UNLABELLED: In systemic lupus erythematosus (SLE) patients photosensitivity is considered as a factor which may cause exacerbation of skin lesions and provoke organ damage. Therefore in all therapeutic standards photo protection is recommended which may diminish vitamin D synthesis. Because of the enhanced activity of the humoral immunity which is present in the course of disease one postulates the possibility of the production of antibodies directed against vitamin D, that would be able to intensify this deficiency independently from consequences of photoprotection. THE AIM of the study was to estimate the frequency of occurrence of antibodies directed against 1,25(OH)2D3 in patients with SLE and to assess serum concentration of 25 (OH)D3 in comparison with clinical and laboratory parameters. MATERIAL AND METHODS: The study encompassed 45 patients with SLE. The control group in the 25(OH)D3 investigation comprised 49 healthy individuals but in autoantibodies against 1,25(OH)2D3 evaluation involved 30 sera obtained from healthy blood donors. In the determination of autoantibodies directed against 1,25(OH)2D3 ELISA method was employed. The concentration of 25 (OH)D3 in the serum was evaluated with automatized electrochemi-luminescence method on the automatic platform Elecsys 2010 in the control system DEQAS (vitamin D external quality assessment scheme). RESULTS: Serum concentration of 25(OH)D3 was significantly decreased in SLE patients in comparison with the control group (15.03 +/- 8.69 vs 23.37 +/- 12.34 ng/ml, respectively; p = 0.0005). Vitamin D deficit (25(OH)D3 < 10 ng/ml) was ascertained in 16 patients (35.55%), deficiency (10-20 ng/ml) in 16 (35.55%) and hypovitaminosis (20-30 ng/ml) in 10 (22.22%). Values within the recommended range (30-80 ng/ml) were established in 3 (6.66%) patients. The risk for vitamin D deficiency was 3.28 folds higher in SLE patients than in healthy controls (OR = 3.28; p = 0.005). Autoantibodies directed against 1,25(OH)2D3 were found in 4 (8.88%) patients. No statistically significant difference in the concentration of 25 (OH)D3 between SLE anti-1,25(OH)2D3 positive and anti-1,25(OH)2D3 negative patients was disclosed. The study did not reveal the correlations between the presence of antibodies directed against 1,25(OH)2D3 and the occurrence of ascertain clinical and laboratory parameters of SLE. The winter times was found to be the risk factor for vitamin D deficiency (OR = 7.33; p = 0.005). Sunscreen usage was revealed to be the predictor of serum 25(OH) vitamin D, concentration (beta = -0.44; p = 0.04). CONCLUSIONS: The low concentration of vitamin D in lupus patients indicates that they are at the essential risk for vitamin D deficiency, however the presence of the antibodies directed against 1,25(OH)2D3 seems not to influence vitamin D status.
UNLABELLED: In systemic lupus erythematosus (SLE) patients photosensitivity is considered as a factor which may cause exacerbation of skin lesions and provoke organ damage. Therefore in all therapeutic standards photo protection is recommended which may diminish vitamin D synthesis. Because of the enhanced activity of the humoral immunity which is present in the course of disease one postulates the possibility of the production of antibodies directed against vitamin D, that would be able to intensify this deficiency independently from consequences of photoprotection. THE AIM of the study was to estimate the frequency of occurrence of antibodies directed against 1,25(OH)2D3 in patients with SLE and to assess serum concentration of 25 (OH)D3 in comparison with clinical and laboratory parameters. MATERIAL AND METHODS: The study encompassed 45 patients with SLE. The control group in the 25(OH)D3 investigation comprised 49 healthy individuals but in autoantibodies against 1,25(OH)2D3 evaluation involved 30 sera obtained from healthy blood donors. In the determination of autoantibodies directed against 1,25(OH)2D3 ELISA method was employed. The concentration of 25 (OH)D3 in the serum was evaluated with automatized electrochemi-luminescence method on the automatic platform Elecsys 2010 in the control system DEQAS (vitamin D external quality assessment scheme). RESULTS: Serum concentration of 25(OH)D3 was significantly decreased in SLEpatients in comparison with the control group (15.03 +/- 8.69 vs 23.37 +/- 12.34 ng/ml, respectively; p = 0.0005). Vitamin D deficit (25(OH)D3 < 10 ng/ml) was ascertained in 16 patients (35.55%), deficiency (10-20 ng/ml) in 16 (35.55%) and hypovitaminosis (20-30 ng/ml) in 10 (22.22%). Values within the recommended range (30-80 ng/ml) were established in 3 (6.66%) patients. The risk for vitamin D deficiency was 3.28 folds higher in SLEpatients than in healthy controls (OR = 3.28; p = 0.005). Autoantibodies directed against 1,25(OH)2D3 were found in 4 (8.88%) patients. No statistically significant difference in the concentration of 25 (OH)D3 between SLE anti-1,25(OH)2D3 positive and anti-1,25(OH)2D3 negative patients was disclosed. The study did not reveal the correlations between the presence of antibodies directed against 1,25(OH)2D3 and the occurrence of ascertain clinical and laboratory parameters of SLE. The winter times was found to be the risk factor for vitamin D deficiency (OR = 7.33; p = 0.005). Sunscreen usage was revealed to be the predictor of serum 25(OH) vitamin D, concentration (beta = -0.44; p = 0.04). CONCLUSIONS: The low concentration of vitamin D in lupuspatients indicates that they are at the essential risk for vitamin D deficiency, however the presence of the antibodies directed against 1,25(OH)2D3 seems not to influence vitamin D status.
Authors: Odirlei André Monticielo; Thaisa de Mattos Teixeira; José Artur Bogo Chies; João Carlos Tavares Brenol; Ricardo Machado Xavier Journal: Clin Rheumatol Date: 2012-06-13 Impact factor: 2.980