Please use this identifier to cite or link to this item: https://www.um.edu.mt/library/oar/handle/123456789/85354
Title: Vitamin D supplementation in systemic lupus erythematosus : relationship to disease activity, fatigue and the interferon signature gene expression
Authors: Magro, Rosalie
Saliba, Christian
Camilleri, Liberato
Scerri, Christian A.
Borg, Andrew A.
Keywords: Vitamin D
Systemic lupus erythematosus
Fatigue
Interferon
Issue Date: 2021
Publisher: BioMed Central Ltd.
Citation: Magro, R., Saliba, C., Camilleri, L., Scerri, C., & Borg, A. A. (2021). Vitamin D supplementation in systemic lupus erythematosus : relationship to disease activity, fatigue and the interferon signature gene expression. BMC Rheumatology, 5, 53.
Abstract: Background: In addition to the well-known role of vitamin D in calcium homeostasis and bone metabolism, vitamin D is important in the modulation of the immune system and inflammatory processes. Vitamin D deficiency is common in patients with systemic lupus erythematosus (SLE), possibly as a result of sun avoidance. The aim of this prospective open-label study was to assess the effect of the treatment of vitamin D deficiency and insufficiency in SLE patients, particularly with regards to disease activity, fatigue and interferon signature gene expression. Methods: 31 SLE patients, 13 with vitamin D deficiency and 18 with vitamin D insufficiency were treated with vitamin D3. They were supplemented with vitamin D3 8000 IU daily for 8 weeks if they were vitamin D deficient, or 8000 IU daily for 4 weeks if they were insufficient. This was followed by 2000 IU daily maintenance. They were assessed at baseline, after 6 and 12 months by means of an interview, filling in questionnaires and blood tests. The expression of 12 interferon signature genes in RNA extracted from whole blood was measured by using QuantiGene Plex technology. Results: An improvement in disease activity measured by systemic lupus erythematosus disease activity index-2K (SLEDAI-2K; p = 0.028) and fatigue measured by fatigue severity scale (FSS; p = 0.071) at 12 months were noted. A significant decrease in anti-double stranded deoxyribonucleic acid (dsDNA) titre (p = 0.045) was also noted. The mean interferon signature gene expression score decreased from baseline to 6 months, however statistical significance was not achieved (p = 0.165). Conclusions: Improved disease activity and fatigue have been noted when Vitamin D has been supplemented in vitamin D deficient/insufficient SLE patients. One possible mechanism could be the suppression of the interferon signature gene expression.
URI: https://www.um.edu.mt/library/oar/handle/123456789/85354
Appears in Collections:Scholarly Works - FacSciSOR



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