Women with recurrent spontaneous abortion have decreased 25(OH) vitamin D and VDR at the fetal-maternal interface.
Braz J Med Biol Res. 2017 Sep 12;50(11):e6527. doi: 10.1590/1414-431X20176527.
Li N1, Wu HM1, Hang F1, Zhang YS2, Li MJ1.
A good level of Vitamin D at the placenta and fetus requires both a good level in blood and a good vitamin D receptor
- Miscarriage in first trimester 2.5X more likely if less than 20 ng of vitamin D – July 2015
- Search VitaminDiiki for MISCARRIAGE OR "Spontaneous abortion" 377 items as of Sept 2017
- Vitamin D genes and pregnancy – 7th study - Sept 2017
- Preterm birth 2X more likely if poor Vitamin D Receptor, 9 X if also had previous miscarriage – June 2017
- Second miscarriage associated with low vitamin D – review June 2018
Immunological mechanisms have been proposed to underlie the pathogenesis of recurrent spontaneous abortion (RSA). Vitamin D has a potent immunomodulatory effect, which may affect pregnancy outcome. The objective of this study was to investigate 25-hydroxyvitamin D [25(OH) D] concentration and vitamin D receptor (VDR) expression in the decidual tissues of RSA patients. Thirty women with RSA (RSA group) and thirty women undergoing elective abortion (control group) were recruited during 2016 from gynecology outpatient clinics. We measured 25(OH) D, interleukin (IL)-17, IL-23, transforming growth factor β (TGF-β), VDR and 1-α-hydroxylase (CYP27B1) in decidual tissues collected during the abortion procedure. In the RSA group, 25(OH) D and TGF-β were significantly decreased while IL-17 and IL-23 were significantly increased compared with the control group.
VDR expression was significantly decreased in the RSA group compared with the control group. Logistic regression analysis showed a significant negative correlation between 25(OH) D in decidual tissues and RSA. These results indicated that vitamin D concentrations in the decidua are associated with inflammatory cytokine production, suggesting that vitamin D and VDR may play a role in the etiology of RSA.
PMID: 28902929 DOI: 10.1590/1414-431X20176527