scholarly journals Clinical significance of vitamin D deficiency and receptor gene polymorphism in systemic lupus erythematosus patients

2017 ◽  
Vol 39 (3) ◽  
pp. 159-164 ◽  
Author(s):  
Kamel H. Gado ◽  
Tarek H. Gado ◽  
Rasha M. Abdel Samie ◽  
Noha M. Khalil ◽  
Safa L. Emam ◽  
...  
Lupus ◽  
2013 ◽  
Vol 22 (7) ◽  
pp. 750-751 ◽  
Author(s):  
J Bogaczewicz ◽  
B Kaleta ◽  
A Sysa-Jedrzejowska ◽  
E Robak ◽  
J Lukaszkiewicz ◽  
...  

2019 ◽  
Author(s):  
Shi-kun Yang ◽  
Na Liu ◽  
Ying-qiu Zhu ◽  
Wei-juan Zhang ◽  
Na Song ◽  
...  

Abstract It is still unclear whether there was an association between vitamin D receptor (VDR) gene polymorphism and systemic lupus erythematosus (SLE). This meta analysis including 19 studies were performed using Stata software. In our analysis, VDR ApaI polymorphism was correlated with SLE susceptibility in general populations (AA vs aa: P=0.003; AA+Aa vs aa: P=0.000). VDR gene ApaI and BsmI polymorphism were correlated with SLE susceptibility in Caucasian populations (BB vs Bb+bb: p=0.005; B vs b: P=0.026; AA vs aa: P =0.038). VDR BsmI and FokI polymorphism were correlated with SLE in African populations (BB+Bb vs bb: P=0.000; FF vs Ff +ff: P=0.000; F vs f: P=0.000; FF vs ff: P=0.000; FF+Ff vs ff: P=0.000). VDR ApaI polymorphism was correlated with SLE in Asian populations (AA+Aa vs aa) when stratified by race. Additionly, ApaI polymorphism was correlated with SLE in female subjects (AA vs aa: P =0.022) when stratified by gender. But there was no association between VDR TaqI polymorphism and SLE susceptibility in our analysis.


2006 ◽  
Vol 26 (10) ◽  
pp. 949-950 ◽  
Author(s):  
Chang-Hai Tsai ◽  
Chung-Ming Huang ◽  
Sui-Foon Lo ◽  
Lei Wan ◽  
Fuu-Jen Tsai

2018 ◽  
Vol 12 (1) ◽  
pp. 226-247 ◽  
Author(s):  
Alessandra Nerviani ◽  
Daniele Mauro ◽  
Michele Gilio ◽  
Rosa Daniela Grembiale ◽  
Myles J. Lewis

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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