Objectives: To identify relationships between vitamin D serum levels and the presence of autoantibodies directed against vitamin D and levels of interleukin(IL)-17 and IL-23 in patients with systemic lupus erythematosus (SLE). Methods: The study included 49 patients with SLE. Serum concentrations of 25(OH)D 3 were measured with electrochemiluminescence immunoassay (ECLIA). Enzyme-linked immunosorbent assays (ELISA) were used to determine antibodies directed against 1,25(OH) 2 D 3 and levels of IL-17 and IL-23 in serum of SLE patients. In evaluation of vitamin D status, the control group consisted of 49 age and gender matched healthy individuals, whereas in assessment of anti-vitamin D antibodies the control group comprised 30 sera from blood donors. Results: Serum concentration of 25(OH)D 3 in SLE patients during the warm season was 18.47 AE 9.14 ng/ml, which was significantly decreased as compared with that of the control group -31.27 AE 12.65 ng/ml (p ¼ 0.0005). During the cold season a trend toward lower concentration of 25(OH)D 3 in SLE patients was revealed; however, it did not reach statistical significance (11.71 AE 7.21 ng/ml vs. 16.01 AE 8.46 ng/ml; p ¼ 0.054). Results within the recommended range for vitamin D (30-80 ng/ml; 70-200 nmol/l) were observed only in three patients. The 25(OH)D 3 concentration was decreased in SLE patients with renal disease or leucopenia as compared with the levels in patients who did not have either problem (p ¼ 0.006 and p ¼ 0.047, respectively). The cold season was found to be a risk factor for vitamin D deficiency (<20 ng/ml) (odds ratio ¼ 9.25; p ¼ 0.005). Autoantibodies directed against 1,25(OH) 2 D 3 were detected in three SLE patients. No significant difference in 25(OH)D 3 serum concentrations was found between SLE patients with and without these autoantibodies. No link was shown between the existence of autoantibodies against 1,25(OH) 2 D 3 and clinical or laboratory findings, including IL-17 and IL-23 levels. However, serum concentrations of IL-23 were lower in patients with vitamin D deficiency (p ¼ 0.037). Conclusions: SLE patients, especially those with leucopenia or renal involvement, are at high risk of vitamin D deficiency and require vitamin D supplementation. Some SLE patient sera contained 1,25(OH) 2 D 3 antibodies, but these antibodies do not appear to affect vitamin D levels. Lupus (2012) 21, 477-484.
This study was supported by 1M15/N/2011 and NK1W grants from the I Faculty of Medicine, Warsaw Medical University. None of the authors has any competing interests to declare.
The objective of this study is to evaluate efficacy and safety of influenza vaccine in systemic lupus erythematosus (SLE) patients. We studied SLE patients and healthy subjects immunised with inactivated influenza vaccine. Efficacy was measured by comparing humoral response to vaccine antigens between groups. Safety was monitored by SLEDAI and serological markers. Subjects attended visits at baseline and on post-vaccination weeks 4 and 12. We enrolled 62 SLE patients and 47 healthy subjects. In post-immunisation week 4, anti-haemagglutinin antibody titres rose in the patient group at least 6.23-fold, compared to 11.90-fold among controls (P < or = 0.05). The seroconversion rate range was 53-56% among patients and 72-85% among controls (P < 0.05 for strains H1N1 and H3N2, NS for strain type B). The seroprotection rate ranged between 62% and 73% and between 90% and 98% in the patient and control group, respectively (P < 0.05). In post-vaccination week 12, the antibody titre was higher at least 3.86-fold in the patient group and 7.65-fold among controls. The seroconversion rate range was 32-40% among patients and 64-70% among controls, while the seroprotection rate ranged between 43% and 50% and between 79% and 94%, respectively (P < 0.005 for three strains). We identified one severe and six mild to moderate SLE exacerbations by week 12. The anti-nuclear antibodies and anti-double-stranded DNA titres grew by post-immunisation week 4 (P < 0.05). The post-vaccination response was weaker in SLE patients compared to healthy subjects. Immunisation did not change underlying disease activity.
The idiopathic inflammatory myopathies are a heterogeneous group of diseases that can involve various systems. Antibodies directed against aminoacyl-tRNA synthetases, such as anti-Jo-1 antibodies, are strongly associated with a syndrome which consists of myositis, interstitial lung disease (ILD), arthritis and Raynaud's phenomenon. Forty-one patients with various forms of idiopathic inflammatory myopathies were assessed: 14 patients with anti-Jo-1 antibodies and 27 patients without anti-Jo-1 antibodies as a control group. We retrospectively analysed clinical symptoms, treatment and outcome in both groups. Patients with anti-Jo-1 antibodies more often had ILD (64.2 vs. 11.1%), arthritis (64.2 vs. 18.1%) and Raynaud's phenomenon (38 vs. 0%). Patients without the anti-Jo-1 antibody presented worse muscle strength and more frequently myalgia (37 vs. 21%), cutaneous rash (18.5 vs. 7%), heliotrope rash (29% vs. 7%) and periungueal changes (22 vs. 0%) than the anti-Jo-1-positive patients. Outcome was good in both groups. Improvement was achieved in the 14 (100%) Jo-1 positive patients, and in 25 (92.5%) controls. Two (7.5%) patients from control group achieved remission.
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