() IV 1,550 Among pregnant women in a After adjusting for potential confounders, there Deficient:<50 maternity service that was an association between GDM and early nmol/L (n=849 Australian recommends routine pregnancy vitamin D deficiency (OR 6.90 [1.66, [55%]) study antenatal screening and 28.7]; p=0.008) or insufficiency (OR 7.6 (1.83, Insufficient: 50-74 advises supplementation 32.0];p=0.005) compared to replete. nmol/L (n=571 where necessary, Vitamin D [37%]) serum concentrations were Replete: >75nmol/L measured in early and late (n=130 [8%]) pregnancy. The relationship between initial vitamin D status, maternal factors and pregnancy outcomes were estimated. () IV 399 Pregnant women living in an A difference of one standard deviation in Mean (+/- SD) Australian subtropical maternal 25-hydroxy vitamin D was inversely fasting plasma Australian environment. related to fasting glucose (fasting glucose lower glucose: study by 0.047 mmol/l, P=0.012) when assessed with 4.5 +/- 0.4 mmol/l. All patients underwent a multiple linear regression after adjusting for blinded 75-g oral glucose Mean (+/- SD) confounders. tolerance test at 24-32 (target serum 25(HO)D: 28) weeks' gestation. Maternal 25-hydroxy vitamin D correlated with 132.5 +/- 44.0 beta-cell function as estimated by the nmol/l. homeostasis model cell function equation (r=0.131, P=0.009), but not with the homeostasis model assessment of insulin resistance. An association between mid-gestational 25(HO)D and fasting glucose was confirmed in a largely normoglycaemic and vitamin D-replete pregnant population. The correlation between 25-hydroxy vitamin D and beta-cell function suggests that vitamin D may influence glucose metabolism through this mechanism.
() IV Australian study 1,550 Among pregnant women in a maternity service that recommends routine antenatal screening and advises supplementation where necessary, Vitamin D serum concentrations were measured in early and late pregnancy. The relationship between initial vitamin D status, maternal factors and pregnancy outcomes were estimated. After adjusting for potential confounders, there was an association between GDM and early pregnancy vitamin D deficiency (OR 6.90 [1.66, 28.7]; p=0.008) or insufficiency (OR 7.6 (1.83, 32.0];p=0.005) compared to replete. Deficient:<50 nmol/L (n=849 [55%]) Insufficient: 50-74 nmol/L (n=571 [37%]) Replete: >75nmol/L (n=130 [8%]) () IV Australian study 399 Pregnant women living in an Australian subtropical environment. All patients underwent a blinded 75-g oral glucose tolerance test at 24-32 (target 28) weeks' gestation. A difference of one standard deviation in maternal 25-hydroxy vitamin D was inversely related to fasting glucose (fasting glucose lower by 0.047 mmol/l, P=0.012) when assessed with multiple linear regression after adjusting for confounders. Maternal 25-hydroxy vitamin D correlated with beta-cell function as estimated by the homeostasis model function equation (r=0.131, P=0.009), but not with the homeostasis model assessment of insulin resistance. An association between mid-gestational 25(HO)D and fasting glucose was confirmed in a largely normoglycaemic and vitamin D-replete pregnant population. The correlation between 25-hydroxy vitamin D and beta-cell function suggests that vitamin D may influence glucose metabolism through this mechanism. Mean (+/- SD) fasting plasma glucose: 4.5 +/- 0.4 mmol/l. Mean (+/- SD) serum 25(HO)D: 132.5 +/- 44.0 nmol/l. cell
Vitamin%20D%20evidence%20evaluation%2022May17.docx