The metabolic bone disease is an important morbidity in premature, very low birth weight and sick infants. If left undiagnosed, leads to structural deformities & spontaneous fractures.It is defined as impaired bone mineralization in a neonate with lower than the estimated bone mineral levels in either fetus or neonate of comparable gestational age / weight coupled with biochemical abnormalities with or without radiological manifestations. It has been reported to occur in 16% to 40% of extremely low birth weight neonates. Insufficient calcium and phosphorous stores during the phase of accelerated growth predispose to it along with use of medications (caffeine, steroids), prolonged parenteral nutrition & chronic immobilization. It presents by 6-16 weeks after birth. Enhanced physical activity in preterm infants facilitates bone mineralization and weight gain. Biochemical abnormalities tend to worsen significantly, as the severity of disease progresses. They consist of hypocalcemia, hypophosphatemia, hyperphosphatasia and secondary hyperparathyroidism. In addition, urinary phosphate wasting and hypo vitaminosis D can complicate these abnormalities. Conversely, biochemical abnormalities may not be accompanied by rachitic changes. Newer diagnostic modalities include bone densitometry by quantitative ultrasound over mid-tibial shaft (noninvasive tool). The management of metabolic bone disease includes adequate calcium, phosphorous and vitamin D supplementation along with optimum nutrition and physical activity. Similarly, preventive strategies for metabolic bone disease should target nutritional enhancement alongside enhanced physical activity. Conclusion: Metabolic bone disease is a preventable morbidity in preterm, VLBW neonates and requires optimum nutritional supplementation and enhanced physical activity.

Neural Tube Defects are the most typical congenital malformations, with almost 300,000 cases annually worldwide. The incidence varies amongst geographical ranges from 0.2 to up to 11 per 1000 live births. In India, incidence is reportedly higher in north than south and can be attributable to diet and genetic variances. Etiology is multifactorial. Severe forms of whitethorn are allied with syndromes. Primary neurulation and secondary neurulation are the most crucial steps in the formation and closure of the neural tube; any interruption can lead to mild to severe NTDs depending on the level of insult during embryogenesis. Various molecular and cellular events take place simultaneously for neural tube bending and closure of the neural tube. Neurological deficit in the newborn is contingent on the level of defect and severity of the structures affected. Survival of the newborn also depends on the severity of the lesion. Folic acid supplementation in all prospective mothers, preferably 4 weeks before conception and at least 12 weeks after conception, can prevent NTDs in folic responsive groups. But there is a significant number of other causes leading to neural tube defects apart from folic acid. Hydrocephalus is the commonest abnormality allied with NTDs in syndromic cases. Conclusion: NTDs are a frequent cause of stillbirths, infant mortality, and palsies in children. There are various reasons for NTDs, but the process of neurulation points towards some factors of NTC, which can be taken care of to lessen the burden of NTDs.

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