Comparison between preterm and full term neonatal cord selenium in correlation to maternal serum selenium levels

Background: Lower concentrations of selenium and glutathione peroxidase activities have been reported in pregnant women. An exposure to a high oxygen concentration at birth, an infection, inflammation, and a deficient antioxidant system make the newborn more susceptible to oxidative stress that can result in bronchopulmonary dysplasia, retinopathy of prematurity, persistent ductus arteriosus, necrotizing enterocolitis, intracranial hemorrhage, and hypoxic ischemic encephalopathy, especially in extremely low-birth-weight infants. Aim: The current study aimed at the detection and comparison of maternal serum and neonatal umbilical cord selenium levels. Methods: A prospective study on 80 mothers and their healthy neonates (40 full term and 40 preterm) enrolled over the period from June to December 2016. Selenium concentrations were measured in the maternal serum and umbilical cord using a spectrophotometer. Results: A significantly higher mean selenium level was detected in term neonates than preterm neonates (P = 0.015) with no gender difference but the difference in selenium concentration between their mothers was not significant. No significant relations found between maternal serum selenium levels and maternal age, weight, height, BMI or pregnancy weeks. The maternal serum selenium was positively correlated with the cord selenium in full-term group (r = 0.59 & P = 0.006). Significantly positive correlations between umbilical cord selenium levels in both full-term and preterm neonates with their gestational age and birth weight. Conclusion: This study indicated that cord Se concentration was different in term and preterm neonates being higher in full terms, so we recommend selenium supplementation to preterm neonates and their mothers to avoid sequelae of selenium deficiency on their health and to reach the levels obtained in full term neonates

Assessment of Preptin peptide level in the sera of rachitic children and in breast milk of their mothers

Abstract Background Preptin is a 34-residue pancreatic hormone that stimulates osteoblast proliferation and reduces osteoblast apoptosis. Research aims To measure levels of serum Preptin in rachitic children and in breastmilk of their mothers and to compare with levels in healthy non-rachitic children. Methods Thirty children with rickets and another 30 non-rachitic age and sex matched controls were subjected to detailed history, physical examination including anthropometric measurements, assessment of signs of rickets and laboratory measurement of serum vitamin D, calcium, phosphorus, alkaline phosphatase and Preptin. Mothers’ breast milk Preptin were also measured. Results Significantly lower serum Preptin (p < 0.001) in rachitic children with a significant negative correlation between serum Preptin and alkaline phosphatase (P < 0.0001). Lower breastmilk Preptin levels in mothers of rachitic children (P < 0.001) with a negative correlation between breastmilk Preptin and both maternal weight and BMI(P < 0.01&P < 0.02). Mothers’ milk Preptin is positively correlated with serum Preptin and calcium in non-rachitic children(P < 0.001&0.04), but negatively correlated with their mothers’ age (P < 0.01). Conclusion Preptin may play a role in the etiology of rickets in children. Further studies are recommended to evaluate Preptin role in treatment of rickets in children

Propionic and Methylmalonic Acidemias: Initial Clinical and Biochemical Presentation

PA and MAA have numerous nonspecific presentations, potentially leading to delayed diagnosis or misdiagnosis. In this paper, we present the clinical and biochemical characteristics of MMA and PA patients at initial presentation. Results. This is a retrospective review of 20 patients with PA (n=10) and MMA (n=10). The most observed symptoms were vomiting (85%) and refusing feeding (70%). Ammonia was 108.75±9.3 μmol/l, showing a negative correlation with pH and bicarbonate and positive correlation with lactate and anion gap. Peak ammonia did not correlate with age of onset (r=0.11 and p=0.64) or age at diagnosis (r=0.39 and p=0.089), nor did pH (r=0.01, p=0.96; r=−0.25, p=0.28) or bicarbonate (r=0.07, p=0.76; r=−0.22, p=0.34). There was no correlation between ammonia and C3 : C2 (r=0.1 and p=0.96) or C3 (r=0.23 and p=0.32). The glycine was 386±167.1 μmol/l, and it was higher in PA (p=0.003). There was a positive correlation between glycine and both pH (r=0.56 and p=0.01) and HCO3 (r=0.49 and p=0.026). There was no correlation between glycine and ammonia (r=−0.435 and p=0.055) or lactate (r=0.32 and p=0.160). Conclusion. Clinical presentation of PA and MMA is nonspecific, though vomiting and refusing feeding are potential markers of decompensation. Blood gas, lactate, and ammonia levels are also good predictors of decompensation, though increasing levels of glycine may not indicate metabolic instability