs further exploration.

Serological and clinical characterization of anti-dsDNA and anti-PM/Scl double-positive patients.

Antibodies to double-stranded desoxyribonucleic acid (dsDNA) and to the polymyositis/scleroderma (PM/Scl) complex are regarded as serological markers for systemic lupus erythematosus (SLE) and PM/Scl overlap syndrome, respectively. In a previous study, serum samples were identified that contained antibodies specific for both dsDNA and PM/Scl. Fourteen of these sera were available for more detailed investigation including the autoantibody profile as determined by several methods including an addressable laser bead assay, Crithidia luciliae indirect immunofluorescence test (CLIFT) and a PM1-Alpha ELISA. Moreover, 300 samples from connective tissue disease patients and 30 PM/Scl positive samples were screened for anti-dsDNA(+)/PM/Scl(+) specimens by CLIFT, dsDNA ELISA, and PM1-Alpha ELISA. We confirmed anti-dsDNA and anti-PM/Scl reactivity in 2/7 samples from the previous study. One sample had also anti-chromatin and anti-SS-A reactivity and the second sample was oligoreactive. In addition, 2/300 (0.7%) unselected samples from connective tissue disease patients were identified with anti-dsDNA and anti-PM/Scl reactivity. In a panel of PM1-Alpha positive samples (n = 30) collected regardless of the diagnosis of the patients, no anti-dsDNA reactivity was found. All anti-dsDNA(+)/anti-PM/Scl(+) patients identified fulfilled sufficient criteria to be classified as definite SLE and also had at least one feature of systemic sclerosis (i.e., sclerodactyly and/or Raynaud's phenomenon). Only 1/4 patients had clinical evidence of dermatomyositis. The combination of anti-dsDNA(+)/anti-PM/Scl(+) in patients suffering from connective tissue disease is less frequently found than previously described when newer assays are used. Clinically, anti-dsDNA(+)/anti-PM/Scl(+) patients may define a small subgroup of SLE patients with additional features of systemic sclerosis.