Routine screening for vitamin D deficiency in early pregnancy

To the Editor: We wish to report Queensland data regarding vitamin D levels during pregnancy, to contribute to the debate on screening during pregnancy raised in Lau and colleagues’ article1 and Ebeling’s accompanying editorial.2

In 2009, we measured serum 25-hydroxyvitamin D (25[OH]D) levels, using a DiaSorin radioimmunoassay (DiaSorin, Stillwater, Minn, USA), in 75 women who attended general antenatal clinics at the Royal Brisbane and Women’s Hospital (RBWH) and Mater Mothers’ Hospital. Both institutions’ Human Research Ethics Committees approved the study. Participants gave written consent. The RBWH Private Practice Fund covered pathology expenses.

Fifty-seven of the 75 women were white; the remainder were Asian (five), Indian Subcontinental (seven), Polynesian (four), Middle Eastern (one) and black African (one). Mean age was 28.6 years (SD, 5.4 years), mean gestational age was 28.7 weeks (SD, 2.7 weeks) and mean body mass index was 26.4 kg/m2 (SD, 5.5 kg/m2). Median serum 25(OH)D level was 92 nmol/L (interquartile range, 74–118 nmol/L). Using cut-offs of < 25 nmol/L for deficiency and < 50 nmol/L for insufficiency, two women were vitamin D deficient (one was Middle Eastern and one was South-East Asian) and five women were vitamin D insufficient (three were white, with lowest serum 25[OH]D level of 40 nmol/L, and two were Indian Subcontinental). The result of a Fisher exact test suggested an association with ethnicity (P = 0.01). A χ2 value of 21.36 (P < 0.001) confirmed that the proportions of deficiency and insufficiency in our study population were significantly different to those of Lau et al’s study population. The majority of serum samples (40) were obtained in winter, followed by spring (21), summer (10) and autumn (three). Six of the seven results of deficiency and insufficiency were from samples obtained in winter; the other was from a sample obtained in September. Excluding autumn, categorical and continuous analyses showed borderline significant variation of 25(OH)D level by season (Mann–Whitney U test [P = 0.08] and Kruskal–Wallis test [P = 0.08], respectively).

Several factors may account for the difference in vitamin D deficiency and insufficiency prevalence between our study and that of Lau et al. The most obvious is the “Sunshine State” factor, because several studies in southern states have reported higher prevalence of vitamin D insufficiency than in our study.3-5 In Lau et al’s study, a large proportion of women were at high risk of vitamin D deficiency (only 19% were white) and the women were recruited from a gestational diabetes mellitus clinic. Care should be taken in extrapolating such findings to the wider population. Although our study was not population based, it included a majority white and healthy general obstetric population, rather than sampling at a clinic where women are at high risk of vitamin D insufficiency.

We are not asserting that gestational vitamin D levels are unimportant. The increasing incidence of rickets in Australia,2 along with other potential hazards, dictate that increased awareness is mandatory. However, as opposed to routine screening in all pregnancies, our data suggest that local assessment of vitamin D status and demographic risk factors (in gestational diabetes mellitus and general obstetric populations) should be the priority.