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Maternal vitamin D deficiency, refractory neonatal hypocalcaemia, and nutritional rickets
  1. S D Shenoy1,
  2. P Swift1,
  3. D Cody1,
  4. J Iqbal2
  1. 1Children’s Hospital, University Hospitals of Leicester NHS Trust, UK
  2. 2Department of Chemical Pathology, University Hospitals of Leicester NHS Trust, UK
  1. Correspondence to:
    Dr D Cody
    Department of Paediatrics, Children’s Hospital, University Hospitals of Leicester NHS Trust, Leicester, UK;

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We read with interest the articles by Allgrove1 and Ladhani and colleagues2 which highlighted the re-emergence of vitamin D deficiency and nutritional rickets as a major public health problem in the UK, especially in the “at risk” ethnic minority groups.

We would like to present our experience from a single centre of maternal vitamin D deficiency, neonatal hypocalcaemia, and nutritional rickets. Leicester City has an estimated proportion of 28% South Asians (Census 2001) and an increasing number of other ethnic groups, including an estimated recently arrived 10 000 people of Somalian origin. Studies in our centre have confirmed that significant numbers of south Asian mothers have vitamin D deficiency at the end of pregnancy, and substantial numbers of children have infantile and adolescent rickets, some of whom have extremely severe bony deformities. In addition there have been increasing numbers of late (5–10 days of age) and late-late (2–12 weeks of age) neonatal hypocalcaemia, presenting predominantly with seizures, which, despite intensive calcium and vitamin D treatment have been difficult to correct biochemically. All the mothers had vitamin D deficiency and were supplemented with oral vitamin D and calcium supplements. None of the mothers, despite being within high risk ethnic groups, had vitamin D supplementation in pregnancy despite the recommendation by COMA (Committee on Medical Aspects of Food Policy in UK) that all at-risk pregnant and lactating mothers should receive 10 μg (400 IU) of vitamin D daily.3 Furthermore, a local audit involving clinicians in antenatal care including general practitioners, midwives, and obstetricians showed that, while health professionals were aware of this issue, there was no clear policy followed.4

At birth, the newborn’s vitamin D status is directly related to maternal vitamin D status and materno-fetal transfer of vitamin D and its metabolites in pregnancy. Babies whose mothers have a marked vitamin D deficiency will have a compromised vitamin D status,5 and this has important long term implications for the health of the offspring.6

As noted by Allgrove there were national and local “stop rickets campaigns” in the 1970s, and in Leicester this appeared to reduce but not remove the spectre of nutritional rickets. In view of our more recent experiences confirming an increasing frequency and severity of neonatal vitamin D deficiency we would strongly agree with Allgrove1 and Ladhani and colleagues2 in emphasising the importance of vitamin D supplementation. It is certainly a serious indictment of our community preventative services not to have protected “high risk” mothers and their offspring. We would propose an urgent review and implementation of the national recommendations on vitamin D supplementation in “high risk” pregnant women and infants to prevent associated infantile co-morbidity.



  • Competing interests: none declared