Background

Vitamin D deficiency is a public health issue which affects a large proportion of the population. Pregnant women and their infants are particularly prone to the risks of this deficiency. Maternal and infants vitamin D levels are highly correlated and low vitamin D levels during pregnancy have been linked to various health outcomes in the offspring. Few cases of hypocalcaemic seizures secondary to vitamin D deficiency have been reported in the literature. We reported here, a case of neonatal convulsions secondary to vitamin D deficiency.

1 Observation

A 25 days old, full term male infant presented two episodes of generalized seizures. Physical examination was within normal. Laboratory investigations in blood, revealed low calcium level at 5.5 mg/dl, elevated phosphatemia level at 9.6 mg/dl and high parathormone (PTH) level at 133.4 pg/ml (N:15-65). Urinary calcium was low at 7.6 mg/24 hours. Other laboratory results were normal. Unfortunately, 25 hydroxy vitamin D assay was not available in the infant but it was low in the mother at 12.9 ng/ml. In this infant hypocalcemia was presumably due to vitamin D deficiency as other causes were unlikely.

The patient was commenced on vitamin D and calcium supplements during some weeks which allowed normalization of calcium levels.

After treatment cessation for several months, the infant was doing well. His development was according to his chronological age. His calcium, phosphatemia and PTH levels were within normal ranges without any treatment.

At nine months of age, without treatment, calcemia level was at 10.1mg/dl, phosphatemia level was at 5.6 mg/dl, and parathormone level was at 20.2 pg/ml.

Reassessment at the age of two years of age without any treatment found a calcium level at 9.8 mg/dl, phosphatemia level at 6.1 mg/dl and PTH level was at 21.4 pg/ml. Vitamin D level was at 27 ng/ml.

In this case, the diagnosis of neonatal vitamin D deficiency secondary to deficiency in the mother was retained, and what was in favor of this later diagnosis was the presence of signs of hypocalcaemia in the mother during pregnancy and low level of 25 hydroxy vitamin D in the mother.

2 Discussion

Hypocalcemia is a frequently observed abnormality in neonates. It is defined as total serum calcium of less than 7 mg/dl (1.75 mmol/l) or ionized calcium less than 4 mg/dL (1 mmol/l) in preterm infants and less than 8 mg/dl (2 mmol/l) or ionized calcium less than 4.8 mg/dl (1.2 mmol/l) in full term neonates (Oden, 2000).

The usual causes of early onset hypocalcaemia occurring within 72 h of life are low birth weight babies, infants of mothers with diabetes and cases of perinatal asphyxia (Venkataraman et al., 1986). Whereas the usual causes of late onset hypocalcaemia occurring after 72 h of life include neonatal hypoparathyroidism, maternal hyperparathyroidism, sick neonate, hypomagnesaemia and vitamin D deficiency (Venkataraman et al., 1985).

Vitamin D deficiency has been increasingly recognized as a worldwide epidemic, affecting children, adults and the elderly alike. Vitamin D deficiency in women in the reproductive age group is also increasing due to lifestyle factors, including increased time spent indoors both in the workplace and domestically with lack of sun exposure, maternal obesity, overuse of broad spectrum sunscreens, pigmented skin, intestinal malabsorption, increased catabolism of vitamin D and other factors (Nozza, 2001).

Prevalence of vitamin D deficiency in pregnancy is considered high in different populations. It vary between 6 and 96% according to the latitude, ethnicity and supplementation of vitamin D, body mass index, season and the cut-off used to define deficiency of vitamin D. This cut-off has been set between 10 and 20 ng/ml depending on the study (Weinert, 2015).

25 hydroxy vitamin D cross the placental barrier and, at birth, cord blood 25 hydroxy vitamin D levels are directly correlated with maternal levels, Plasma levels of vitamin D in the neonate correspond to approximately 60–70% of maternal levels. In contrast, fetal 1, 25 dihydroxy vitamin D appear to be largely synthesized in the fetal kidney with some contribution from placenta-derived 1, 25 dihydroxy vitamin D (Perez-Lopez, 2007).

Vitamin D deficiency in neonates secondary to vitamin D deficiency in their mothers is not uncommon and may lead to hypocalcemia as vitamin D plays crucial role in calcium homeostasis (Camadoo, 2007). Maternal vitamin D deficiency results in poor transplacental transfer of vitamin D during pregnancy and reduced stores in the newborns.

During pregnancy, vitamin D has numerous actions in both the mother and the fetus, its deficiency will have detrimental effects in both. It is essential for fetal skeletal development. Vitamin D deficiency in the pregnant women has been associated with adverse outcomes to the mother, such as gestational diabetes mellitus and preeclampsia, and to the offspring, such as seizures small for gestational age newborns and respiratory distress (Principi et al., 2013).

In their study, Toaima and al, reported a case series of 19 newborn infants presented with symptomatic hypocalcemia in a 2-year period only. Vitamin D deficiency in both the infants and their mothers was the attributed cause in all studied patients and out of the 19 patients, nine had an associated unexpected response of PTH, which might be explained by immature calcium–vitamin D–parathyroid hormone axis at this early age (Toaimi, 2010).

3 Conclusions

This case illustrates the importance of checking the calcium levels in neonates who present with seizures and to check their vitamin D status in those found to be hypocalcaemic.

There is also a need to screen for vitamin D deficiency during pregnancy and provide supplementation when indicated.

Conflicts of interests

The authors have declared that no competing interests exist.

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