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.