Vitamin D receptor gene polymorphism influences lipid profile in patients with juvenile idiopathic arthritis
Clin Rheumatol (2018). https://doi.org/10.1007/s10067-018-4264-2
Jelena Bašić Email author Jelena Vojinović Tatjana Jevtović-Stoimenov Milena DespotovićGordana SušićDragana LazarevićVuk MiloševićMina CvetkovićDušica Pavlović
- Knee osteoarthritis strongly associated with low Boron – 2015
- More UVB at 12th week of pregnancy associated with less Juvenile Idiopathic Arthritis – Oct 2018
- Rheumatoid arthritis and many other diseases associated with low Boron – 2012
Items in both categories Rheumatoid Arthritis and Infant-Child are listed here:
- Taking vitamin D for health problems has raised D levels a bit (child Arthritis this case) – July 2021
- World Arthritis Day - Children who suffer with arthritis are lacking Vitamin D - Oct 2019
- More UVB at 12th week of pregnancy associated with less Juvenile Idiopathic Arthritis – Oct 2018
- Arthritic children have low vitamin D (84 percent of the studies) – May 2018
- Juvenile idiopathic arthritis 2.2 X more likely if poor Vitamin D Receptor – Aug 2018
- Juvenile Rheumatoid Arthritis 8 X more likely if poor Vitamin D receptor – Dec 2017
- Children with Idiopathic arthritis have very low Boron levels – Jan 2016
- 2,000 IU vitamin D recommended for pediatric rheumatology – May 2015
- Juvenile Idiopathic Arthritis is strongly associated with low vitamin D – many studies
- Juvenile Rheumatoid Arthritis associated with low vitamin D, but how low – meta-analysis Jan 2013
The risk of 43 diseases at least double with poor Vitamin D Receptor as of Oct 2019
PDF is available free at Sci-Hub 10.1007/s10067-018-4264-2
Vitamin D receptor (VDR) gene FokI (rs2228570) polymorphism was postulated to influence outcome of several inflammatory diseases. The aim of this study was to evaluate the influence of rs2228570 polymorphism on lipid profile and on outcome in patients with juvenile idiopathic arthritis (JIA) treated with etanercept. A total of 153 subjects (62 JIA patients and 91 controls) were screened for the rs2228570 using the PCR-RFLP method. Lipid profile (cholesterol, triacylglycerol, HDL-C, and LDL-C) was determined using standard biochemical analysis in controls, while in JIA patients, it was determined prior to and 12 months after anti-TNF (etanercept) therapy. Clinical outcome was assessed using the JIA—American College of Rheumatology (ACR) response criteria.
There were significant differences in the distribution of genotypes (p = 0.024) and alleles (p = 0.006; OR = 2.222, 95% CI 1.136–4.348) of the rs2228570 between patients and controls. Etanercept treatment significantly increased HDL-C levels (p = 0.006) in JIA patients with FF genotype in comparison to baseline values. No significant differences were seen in JIA—ACR 30/50/70 responses at month 12 between FF and Ff/ff genotype carriers. This is the first study to demonstrate the protective effect of the VDR FokI FF genotype on lipid profile in JIA patients treated with etanercept. However, this has to be confirmed in a larger cohort of patients.