Pregnancy and Vitamin D Deficiency
Posted by: Kevin FlattIt is well recognised that maternal vitamin D deficiency during pregnancy and during the period of breastfeeding contributes to the development of rickets in infancy.
However, seizures in infants during the first month after birth caused by a deficiency of calcium in the blood, as a consequence of maternal vitamin D deficiency is not well described in western societies.
In 1991, the Committee on Medical Aspects of Food Policy recommended that all pregnant and lactating mothers should receive 10 micrograms vitamin D (400 IU) daily (Department of Health Dietary reference values for food energy and nutrients for the United Kingdom London: HMSO 1991. Report on health and social subjects 41).
This policy has not been implemented widely.
It is not uncommon to find vitamin D insufficiency in otherwise, healthy pregnant women.
Infants born to such mothers have reduced umbilical cord blood concentrations of 25-hydroxycholecalciferol (the first step in the biologic conversion of vitamin D3 to the more active form, calcitriol. It is more potent than vitamin D3).
In addition, breast milk contains only about 1 microgram of vitamin D per litre. This varies according to maternal vitamin D status (Am J Dis Child 1985, 139:1134-7).
Infants born to mothers who are deficient in vitamin D and or calcium, usually due to cultural modifications in their diets or clothing habits, and in addition are breastfed, are at risk of developing vitamin D deficiency and a deficiency of calcium.
Researchers from Queensland, Australia, and the UK presented a case in the September 2007 issue of Nutrition Journal of neonatal seizures (seizures in an infant during the first month after birth) secondary to hypocalcaemia (a deficiency of calcium in the blood) where the only other abnormal findings were low vitamin D levels both in the infant and in the mother, and low levels of calcium in the baby.
Case Presentation
A one week old, full term male infant presented to Accident and Emergency with generalised seizures. He was exclusively breast fed since birth. Both parents were vegetarians, from Asian origin, and mother dressed in her cultural customs, where most of her body was covered. Mother was neither taking nutritional, nor vitamin supplements during pregnancy.
Physical as well as neurological examinations were within normal limits. His parents had recorded the “attacks” by video camera, and tonic-clonic generalised movements were well identified on the screen. Magnetic resonance imaging of the brain was normal. Electroencephalography showed no epileptiform phenomenon.
Other than low vitamin D and calcium levels all other laboratory results (liver function tests, urea and electrolytes, C reactive protein, lumbar puncture, blood culture, lactate) were normal.
Baby did not receive anti-epileptic medications.
Within 6 hours of admission, once the initial laboratory tests became available, the patient was commenced on vitamin D (100 nanograms/kg once a day, which were reduced to 50 nanograms/kg/day after 1 week), and calcium supplements (0.25 millimole/kg/day).
(Note: Very small amounts were administered for a very young baby).
After four days the calcium levels had returned to normal. He remained on vitamin D until ten weeks of age and then was changed onto Abidec 0.6 mls/day (vitamin A, B, C and D supplement).
His seizures ceased within three days of starting treatment.
After 6 months, the baby was doing well, with normal calcium levels and normal total vitamin D levels, and his development was according to his chronological age.
Our case illustrates the importance of checking the calcium levels in neonates (infants during the first month after birth) who present with seizures and in those found to have a deficiency of calcium in the blood to check their vitamin D status as this is an easily correctable condition.
Extracted and adapted from: Laxmi Camadoo, Rebecca Tibbott and Fernando Isaza. Maternal vitamin D deficiency associated with neonatal hypocalcaemic convulsions. Nutrition Journal 2007, 6:23doi:10.1186/1475-2891-6-23. © 2007 Camadoo et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
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