Neonatal mortality rates in Indonesia are still at an alarming rate, with preterm birth as one of the causes. Nutritional deficiencies such as low level of vitamin D is suspected to be the risk factors of preterm birth but still a little knowledge about it. Vitamin D metabolism includes 25-hydroxyvitamin D3 (25(OH)D3) and 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), as the inactive and active form, with the help of 1α-hydroxylase (CYP27B1) enzyme. Our study aims to determine the differences of 25(OH)D3, 1,25(OH)2D3 and CYP27B1 enzyme in term and preterm birth. A cross-sectional study was performed in Cipto Mangunkusumo National General Hospital, Jakarta, Indonesia, in January–June 2017. The blood sample was taken soon after delivery, to examine maternal 25(OH)D3 and 1,25(OH)2D3 in serum and tissue placenta, as well as placental CYP27B1 enzyme. Statistical analysis using SPPS version 20 was used to find significances. There were a total of sixty subjects in this study, with term-preterm birth group ratio 1:1. We found that placental 25(OH)D3 was significantly low (P = 0⋅001), and CYP27B1/25(OH)D3 ratio was high in preterm birth. Also, there were significant negative correlations found in CYP27B1 level and both placental 25(OH)D3 (r 0⋅481, P < 0⋅001) and 1,25(OH)2D3 (r −0⋅365, P = 0⋅004) levels. Our study concludes that preterm birth showed lower placental 25(OH)D3 status, and higher CYP27B1/25(OH)D3 ratio compared to term pregnancy.

The ability to synthesise sufficient vitamin D through sunlight in human subjects can be limited. Thus, diet has become an important contributor to vitamin D intake and status; however, there are only a few foods (e.g. egg yolk, oily fish) naturally rich in vitamin D. Therefore, vitamin D-enriched foods via supplementing the animals’ diet with vitamin D or vitamin D fortification of foods have been proposed as strategies to increase vitamin D intake. Evidence that cholecalciferol (vitamin D3) and calcifediol (25(OH)D3) content of eggs, fish and milk increased in response to vitamin D3 supplementation of hens, fish or cows’ diets was identified when vitamin D-enrichment studies were reviewed. However, evidence from supplementation studies with hens showed only dietary 25(OH)D3, not vitamin D3 supplementation, resulted in a pronounced increase of 25(OH)D3 in the eggs. Furthermore, evidence from randomised controlled trials indicated that a 25(OH)D3 oral supplement could be absorbed faster and more efficiently raise serum 25(OH)D concentration compared with vitamin D3 supplementation. Moreover, evidence showed the relative effectiveness of increasing vitamin D status using 25(OH)D3 varied between 3·13 and 7·14 times that of vitamin D3, probably due to the different characteristics of the investigated subjects or study design. Therefore, vitamin D-enrichment or fortified foods using 25(OH)D3 would appear to have advantages over vitamin D3. Further well-controlled studies are needed to assess the effects of 25(OH)D3 enriched or fortified foods in the general population and clinical patients.