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Journal articles on the topic 'Lupus, mice, vitamin D'

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Published: 14 March 2023

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1

Yamamoto, Erin A., Jane K. Nguyen, Jessica Liu, Emma Keller, Nicole Campbell, Cun-Jin Zhang, Howard R. Smith, Xiaoxia Li, and Trine N. Jørgensen. "Low Levels of Vitamin D Promote Memory B Cells in Lupus." Nutrients 12, no. 2 (January 22, 2020): 291. http://dx.doi.org/10.3390/nu12020291.

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Background: Vitamin D deficiency is a known risk factor for Systemic Lupus Erythematosus (SLE), yet clinical trials have not demonstrated efficacy and few studies have utilized lupus models to understand the mechanism underlying this relationship. The Act1-/- mouse is a spontaneous model of lupus and Sjögren’s syndrome, characterized by increased Th17 cells and peripheral B cell expansion. Vitamin D3 has anti-inflammatory properties, reduces Th17 cells and impairs B cell differentiation/activation. Therefore, we assessed how varying amounts of vitamin D3 affected lupus-like disease in the Act1-/- mouse. Methods: Act1-/- mice were fed either low/restricted (0 IU/kg), normal (2 IU/kg), or high/supplemented (10 IU/kg) vitamin D3 chow for 9 weeks, after which lupus-like features were analyzed. Results: While we found no differences in Th17 cells between vitamin D3 groups, vitamin D3 restriction specifically promoted memory B cell development, accompanied by elevated levels of serum IgM, IgG1, IgG3, and anti-dsDNA IgG. A similar significant negative association between serum vitamin D and memory B cells was confirmed in a cohort of SLE patients. Conclusion: Low levels of vitamin D3 are associated with elevated levels of memory B cells in an animal model of lupus and well-controlled SLE patients.
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Barsotti, S., C. Tani, A. Kuhl, S. Pacini, S. Vagnani, and M. Mosca. "AB0124 NO EFFECTS OF HIGH DOSE 25OH-VITAMIN D SUPPLEMENTATION ON LUPUS NEPHRITIS IN AN ANIMAL MODEL OF SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1362.2–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4250.

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Background:25OH Vitamin D (25-OH-D3) is a fat-soluble steroid-derived molecule involved in the calcium homeostasis. Low levels of 25-OH-D3 are commonly found in patients with systemic lupus erythematosus (SLE) and have been correlated to higher disease activity and severity. Several recent studies have demonstrated that high dose Vitamin D may influence several aspects of the innate and adaptive immune response and some authors hypothesized that high dose 25-OH-D3 may have a role in the treatment of SLE. Despite these observations, the immunomodulatory effect of high dose 25-OH-D3in vivostill needs to be demonstrated.Objectives:The aim of our study was to identify the effect of 25-OH-D3 on proteinuria, survival and renal biopsy in New Zealand Black/White F1 mice (NZ), that develop a disease very similar to human SLE nephritis.Methods:We administered to 20 NZ mice a diet enriched with high dose 25-OH-D3 10,000 UI/Kg starting from 8 weeks of age. Mice were divided in 7 experimental groups (5 mice each). The first group was sacrificed before the start of the treatment (8 week of age), three groups were treated (treated mice – TM) with 25-OH-D3 and sacrificed at 16, 26 and 36 weeks of age. The other three groups were enrolled as controls and sacrificed at 16, 26 and 36 weeks of age respectively (untreated mice – UM). The parameters collected included: total urinary protein and kidney histology for the evaluation of lupus nephritis (LN): glomerulonephritis, interstitial nephritis and vascular lesions according to a 5 points scale to obtain a total score (ranging from 0 to 12).Results:In UM, proteinuria tended to increase over 1 mg/day at 12 weeks of age (1.7±0.43mg/day) and further increased until to reach a plateau after 28 weeks of age (10±2.0 mg/day).In TM, a significant increase in proteinuria over 1 mg/day was observed at 24 weeks, when the mean proteinuria was 1.7±1.33 which was lower than controls at the same age although without statistical significance (2.9±2.6); thereafter proteinuria started to increase also in treated mice and at week 30 was higher in TM compared with UM (10,3±8.8 vs 4.3±3.5 p=0.05). Figure 1.Kidney histology showed, in mice sacrificed before the start of the treatment no signs of LN. In mice sacrificed at 16 weeks minimal interstitial nephritis (score 1) was identified in 2 mice only in UM. At 26 weeks of age, a higher total LN score was identified in TM compared with UM (3.4±3.8 vs 0.4 ±0.9) with higher score for all three parameters analyzed. At 36 weeks of age, the TM group maintained a higher total LN score compared to UM (6.5±1.7 vs 6.0±2.6) with higher score for glomerulonephritis and interstitial nephritis.In the TM group, three mice spontaneously died at 26, 30 and 32 weeks of age, while in the UM only one mouse died at 36 weeks of age.Conclusion:Our data suggest that, in this animal model of SLE, 25-OH-D3 administration seems to delay the onset of proteinuria, although has no effect on the overall disease control. In addition, it may have a negative effect on renal histology and survival with earlier development of LN.Figure:Disclosure of Interests:None declared
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Yan, Lijun, Ping Wu, Dong-Mei Gao, Jie Hu, Qian Wang, Nan-Fang Chen, Sheng-Quan Tong, Li Rao, and Jing Liu. "The Impact of Vitamin D on Cognitive Dysfunction in Mice with Systemic Lupus Erythematosus." Medical Science Monitor 25 (June 25, 2019): 4716–22. http://dx.doi.org/10.12659/msm.915355.

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4

Alves, I., V. Pinto, B. Santos-Pereira, A. Campar, J. R. Vizcaino, F. Carneiro, C. Vasconcelos, A. Marinho, and S. Pinho. "AB0123 CHANGES IN CELLULAR GLYCOSYLATION AS A KEY FACTOR IN THE IMMUNOPATHOGENESIS OF SYSTEMIC LUPUS ERYTHEMATOSUS." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 1361.1–1362. http://dx.doi.org/10.1136/annrheumdis-2020-eular.1231.

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Background:Systemic Lupus Erythematous (SLE) is one of the most challenging autoimmune diseases as it may be presented as a severe, relapsing and disabling immune-mediated disorder still remaining incurable (1,2).Protein glycosylation is an essential post translational modification that participate in the correct recognition of cells by the immune system (3–5). Moreover, glycosylation changes in T cells (specifically loss of branchedN-glycans mediated by GnTV, encoded byMGAT5gene) have been shown to impact its intrinsic function and activity in a diverse panel of autoimmune diseases (3,4,6)Objectives:To evaluate the impact of glycans in the cellular and molecular mechanisms underlying the loss of immune-tolerance, envisioning the identification of a new targeted-specific mechanism.Methods:We have analysed the profile of cellular glycosylation of a subset of biopsy-proven lupus nephritis from SLE patients and normal kidney tissue (from two Porto Centre Hospitals), through immunohistochemistry (IHC) as well as by real time PCR using RNA extracted from paraffin tissues. Blood samples were collected and were analysed by flow cytometry.Mgat5null mice with 15-months old were monitored for autoimmune signs by evaluating proteinuria, weight loss and colon and kidney tissues were analysed by IHC and FACS.Results:SLE patients revealed a significant decreased expression of complexN-glycans in the renal parenchyma, when compared to healthy kidney. In addition, we have identified in lupus nephritis patients a unique subset of circulatory CD3+T cells with an abnormal glycosignature and displaying an increased expression of specific glycan-binding receptors. Interestingly,Mgat5null mice develop clinical signs compatible within autoimmune-like syndrome together with an increased infiltration of specific CD3+T cells subset identified in SLE patients.Conclusion:These findings point towards the identification of a novel immune player with increased ability to sense abnormalN-glycans, modulating the surrounding immune response. We propose glycosylation as a regulatory mechanism that tips the balance between homeostasis/self-tolerance and autoimmunity opening a potential novel targeted-specific mechanism in SLE pathogenesis.References:[1]Tsokos GC et al. New insights into the immunopathogenesis of systemic lupus erythematosus. Nat Rev Rheumatol. 2016 Nov 22;12(12):716–30.[2]Marinho A et al. Vitamin D supplementation effects on FoxP3 expression in T cells and FoxP3+/IL-17A ratio and clinical course in systemic lupus erythematosus patients: a study in a Portuguese cohort. Immunol Res. 2017 Feb 16;65(1):197–206.[3]Dias AM et al. Metabolic control of T cell immune response through glycans in inflammatory bowel disease. Proc Natl Acad Sci U S A. 2018 May 15;115(20):E4651–60.[4]Pereira MS & Alves I. et al. Glycans as Key Checkpoints of T Cell Activity and Function. Front Immunol. 2018 Nov 27;9:2754.[5]Pinho SS, Reis CA. Glycosylation in cancer: mechanisms and clinical implications. Nat Rev Cancer. 2015 Sep 20;15(9):540–55.[6]Verhelst X et al. Protein Glycosylation as a Diagnostic and Prognostic Marker of Chronic Inflammatory Gastrointestinal and Liver Diseases. Gastroenterology. 2020 Jan 1;158(1):95–110.Acknowledgments:S.S.P. and I.A. acknowledge Group of Studies for Autoimmune diseases (NEDAI) from Portuguese Society of Internal Medicine (SPMI) for Funding and for supporting the attendance at this meeting.Disclosure of Interests:None declared
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5

Simioni, Juliana A., Flavia Heimovski, and Thelma L. Skare. "On lupus, vitamin D and leukopenia." Revista Brasileira de Reumatologia (English Edition) 56, no. 3 (May 2016): 206–11. http://dx.doi.org/10.1016/j.rbre.2015.08.008.

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6

Sangüesa Gómez, Clara, Bryan Josué Flores Robles, and José Luis Andréu. "Bone Health, Vitamin D and Lupus." Reumatología Clínica (English Edition) 11, no. 4 (July 2015): 232–36. http://dx.doi.org/10.1016/j.reumae.2014.12.006.

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7

Cutolo, M., and K. Otsa. "Review: Vitamin D, immunity and lupus." Lupus 17, no. 1 (January 2008): 6–10. http://dx.doi.org/10.1177/0961203307085879.

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8

Klyukvina, N. G. "Systemic lupus erythematosus and vitamin D." Modern Rheumatology Journal 9, no. 2 (June 9, 2015): 57. http://dx.doi.org/10.14412/1996-7012-2015-2-57-65.

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9

Kamen, Diane, and Cynthia Aranow. "Vitamin D in systemic lupus erythematosus." Current Opinion in Rheumatology 20, no. 5 (September 2008): 532–37. http://dx.doi.org/10.1097/bor.0b013e32830a991b.

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10

Kamen, Diane L., Glinda S. Cooper, Henda Bouali, Stephanie R. Shaftman, Bruce W. Hollis, and Gary S. Gilkeson. "Vitamin D deficiency in systemic lupus erythematosus." Autoimmunity Reviews 5, no. 2 (February 2006): 114–17. http://dx.doi.org/10.1016/j.autrev.2005.05.009.

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11

red. "Ist Vitamin D bei Lupus erythematodes wirksam?" hautnah dermatologie 28, no. 6 (November 2012): 352. http://dx.doi.org/10.1007/s15012-012-0249-z.

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12

Nerviani, Alessandra, Daniele Mauro, Michele Gilio, Rosa Daniela Grembiale, and Myles J. Lewis. "To Supplement or not to Supplement? The Rationale of Vitamin D Supplementation in Systemic Lupus Erythematosus." Open Rheumatology Journal 12, no. 1 (December 27, 2018): 226–47. http://dx.doi.org/10.2174/1874312901812010226.

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Background: Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease characterised by abnormal activation of the immune system, chronic inflammation and organ damage. Lupus patients are more prone to be vitamin D deficient. However, current evidence is not conclusive with regards to the role played by vitamin D in SLE development, progression, and clinical manifestations. Objective: Here, we will summarise the current knowledge about vitamin D deficiency prevalence, risk factors, molecular effects, and potential pathogenic role in SLE. We will focus on the link between vitamin D deficiency and lupus clinical manifestations, and on the clinical trials assessing the effects of vitamin D supplementation in SLE. Method: A detailed literature search was performed exploiting the available databases, using “vitamin D and lupus/SLE” as keywords. The relevant interventional trials published over the last decade have been considered and the results are reported here. Conclusion: Several immune cells express vitamin D receptors. Thus, an immunomodulatory role for vitamin D in lupus is plausible. Numerous observational studies have investigated the relationship between vitamin D levels and clinical/serological manifestations of SLE with contrasting results. Negative correlations between vitamin D levels and disease activity, fatigue, renal and cardiovascular disease, and anti-dsDNA titres have been described but not conclusively accepted. In experimental models of lupus, vitamin D supplementation can improve the disease. Interventional trials have assessed the potential therapeutic value of vitamin D in SLE, but further larger studies are needed.
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Miskovic, Rada, Aleksandra Plavsic, Jasna Bolpacic, Sanvila Raskovic, and Mirjana Bogic. "Role of Vitamin D in Systemic Lupus Erythematosus." Open Access Macedonian Journal of Medical Sciences 2, no. 4 (December 15, 2014): 662–67. http://dx.doi.org/10.3889/oamjms.2014.119.

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Vitamin D is a steroid hormone that in addition to its well known role in the metabolism of calcium and phosphorus exerts immunoregulatory properties. Data from animal studies and from prospective clinical trials on patients with rheumatoid arthritis, multiple sclerosis and type 1 diabetes point to the potential role of vitamin D as important environmental factor in the development of autoimmune diseases. Such role of vitamin D in systemic lupus erythematosus (SLE) has not yet been sufficiently studied. This review shows the sources, metabolism and mechanism of action of vitamin D, its effect on the cells of the immune system, prevalence and causes of vitamin D deficiency in patients with SLE, the link between vitamin D status and disease activity as well as recommendations for vitamin D supplementation.
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14

Cutillas-Marco, E., A. Marquina-Vila, WB Grant, JJ Vilata-Corell, and MM Morales-Suárez-Varela. "Vitamin D and cutaneous lupus erythematosus: effect of vitamin D replacement on disease severity." Lupus 23, no. 7 (February 6, 2014): 615–23. http://dx.doi.org/10.1177/0961203314522338.

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15

Abdelhamid, Leila, Xavier Cabana-Puig, Brianna Swartwout, Jing Zhu, Yaqi Li, A. Catharine Ross, Thomas E. Cecere, Phillip Ruiz, Christopher M. Reilly, and Xin M. Luo. "Vitamin A Deficiency Deteriorates Lupus Nephritis." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 61.05. http://dx.doi.org/10.4049/jimmunol.206.supp.61.05.

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Abstract Vitamin A deficiency (VAD) is observed in both human and mice with lupus nephritis (LN). However, whether VAD is a driving factor for LN progression is unclear. Here, we investigated the effect of VAD on the progression of LN in a lupus-prone mouse model, MRL/lpr. In these mice, while LN is not apparent before 8 weeks of age, the inflammation of lymphoid tissues suggesting initiation of lupus is evident at weaning. Thus, we initiated VAD either before or after weaning to reveal a potential time-dependent effect. At around 15 weeks of age with both types of VAD, we found exacerbated LN that was characterized by deteriorated kidney inflammation, impaired renal epithelial integrity, and dramatic squamous metaplasia of the renal pelvic urothelium. Both types of VAD provoked severe neutrophilic tubulointerstitial nephritis and accelerated renal failure. This was concomitant with significantly higher mortality in all VAD mice. Looking at an earlier time point of 7 weeks of age and before the onset of clinical LN, both types of VAD increased splenomegaly, lymphadenopathy, and circulating autoantibodies; three additional hallmarks of lupus, as well as renal infiltration of conventional and plasmacytoid dendritic cells. These results suggest VAD-driven deterioration of LN regardless of the time of VAD initiation. Our findings raise significant public health concerns that concurrent lupus and VAD may lead to more severe SLE. Future studies will elucidate the underlying mechanisms of how VAD modulates myeloid cells to accelerate the initiation of LN.
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Chiruvolu, Neha V., Yasaman Safarpour, and Vaneet K. Sandhu. "Vitamin D and Lupus: Are we doing enough?" Journal of Community Hospital Internal Medicine Perspectives 11, no. 5 (September 3, 2021): 624–28. http://dx.doi.org/10.1080/20009666.2021.1956049.

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Mok, Chi Chiu. "Vitamin D and systemic lupus erythematosus: an update." Expert Review of Clinical Immunology 9, no. 5 (May 2013): 453–63. http://dx.doi.org/10.1586/eci.13.19.

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Yap, Kristy S., and Eric F. Morand. "Vitamin D and systemic lupus erythematosus: continued evolution." International Journal of Rheumatic Diseases 18, no. 2 (December 19, 2014): 242–49. http://dx.doi.org/10.1111/1756-185x.12489.

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WALSH, NANCY. "Low Levels of Vitamin D Seen in Lupus." Skin & Allergy News 39, no. 6 (June 2008): 48. http://dx.doi.org/10.1016/s0037-6337(08)70428-5.

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Albuquerque, Lucas Tavares Cruz de, Caroline Pereira Modesto, Pedro De Sousa Leite, Ana Aurélia Tavares da Cruz, and Djailson Ricardo Malheiro. "THE IMMUNOMODULATORY ROLE OF VITAMIN D IN SYSTEMIC LUPUS ERYTHEMATOSUS: AN INTEGRATING LITERATURE REVIEW." Amadeus International Multidisciplinary Journal 2, no. 4 (July 6, 2018): 88–99. http://dx.doi.org/10.14295/aimj.v2i4.34.

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Vitamin D, conceptually, is a pre-hormone. Many studies have shown that the vitamin D deficiency may be associated to a higher incidence of autoimmune diseases, including Systemic Lupus Erythematosus. So, this work’s purpose is identify what the scientific literature approaches about the vitamin D, highlighting its immunomodulatory role with the Systemic Lupus Erythematosus. We used the article survey that ran upon the subject in the Medline, Scielo and Lilacs databases with the descriptors: vitamin D, Systemic Lupus Erythematosus and autoimmune disease. The selected articles pointed out higher prevalence in the vitamin D deficiency and insufficiency in Lupus patients. In these, the supplementation appeared to improve the disease activity and inflammatory markers and shows a tendency for subsequent clinical improvement. However, there is a lack of adequate intake guidelines. In this way, researches about the best dosage of vitamin D are needed for these patients in order to improve their condition.
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Bouillon, Roger, Geert Carmeliet, Lieve Verlinden, Evelyne van Etten, Annemieke Verstuyf, Hilary F. Luderer, Liesbet Lieben, Chantal Mathieu, and Marie Demay. "Vitamin D and Human Health: Lessons from Vitamin D Receptor Null Mice." Endocrine Reviews 29, no. 6 (October 1, 2008): 726–76. http://dx.doi.org/10.1210/er.2008-0004.

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Abstract The vitamin D endocrine system is essential for calcium and bone homeostasis. The precise mode of action and the full spectrum of activities of the vitamin D hormone, 1,25-dihydroxyvitamin D [1,25-(OH)2D], can now be better evaluated by critical analysis of mice with engineered deletion of the vitamin D receptor (VDR). Absence of a functional VDR or the key activating enzyme, 25-OHD-1α-hydroxylase (CYP27B1), in mice creates a bone and growth plate phenotype that mimics humans with the same congenital disease or severe vitamin D deficiency. The intestine is the key target for the VDR because high calcium intake, or selective VDR rescue in the intestine, restores a normal bone and growth plate phenotype. The VDR is nearly ubiquitously expressed, and almost all cells respond to 1,25-(OH)2D exposure; about 3% of the mouse or human genome is regulated, directly and/or indirectly, by the vitamin D endocrine system, suggesting a more widespread function. VDR-deficient mice, but not vitamin D- or 1α-hydroxylase-deficient mice, and man develop total alopecia, indicating that the function of the VDR and its ligand is not fully overlapping. The immune system of VDR- or vitamin D-deficient mice is grossly normal but shows increased sensitivity to autoimmune diseases such as inflammatory bowel disease or type 1 diabetes after exposure to predisposing factors. VDR-deficient mice do not have a spontaneous increase in cancer but are more prone to oncogene- or chemocarcinogen-induced tumors. They also develop high renin hypertension, cardiac hypertrophy, and increased thrombogenicity. Vitamin D deficiency in humans is associated with increased prevalence of diseases, as predicted by the VDR null phenotype. Prospective vitamin D supplementation studies with multiple noncalcemic endpoints are needed to define the benefits of an optimal vitamin D status.
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Whitcomb, James P., Mary DeAgostino, Mark Ballentine, Jun Fu, Martin Tenniswood, JoEllen Welsh, Margherita Cantorna, and Mary Ann McDowell. "The Role of Vitamin D and Vitamin D Receptor in Immunity toLeishmania majorInfection." Journal of Parasitology Research 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/134645.

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Vitamin D signaling modulates a variety of immune responses. Here, we assessed the role of vitamin D in immunity to experimental leishmaniasis infection in vitamin D receptor-deficient mice (VDRKO). We observed that VDRKO mice on a genetically resistant background have decreasedLeishmania major-induced lesion development compared to wild-type (WT) mice; additionally, parasite loads in infected dermis were significantly lower at the height of infection. Enzymatic depletion of the active form of vitamin D mimics the ablation of VDR resulting in an increased resistance toL. major. Conversely, VDRKO or vitamin D-deficient mice on the susceptible Th2-biased background had no change in susceptibility. These studies indicate vitamin D deficiency, either through the ablation of VDR or elimination of its ligand, 1,25D3, leads to an increase resistance toL. majorinfection but only in a host that is predisposed for Th-1 immune responses.
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Miskovic, Rada, Aleksandra Plavsic, Sanvila Raskovic, Zikica Jovicic, and Jasna Bolpacic. "Vitamin D Status in Patients with Systemic Lupus Erythematosus in Serbia: Correlation with Disease Activity and Clinical Manifestations." Open Access Macedonian Journal of Medical Sciences 3, no. 2 (May 4, 2015): 256–61. http://dx.doi.org/10.3889/oamjms.2015.052.

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BACKGROUND: Numerous studies indicate potential role of vitamin D as an important factor in the development of many autoimmune diseases including systemic lupus erythematosus (SLE). Patients with SLE are especially prone to the development of vitamin D deficiency due to the nature of their illness.AIM: The aims of our study were to determine the prevalence of vitamin D insufficiency and deficiency in patients with SLE in Serbia, to identify clinical variables associated with vitamin D status and to examine the impact of vitamin D status on disease activity and presence of specific lupus autoantibodies.MATERIAL AND METHODS: The study included 46 patients with SLE. Serum 25(OH)D concentration was measured by electrohemiluminiscent immunoassay.RESULTS: The mean serum concentration of 25(OH)D was 11.9 ± 7.3 ng/ml. The prevalence of insufficiency was 32.6%, while the prevalence of deficiency was 67.4%. There was no association between vitamin D status and photosensitivity, skin lesions, arthritis and lupus nephritis. Vitamin D status was not associated with the presence of specific autoantibodies. There was no correlation between disease activity assessed by SLEDAI scale with the concentration of 25(OH)D. Patients who used vitamin D supplements and calcium did not have a significantly higher concentration of 25(OH)D.CONCLUSION: In conclusion, vitamin D deficiency is common in patients with SLE.
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Tri Utami, Amalia. "Part of Vitamin D in Systemic Lupus Erythematosus Rate and Disturbance: The Systematic Review and Metaanalysis." Journal of Clinical Case Reports and Studies 3, no. 6 (June 28, 2022): 01–07. http://dx.doi.org/10.31579/2690-8808/112.

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Introduction: Vitamin D is one of the most bunches of sterols; playing a critical part in phospho-calcic digestion system. The change of 7-dehydrocholesterol to pre- vitamin D3 within the skin, through sun oriented bright B radiation, is the most source of vitamin D. Since lupus patients are more often than not photosensitive, the chance of creating vitamin D lack in is tall in this populace. In spite of the fact that confirmations appeared the intention between systemic lupus erythematosus (SLE) and vitamin D through which SLE can lead to lower vitamin D levels, it is additionally imperative to consider the plausibility that vitamin D insufficiency may have a causative part in SLE etiology. This paper analyzes existing information from different thinks about to highlight the part of vitamin D lack in SLE event and disturbance and the plausible adequacy of vitamin D supplementation on SLE patients. Method: This study using systematic review that search using keyword Vitamin D and Systemic Lupus Erythematosus in PubMed, Google Scholar and Science Direct. Result: After final screening the author analysize 4 articles. As in methods, the author summarize 4 articles. Conclusion: Confirmations appear that vitamin D plays an critical part within the pathogenesis and movement of SLE and vitamin D supplementation appears to improve incendiary and hemostatic markers; so, can progress clinical ensuing.
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Zamani, Batool, Hossein Akbari, Mehrdad Mahdian, and Ehsan Dadgostar. "The Relationship Between Serum Vitamin D Level and Systemic Lupus Erythematosus Activity." International Journal of Epidemiologic Research 7, no. 1 (March 26, 2020): 1–5. http://dx.doi.org/10.34172/ijer.2020.01.

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Background and aims: : Systemic lupus erythematosus (SLE) is an autoimmune disease which involves various organs. Vitamin D is an essential ingredient in regulating the immune system. This study aimed to investigate the relationship between vitamin D and the severity of lupus activity. Materials and Methods: This case-control study was carried out on 38 patients with lupus on the basis of the American College of Rheumatology (ACR) criteria and 44 healthy subjects with no history of rheumatologic disease. To measure the level of 25-hydroxy vitamin D, venous blood samples (5 cc) were taken from each participant and the activity of the lupus disease was measured by the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) scale. Finally, the chi-square test, independent sample t test, one-way ANOVA, and multiple linear regression analysis were used to measure multivariate effects. The level of significance was set to be P<0.05. Results: Thirty-five lupus patients and 40 healthy subjects were females (P=0.847). Vitamin D deficiency was observed in the case (42.1%) and control (11.4%) groups. The mean value of serum vitamin D3 level was 35.3 ng/mL in the control group, as well as 24.6 ng/mL and 21.3 ng/mL in patients with mild and severe SLE, respectively (P=0.024). Conclusion: In this study, high levels of 25-hydroxy vitamin D were observed among the healthy subjects compared to patients with SLE. Eventually, the level of vitamin D significantly decreased by increasing the severity of SLE activity.
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Messaurina, Aninditya Dwi, Agung Triono, Retno Palupi Baroto, Cahya Dewi Satria, and Sumadiono Sumadiono. "Hubungan antara Kadar 25-OH D3 dengan Derajat Fungsi Ginjal pada Pasien Lupus Sistemik Eritematosus." Sari Pediatri 21, no. 4 (January 31, 2020): 213. http://dx.doi.org/10.14238/sp21.4.2019.213-7.

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Latar belakang. Defisiensi vitamin D banyak ditemukan pada anak lupus eritematosus sistemik (LSE) dibandingkan dengan anak normal. Berbagai penelitian membuktikan defisiensi vitamin D berkontribusi terhadap perkembangan chronic kidney disease. Belum ada penelitian hubungan vitamin D dengan derajat fungsi ginjal pada anak Lupus. Tujuan. Mengetahui hubungan antara 25-hidroksivitamin D dengan derajat fungsi ginjal pada anak Lupus.Metode. Menggunakan desain cross sectional dengan melibatkan 62 anak Lupus di bagian Ilmu Kesehatan Anak RSUP Dr. Sardjito yang telah mendapatkan protokol dari Januari 2014 sampai April 2018. Hubungan antara kadar serum 25-hidroksivitamin D dan derajat fungsi ginjal dianalisis menggunakan Independent T-test, sedangkan jenis kelamin, kalsium, steroid, dan aktivitas penyakit dengan uji chi-square. Defisiensi vitamin D didefinisikan konsentrasi 25-hidroksivitamin D<20 ng/ml, sedangkan gangguan ginjal didefinisikan GFR<90/ml/mnt/1.73m2.Hasil. Sebagian besar subyek berjenis kelamin perempuan, 93,5% vs 6,5% dengan rerata usia 14,6±3,1 tahun, dan rerata skor Mex-SLEDAI 7,6±5,6. Secara keseluruhan 66% subyek penelitian mengalami defisiensi vitamin D. Analisis dengan Independent T-tes menunjukkan rerata vitamin D yang mengalami gangguan ginjal 14,14±4,9 lebih rendah dibandingkan normal dengan rerata 19,43±10,3 dengan perbedaan yang bermakna p=0,004. Jenis kelamin, kalsium, steroid, dan aktivitas penyakit tidak berpengaruh signifikan terhadap derajat fungsi ginjal, p>0,05.Kesimpulan. Terdapat hubungan signifikan 25-hidroksivitamin D dengan derajat fungsi ginjal pada anak lupus.
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Sukamto Koesnoe. "Peran Vitamin D dalam Aktivitas Penyakit Lupus Eritematosus Sistemik (LES)." MEDICINUS 35, no. 2 (April 1, 2022): 3–9. http://dx.doi.org/10.56951/medicinus.v35i2.87.

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Lupus eritematosus sistemik (LES) merupakan suatu penyakit autoimun sistemik yang menyebabkan terjadinya disregulasi yang luas pada sistem imun. Penyakit ini memiliki patofisiologi yang kompleks karena adanya interaksi antarfaktor yang dapat menghasilkan respons imun yang abnormal. Respons imun yang abnormal ini mengakibatkan timbulnya reaksi inflamasi di berbagai organ yang berujung pada terjadinya kerusakan jaringan dan organ. Studi menunjukkan bahwa vitamin D memiliki aktivitas sebagai imunomodulator sehingga berpotensi menjadi bagian dari tata laksana kasus LES. Potensi suplementasi vitamin D dalam perbaikan klinis pasien LES telah cukup banyak diteliti. Dalam beberapa studi, dijumpai efek positif dari pemberian suplementasi vitamin D pada pasien LES. Hal ini berkaitan dengan kondisi defisiensi vitamin D yang diketahui berasosiasi dengan aktivitas penyakit LES serta frekuensi eksaserbasi. Vitamin dalam bentuk aktifnya, calcitriol, juga diketahui memiliki peran penting dalam patogenesis LES. Suplementasi vitamin D dilaporkan dapat membantu mengurangi aktivitas penyakit serta memperbaiki kondisi klinis pasien LES.
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Witan, Kereun Yobelium, Elli Arsita, and Todung Donald Aposan Silalahi. "Kadar 25(OH)D pada Pasien Lupus Eritematosus Sistemik di Indonesia." Jurnal Kedokteran Meditek 28, no. 2 (May 7, 2022): 193–98. http://dx.doi.org/10.36452/jkdoktmeditek.v28i2.2267.

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Vitamin D memiliki peran dalam sistem kekebalan tubuh, terutama sistem imun adaptif dalam toleransi diri dan menghasilkan antibodi pada pasien dengan autoimun. Defisiensi vitamin D merupakan hal yang sering ditemukan pada pasien Lupus Eritematosus Sistemik (LES). Hal ini dapat dikarenakan pantangan terhadap paparan sinar matahari, insufisiensi ginjal, penggunaan obat–obatan yang menurunkan regulasi reseptor vitamin D, dan penggunaan sunscreen. Tujuan penulisan ilmiah ini adalah untuk mengetahui kadar vitamin D pada pasien LES di Indonesia. Data didapatkan dari jurnal penelitian yang diambil melalui Google Scholar, Proquest, Pubmed, dan Science Direct. Hasil pencarian didapatkan 4 artikel yang mengambil lokasi penelitian di Malang, 2 artikel di Jakarta, dan 1 artikel di Yogyakarta. Simpulannya adalah bahwa 63,74% pasien LES di Indonesia memiliki defisiensi kadar vitamin D yang disebabkan oleh kurangnya paparan sinar matahari, warna kulit, penggunaan sunblock, memiliki manifestasi klinis nefritis, penggunaan obat–obatan (kortikosteroid dan anti malaria), Indeks Masa Tubuh (IMT) di atas normal, kurangnya konsumsi makanan yang mengandung vitamin D, dan konsumsi suplemen vitamin D yang tidak adekuat.
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Attar, Suzan M., and Aisha M. Siddiqui. "Vitamin D Deficiency in Patients with Systemic Lupus Erythematosus." Oman Medical Journal 28, no. 1 (January 16, 2013): 42–47. http://dx.doi.org/10.5001/omj.2013.10.

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WALSH, NANCY. "Lupus Patients Have Extremely Low Levels of Vitamin D." Internal Medicine News 41, no. 12 (June 2008): 12. http://dx.doi.org/10.1016/s1097-8690(08)70668-1.

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Brown, Alex J., Adriana Dusso, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 277, no. 2 (August 1, 1999): F157—F175. http://dx.doi.org/10.1152/ajprenal.1999.277.2.f157.

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The vitamin D endocrine systems plays a critical role in calcium and phosphate homeostasis. The active form of vitamin D, 1,25-dihydroxyvitamin D3[1,25(OH)2D3], binds with high affinity to a specific cellular receptor that acts as a ligand-activated transcription factor. The activated vitamin D receptor (VDR) dimerizes with another nuclear receptor, the retinoid X receptor (RXR), and the heterodimer binds to specific DNA motifs (vitamin D response elements, VDREs) in the promoter region of target genes. This heterodimer recruits nuclear coactivators and components of the transcriptional preinitiation complex to alter the rate of gene transcription. 1,25(OH)2D3also binds to a cell-surface receptor that mediates the activation of second messenger pathways, some of which may modulate the activity of the VDR. Recent studies with VDR-ablated mice confirm that the most critical role of 1,25(OH)2D3is the activation of genes that control intestinal calcium transport. However, 1,25(OH)2D3can control the expression of many genes involved in a plethora of biological actions. Many of these nonclassic responses have suggested a number of therapeutic applications for 1,25(OH)2D3and its analogs.
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El Omri, Naoual, Fadwa Mekouar, Youssef Sekkach, Mohamed Jira, Mohamed El Qatni, Naoufal Assoufi, Salaheddine El Khader, Taoufik Amezyane, Driss Ghafir, and Rachid Eljaoudi. "Serum vitamin D and vitamin D receptor gene polymorphism in Moroccan patients with systemic lupus erythematosus." International Journal of Research in Medical Sciences 5, no. 3 (February 20, 2017): 811. http://dx.doi.org/10.18203/2320-6012.ijrms20170467.

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Background: Vitamin D plays an important role in the immunomodulation and could be involved in the development of autoimmune diseases such as systemic lupus erythematous (SLE). The study of the polymorphism of the Vitamin D Receptor (VDR) gene may be of interest in explaining the pathophysiology of SLE.Methods: In this study, we aimed to examine the characteristics of VDR gene BsmI polymorphism for the first time in Moroccan patients with SLE and their relationship with clinical manifestations of the disease. We also measured the serum level of 25-hyroxyvitamin D3 to assess its relation to such polymorphism.Results: The study included 66 SLE patients and 91 healthy controls. Our results showed that there were no differences observed in VDR genotypes and allelic distribution within the two groups. Both groups were in Hardy-Weinberg equilibrium, with no significant P values for the observed and expected genotype frequencies. 25-hyroxyvitamin D3 serum levels were the same in the two groups.Conclusions: Based on the results of the present study. We cannot verify any association between VDR gene BsmI polymorphism and SLE. This polymorphism could not be regarded as a genetic marker of the SLE. A larger study examining BsmI and other VDR gene polymorphisms is needed.
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Andreoli, L. "SP0155 Vitamin D and Systemic Lupus Erythematosus: When and How To Treat Vitamin D Insufficiency/deficiency." Annals of the Rheumatic Diseases 75, Suppl 2 (June 2016): 38.3–38. http://dx.doi.org/10.1136/annrheumdis-2016-eular.6346.

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Wang, Jingxuan, Yixuan Li, Liang Zhao, Fazheng Ren, and Huiyuan Guo. "Lactoferrin stimulates the expression of vitamin D receptor in vitamin D deficient mice." Journal of Functional Foods 55 (April 2019): 48–56. http://dx.doi.org/10.1016/j.jff.2019.02.012.

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Lubis, Ahmad Fauzi, Zuhrial Zubir, and Ananda Wibawanta Ginting. "The Relationship of Neutrophil Lymphocyte Ratio and Levels of Vitamin D against Disease Activity Systemic Lupus Erythematosus." International Journal of Research and Review 8, no. 10 (October 21, 2021): 320–25. http://dx.doi.org/10.52403/ijrr.20211043.

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Background: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of autoantibodies against cell nuclei and immune complexes involving multiple organ systems in the body. The Lupus Foundation estimates about 1.5 million cases of SLE in America and at least 5 million cases of SLE in the world and from year to year, the number of people with lupus also tends to increase. Several laboratory findings are also associated with signs and symptoms of SLE activity including the ratio of neutrophil lymphocytes and vitamin D levels. Method: This study is an observational analytic study using medical record data from central installation patients at H. Adam Malik Hospital in the period December 2019 to March 2021. The sample is calculated using the large proportion estimation formula. Then the distribution test was carried out with the Shapiro Wilk test. Bivariate analysis was carried out to determine the relationship between neutrophil lymphocyte ratio and vitamin D levels with the MEX SLEDAI score using the ANOVA test if the data was normally distributed. Results: 75 subjects participated in the study and there were 12 people (16%) experiencing mild systemic lupus erythematosus, 38 people (51%) moderate degree, and 25 people (33%) severe degree. The neutrophil-lymphocyte ratio was associated with systemic lupus erythematosus disease activity (p=0.001) and vitamin D levels were associated with systemic lupus erythematosus disease activity. Conclusion: Neutrophil-lymphocyte ratio and vitamin D levels are associated with systemic lupus erythematosus disease activity. Keywords: neutrophil lymphocyte ratio, vitamin D levels, systemic lupus erythematosus.
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Tedeschi, Sara K., Cynthia Aranow, Diane L. Kamen, Meryl LeBoff, Betty Diamond, and Karen H. Costenbader. "Effect of vitamin D on serum markers of bone turnover in SLE in a randomised controlled trial." Lupus Science & Medicine 6, no. 1 (September 2019): e000352. http://dx.doi.org/10.1136/lupus-2019-000352.

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ObjectiveBone health in SLE is adversely affected by vitamin D deficiency, inflammatory cytokines and glucocorticoid use. We hypothesised that vitamin D supplementation would increase markers of bone formation and decrease markers of bone resorption in SLE subjects.MethodsWe studied 43 vitamin D-deficient SLE subjects who participated in a 12-week randomised controlled trial of 2000–4000 IU/day vitamin D supplementation versus placebo. Subjects had inactive SLE (SLE Disease Activity Index ≤4) and were taking <20 mg prednisone daily at baseline. We assayed baseline and week 12 serum 25-hydroxyvitamin D, N-terminal propeptide of type 1 collagen (P1NP) and C-telopeptide (CTX). We tested the effect of vitamin D versus placebo on change (Δ) in P1NP and ΔCTX in an intention-to-treat analysis. Secondary analyses evaluated whether vitamin D affected bone turnover among subjects achieving vitamin D repletion (≥30 ng/mL) or currently taking glucocorticoids.Results28 subjects were randomised to vitamin D and 15 to placebo. Mean age was 39 years and 40% were using glucocorticoids at enrolment. Repletion was achieved by 46% in the vitamin D group versus none in the placebo group. Changes in bone turnover markers were not significantly different in the vitamin D group versus placebo group (median ΔP1NP −0.2 vitamin D group vs −1.1 placebo group (p=0.83); median ΔCTX +3.5 vitamin D group vs −37.0 placebo group (p=0.50)). The effect of vitamin D did not differ based on achieving vitamin D repletion or baseline glucocorticoid use.ConclusionVitamin D supplementation did not affect the 12-week change in bone turnover markers among SLE subjects in this trial.
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Shimada, Takashi, Yuji Yamazaki, Motoo Takahashi, Hisashi Hasegawa, Itaru Urakawa, Takeshi Oshima, Kaori Ono, et al. "Vitamin D receptor-independent FGF23 actions in regulating phosphate and vitamin D metabolism." American Journal of Physiology-Renal Physiology 289, no. 5 (November 2005): F1088—F1095. http://dx.doi.org/10.1152/ajprenal.00474.2004.

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FGF23 suppresses both serum phosphate and 1,25-dihydroxyvitamin D [1,25D] levels in vivo. Because 1,25D itself is a potent regulator of phosphate metabolism, it has remained unclear whether FGF23-induced changes in phosphate metabolism were caused by a 1,25D-independent mechanism. To address this issue, we intravenously administered recombinant FGF23 to vitamin D receptor (VDR) null (KO) mice as a rapid bolus injection and evaluated the early effects of FGF23. Administration of recombinant FGF23 further decreased the serum phosphate level in VDR KO mice, accompanied by a reduction in renal sodium-phosphate cotransporter type IIa (NaPi2a) protein abundance and a reduced renal 25-hydroxyvitamin D-1α-hydroxylase (1αOHase) mRNA level. Thus FGF23-induced changes in NaPi2a and 1αOHase expression are independent of the 1,25D/VDR system. However, 24-hydroxylase (24OHase) mRNA expression remained undetectable by the treatment with FGF23. We also analyzed the regulatory mechanism for FGF23 expression. The serum FGF23 level was almost undetectable in VDR KO mice, whereas dietary calcium supplementation significantly increased circulatory levels of FGF23 and its mRNA abundance in bone. This finding indicates that calcium is another determinant of FGF23 production that occurs independently of the VDR-mediated mechanism. In contrast, dietary phosphate supplementation failed to induce FGF23 expression in the absence of VDR, whereas marked elevation in circulatory FGF23 was observed in wild-type mice fed with a high-phosphate diet. Taken together, FGF23 works, at least in part, in a VDR-independent manner, and FGF23 production is also regulated by multiple mechanisms involving VDR-independent pathways.
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Peplow, Philip V. "False Positive ANA Testing In The Setting Of Hypovitaminosis D." Clinical Studies & Medical Case Reports 7, no. 3 (December 31, 2020): 1–5. http://dx.doi.org/10.24966/csmc-8801/100098.

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Vitamin D deficiency has been associated with autoimmune diseases, which include systemic lupus erythematosus, and may affect the outcome and activity of these diseases that result from aberrant activation of the immune system. Patients with the systemic autoimmune diseases may have a positive blood test for Antinuclear Antibodies (ANA). The ANA test is very sensitive for the diagnosis of autoimmune diseases but results in many false positives. It has been reported that up to 15% of completely healthy individuals have a positive ANA test without an autoimmune disease and that ANAs are measurable in approximately 25% of the population. Only about 10-13% of persons with a positive ANA test are found to have lupus. Vitamin D insufficiency/deficiency is prevalent in patients with autoimmune disease and vitamin supplementation has a therapeutic effect on disease severity and progression. Though there are many studies supporting the clinical picture that lupus patients are more prone to vitamin D deficiency, there are only a few articles that have considered the possibility that hypovitaminosis D is associated with false positive ANA testing. A case of an anemic patient who was initially evaluated and managed as a case of lupus is presented.
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Wang, Jiadian, Muzi Cui, Siyi Wang, Xiao Xue, Kerong Ren, ZhiLu Li, Saijia Li, and Pingping Yan. "Study on the Role of Vitamin D in Systemic Lupus Erythematosus." Journal of Advances in Medicine Science 4, no. 1 (February 25, 2021): 23. http://dx.doi.org/10.30564/jams.v4i1.2728.

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Vitamin D is a hormone precursor with multiple biological effects. It binds to vitamin D receptors on target cells. It is an important participant in the metabolism of calcium and phosphorus in vivo. It is closely related to cell cycle, cell proliferation, differentiation, apoptosis, signal transduction and immune regulation. Its role in the treatment of infection, tumor and even immune diseases has been gradually recognized and studied. Patients with systemic lupus erythematosus generally have decreased levels of active vitamin D, and low levels of vitamin D are associated with disease occurrence, disease activity and complications. In the past ten years, a large number of studies have been carried out on it globally to explore the role of vitamin D in the occurrence and development of systemic lupus erythematosus. This paper summarizes its recent research progress.
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Breslin, Leanne C., Pamela J. Magee, Julie M. W. Wallace, and Emeir M. McSorley. "An evaluation of vitamin D status in individuals with systemic lupus erythematosus." Proceedings of the Nutrition Society 70, no. 4 (August 24, 2011): 399–407. http://dx.doi.org/10.1017/s0029665111001613.

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Systemic lupus erythematosus (SLE) is a multi-system inflammatory disease where genetic susceptibility coupled with largely undefined environmental factors is reported to underlie the aetiology of the disease. One such factor is low vitamin D status. The primary source of vitamin D is endogenous synthesis following exposure of the skin to UVB light. Photosensitivity, sunlight avoidance and the use of sun protection factor in combination with medications prescribed to treat the symptoms of the disease, puts SLE patients at increased risk of vitamin D deficiency. Decreased conversion of 25-hydroxyvitamin D to the metabolically active form, 1,25-dihydroxyvitamin D3, is possible, due to renal impairment common in SLE putting additional stress on vitamin D metabolism. The majority of studies have identified low 25-hydroxyvitamin D in SLE patients, albeit using varying cut-offs (<25 to <80 nmol/l). Of these studies, fifteen have investigated a link between status and disease activity with conflicting results. Variation with disease activity index measures used alongside methodological limitations within the study design may partially explain these findings. This review discusses the importance of optimal vitamin D status in SLE, critically evaluates research carried out to date that has investigated vitamin D in SLE, and highlights the need for a well-designed observational study that controls for diet, medication use, dietary supplements, UV exposure and seasonality, that uses sensitive methods for measuring vitamin D status and disease activity in SLE to conclusively establish the role of vitamin D in SLE.
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Dusso, Adriana S., Alex J. Brown, and Eduardo Slatopolsky. "Vitamin D." American Journal of Physiology-Renal Physiology 289, no. 1 (July 2005): F8—F28. http://dx.doi.org/10.1152/ajprenal.00336.2004.

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The vitamin D endocrine system plays an essential role in calcium homeostasis and bone metabolism, but research during the past two decades has revealed a diverse range of biological actions that include induction of cell differentiation, inhibition of cell growth, immunomodulation, and control of other hormonal systems. Vitamin D itself is a prohormone that is metabolically converted to the active metabolite, 1,25-dihydroxyvitamin D [1,25(OH)2D]. This vitamin D hormone activates its cellular receptor (vitamin D receptor or VDR), which alters the transcription rates of target genes responsible for the biological responses. This review focuses on several recent developments that extend our understanding of the complexities of vitamin D metabolism and actions: the final step in the activation of vitamin D, conversion of 25-hydroxyvitamin D to 1,25(OH)2D in renal proximal tubules, is now known to involve facilitated uptake and intracellular delivery of the precursor to 1α-hydroxylase. Emerging evidence using mice lacking the VDR and/or 1α-hydroxylase indicates both 1,25(OH)2D3-dependent and -independent actions of the VDR as well as VDR-dependent and -independent actions of 1,25(OH)2D3. Thus the vitamin D system may involve more than a single receptor and ligand. The presence of 1α-hydroxylase in many target cells indicates autocrine/paracrine functions for 1,25(OH)2D3in the control of cell proliferation and differentiation. This local production of 1,25(OH)2D3is dependent on circulating precursor levels, providing a potential explanation for the association of vitamin D deficiency with various cancers and autoimmune diseases.
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Athanassiou, Lambros, Ifigenia Kostoglou-Athanassiou, Pavlos Tsakiridis, Eirini Devetzi, Maria Mavroudi, Pantelis Fytas, Michael Koutsilieris, and Panagiotis Athanassiou. "Vitamin D levels in Greek patients with systemic lupus erythematosus." Lupus 31, no. 1 (January 2022): 125–32. http://dx.doi.org/10.1177/09612033211066462.

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Objectives Vitamin D deficiency has been observed in autoimmune rheumatic diseases, such as rheumatoid arthritis. The aim was to study vitamin D in patients with systemic lupus erythematosus (SLE) and its relationship with disease activity. Methods In a cohort of 45 patients with SLE, 41 females and 4 males, aged 47.07 ± 2.17 years (mean ± SEM), and range = 21–79 years, 25(OH)D3 levels were determined by electrochemiluminescence. C3 and C4 levels were also analyzed. SLE disease activity was estimated by SLEDAI-2K. Observations were also performed in a control group matched for age and sex. Results In this cohort of SLE patients, 25(OH)D3 levels were 40.36 ± 2.41 nmol/L (mean ± SEM) as opposed to 60.98 ± 4.28 nmol/L in the control group ( p < 0.001, Student’s t test). Vitamin D levels were related to C3 ( p < 0.001, linear regression analysis), correlation coefficient 0.106, r2 = 0.011, and C4 ( p < 0.001); correlation coefficient 0.316 and r2 = 0.100; and inversely related to disease activity ( p < 0.001), correlation coefficient −0.572 and r2 = 0.327. 25(OH)D3 levels were 17.73 ± 1.20 nmol/L and 12.24 ± 0.93 nmol/L, in the groups without and with renal involvement, respectively ( p = 0.001, Student’s t test). Conclusions Vitamin D levels are low in SLE patients and are inversely related to disease activity. Routine screening for vitamin D levels should be performed in SLE patients.
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Duchow, Elizabeth G., Nancy E. Cooke, Jeremy Seeman, Lori A. Plum, and Hector F. DeLuca. "Vitamin D binding protein is required to utilize skin-generated vitamin D." Proceedings of the National Academy of Sciences 116, no. 49 (November 20, 2019): 24527–32. http://dx.doi.org/10.1073/pnas.1915442116.

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Vitamin D is produced in the skin following exposure to sunlight. Ultraviolet (UV) B (UVB, 280–310 nm) results in isomerization of 7-dehydrocholesterol to previtamin D that spontaneously isomerizes to vitamin D. This pool of skin-derived vitamin D is the major source of vitamin D for animals. However, the mechanisms by which it becomes available remain undefined. It has been assumed that cutaneous vitamin D is transported into the circulation by vitamin D binding protein (DBP), but experimental evidence is lacking. To determine whether cutaneous vitamin D is transported by DBP, we utilized DBP−/− mice that were made vitamin D-deficient. These animals lack measurable 25(OH)D in blood and are hypocalcemic. As controls, DBP+/+ animals were vitamin D depleted and made equally hypocalcemic. UV irradiation of DBP+/+ animals restored serum calcium and serum 25(OH)D while the same treatment of DBP−/− animals failed to show either a serum calcium or 25(OH)D response despite having normal vitamin D production in skin. Intravenous injection of small amounts of recombinant DBP to the vitamin D-deficient DBP−/− mice restored the response to UV light. These results demonstrate a requirement for DBP to utilize cutaneously produced vitamin D.
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Ospina-Caicedo, Ana Isabel, Alex Darío Cardona-Rincón, Juan Manuel Bello-Gualtero, Rafael Valle-Oñate, Consuelo Romero-Sánchez, Philippe Chalem-Choueka, and Gloria Vásquez Duque. "Lower Levels of Vitamin D Associated with Disease Activity in Colombian Patients with Systemic Lupus Erythematosus." Current Rheumatology Reviews 15, no. 2 (April 5, 2019): 146–53. http://dx.doi.org/10.2174/1573397114666181015161547.

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Background: Systemic Lupus Erythematosus (SLE) involves genetic, environmental, and hormonal alterations, including Vitamin D deficiency. Objective: To evaluate the association between vitamin D levels with anti-dsDNA, complement proteins, immunoglobulins levels and disease activity scores. Methods: : A cross-sectional study was performed. The levels of 25-OH vitamin D were measured in patients older than 18 years with SLE according to ACR/97 [American College of Rheumatology 1997] from 2013 to 2015. The association was assessed by Mann-Whitney U and Kruskal Wallis tests for continuous variables, and by the Chi or Fisher exact test for the nominal variables. Results: Sixty-nine patients were included; 82% were women; the mean age was 38.5 years; 36.2% had low levels of vitamin D with higher consumption [p=0.006] of C4 and C3 complement proteins, plus higher levels of anti-dsDNA. Lower values of vitamin D were observed in patients with moderate to severe activity [p=0.0001] by SLEDAI [Systemic Lupus Erythematosus Activity Index] and general domain [p=0.039] and renal domain [p=0.009] by BILAG [British Isles Lupus Assessment Group] 2004. The mean vitamin D levels were higher in the group not receiving steroids when compared to those groups with dosages of 0.5-1mg/kg/d [p=0.048]. Conclusion: Lower levels of vitamin D are associated with greater complement protein consumption and higher disease activity rates. Therefore, it is important to evaluate vitamin D supplementation in patients with SLE as part of the treatment, especially when it includes the use of steroids.</P>
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Correa-Rodríguez, María, Gabriela Pocovi-Gerardino, Irene Medina-Martínez, Sara Del Olmo-Romero, Norberto Ortego-Centeno, and Blanca Rueda-Medina. "Vitamin D Supplementation Is Associated with Disease Activity in Systemic Lupus Erythematosus Patients." Proceedings 61, no. 1 (October 30, 2020): 1. http://dx.doi.org/10.3390/iecn2020-07013.

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Systemic lupus erythematosus (SLE) is a chronic disease characterized by inflammatory response and abnormal autoimmune disease. Vitamin D is essential in phosphorus-calcium metabolism, has immunosuppressive properties, and is considered a therapeutic option. Controversy exists about the role of this vitamin in the pathogenesis of SLE. Thus, the aim of this study was to investigate the influence of the dietary intake of vitamin D and its supplementation in a cohort of patients with SLE. A cross-sectional study including a total 285 patients with SLE was conducted (248 females and 26 males; mean age 46.99 ± 12.89 years). The SLE disease activity index (SLEDAI-2K) and the SLICC/ACR damage index (SDI) were used to assess disease activity and disease-related damage, respectively. Levels of C-reactive protein (CRP; mg/dL), homocysteine (Hcy; mol/L), anti-double stranded DNA antibodies (anti-dsDNA) (IU/mL), complement C3 (mg/dL), and complement C4 (mg/dL), among other biochemical markers, were measured. The dietary intake of vitamin D and the intake of vitamin D supplement were obtained via a 24-h patient diary. A share of 57.1% of the patients took vitamin D supplements and the average of dietary vitamin D was 2.08 ± 2.94 μg/day. Note that 98.2% of patients did not reach the recommended dietary intakes for vitamin D intake. Multivariate regression analysis revealed that clinical and laboratory variables are not significantly affected by vitamin D intake levels after adjusting for age, gender, energy intake, and medical treatment (immunosuppressants, corticosteroids, and antimalarials). Patients with SLE who took vitamin D supplements had significantly higher serum complement C3 levels compared to patients who did not take them after adjusting for covariates (110.28 ± 30.93 vs. 107.38 ± 24.18; p = 0.018). Our findings suggest a potential impact of supplementation of vitamin D on the activity of SLE. Future longitudinal research on SLE patients, including intervention trials, are required to validate these preliminary data.
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Reynolds, John A., and Ian N. Bruce. "Vitamin D in systemic lupus erythematosus: potential beyond bone health." International Journal of Clinical Rheumatology 4, no. 3 (June 2009): 297–309. http://dx.doi.org/10.2217/ijr.09.19.

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Mahmoud, Heba, Mahmoud Ahmed, Shaimaa Abd elkareem, and Hanaa Rabie. "Relation between Vitamin D Receptors Gene Polymorphism and Lupus Nephritis." Egyptian Journal of Medical Research 3, no. 3 (July 1, 2022): 146–54. http://dx.doi.org/10.21608/ejmr.2022.256658.

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48

Pakpoor, Julia, and Jina Pakpoor. "Vitamin D Deficiency and Systemic Lupus Erythematosus: Cause or Consequence?" Oman Medical Journal 28, no. 4 (July 16, 2013): 295. http://dx.doi.org/10.5001/omj.2013.83.

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49

Cutolo, M., K. Otsa, S. Paolino, M. Yprus, T. Veldi, and B. Seriolo. "Vitamin D involvement in rheumatoid arthritis and systemic lupus erythaematosus." Annals of the Rheumatic Diseases 68, no. 3 (February 12, 2009): 446–47. http://dx.doi.org/10.1136/ard.2008.093476.

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50

Monticielo, O. A., J. A. B. Chies, G. G. Rucatti, M. S. Carlucci, N. C. Sartor, E. A. Souza, P. S. B. Rabaioli, R. Pirolli, R. M. Xavier, and J. C. T. Brenol. "AB0210 Vitamin D and cardiovascular disease in systemic lupus erythematosus." Annals of the Rheumatic Diseases 71, Suppl 3 (June 2013): 649.11–649. http://dx.doi.org/10.1136/annrheumdis-2012-eular.210.

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