INTRODUCTION
25-hydroxy vitamin D (25(OH)D) is the most abundant form of vitamin D and is recommended for measurement of the total body concentration of the vitamin (1). The definition of hypovitaminosis D in pregnancy is having a 25(OH)D below 50nmol/l, whereas in newborns the cutoff for deficiency is 30nmol/L. However, it has been argued that the ideal level in adults should be >75 nmol/L (30 ng/mL) (2). Vitamin D is essential to the human body. Historically, the vitamin is known for its role in calcium and phosphate metabolism, with deficiencies leading to rickets and osteomalaci. As important, upcoming data have shown that vitamin D is linked to numerous essential functions such as reducing inflammation, modulation of the neuromuscular system, regulating glucose metabolism and cell growth (by modulating the genes regulating cell proliferation, differentiation and apoptosis) (3,4) In pregnancy low vitamin D has been associated with increased risk for preeclampsia, preterm rupture of membranes, small for gestational age fetus, and dystocia but according to WHO the evidence is low and more trials are warranted (2,5,6). Importantly, the fetal level of vitamin D entirely depends on 25(OH)D transfer over the placenta. It is a general assumption that the fetal vitamin D level is lower than the maternal and that there is no transport of 25(OH)D over the placenta with low maternal levels, though of low grade evidence (5,7,8). In the United Arab Emirates, up to 69% of pregnant women has 25(OH)D < 30nmol/L, and the awareness of the importance, also in well-educated women is low (9).
This study aimed to study the maternal and umbilical cord levels of 25(OH)D at delivery and to investigate if obesity, diabetes, amount of supplementation, delivery mode influenced the maternal level and the correlation between maternal and umbilical cord blood levels. Secondary to study certain risks associated with 25(OH)D levels < 50nmol/L.