The role of parathyroid hormone during pregnancy on the relationship between maternal vitamin D deficiency and fetal growth restriction: a prospective birth cohort study

Previous studies have shown conflicting findings regarding the relationship between maternal vitamin D deficiency (VDD) and fetal growth restriction (FGR). We hypothesised that parathyroid hormone (PTH) may be an underlying factor relevant to this potential association. In a prospective birth cohort study, descriptive statistics were evaluated for the demographic characteristics of 3407 pregnancies in the second trimester from three antenatal clinics in Hefei, China. The association of the combined status of vitamin D and PTH with birth weight and the risk of small for gestational age (SGA) was assessed by a multivariate linear and binary logistic regression. We found that declined status of 25-hydroxyvitamin D is associated with lower birth weight (for moderate VDD: adjusted beta= -49 center dot 4 g, 95 % CI -91 center dot 1, -7 center dot 8,P< 0 center dot 05; for severe VDD: adjusted beta= -79 center dot 8 g, 95 % CI -127 center dot 2, -32 center dot 5,P< 0 center dot 01), as well as ascended levels of PTH (for elevated PTH: adjusted beta= -44 center dot 5 g, 95 % CI -82 center dot 6, -6 center dot 4,P< 0 center dot 05). Compared with the non-VDD group with non-elevated PTH, pregnancies with severe VDD and elevated PTH had the lowest neonatal birth weight (adjusted beta= -124 center dot 7 g, 95 % CI -194 center dot 6, -54 center dot 8,P< 0 center dot 001) and the highest risk of SGA (adjusted risk ratio (RR) = 3 center dot 36, 95 % CI 1 center dot 41, 8 center dot 03,P< 0 center dot 01). Notably, the highest risk of less Ca supplementation was founded in severe VDD group with elevated PTH (adjusted RR = 4 center dot 67, 95 % CI 2 center dot 78, 7 center dot 85,P< 0 center dot 001). In conclusion, elevated PTH induced by less Ca supplementation would further aggravate the risk of FGR in pregnancies with severe VDD through impaired maternal Ca metabolism homoeostasis.