|Year : 2016 | Volume
| Issue : 2 | Page : 142-144
Selenium supplementation for the preterm Indian neonate
Geeta Gathwala1, Rahul Aggarwal2
1 Professor and Head, Department of Pediatrics, Neonatal Services Division, Pandit Bhagwat Dayal Sharma Post-Graduate Institute of Medical Sciences, Rohtak, Haryana, India
2 Junior Resident, Department of Pediatrics, Neonatal Services Division, Pandit Bhagwat Dayal Sharma Post-Graduate Institute of Medical Sciences, Rohtak, Haryana, India
|Date of Web Publication||23-Jun-2016|
6 J/8, Medical Campus, Pandit Bhagwat Dayal Sharma Post-Graduate Institute of Medical Sciences, Rohtak, Haryana
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Deficient antioxidant defenses in preterm infants have been implicated in diseases such as bronchopulmonary dysplasia, retinopathy of prematurity, necrotizing enterocolitis, periventricular leukomalacia, and intraventricular hemorrhage. The antioxidant properties of selenium make it important in the nutrition of very low-birth weight (VLBW) infants. Selenium is a component of glutathione peroxidase (GPX), an enzyme that prevents the production of free radicals. Preterm infants have low selenium stores and require supplementation by parenteral and enteral routes. This communiquι reviews the beneficial role that selenium supplementation might play in improving neonatal outcomes.
Keywords: Antioxidant defense, neonate, preterm, selenium
|How to cite this article:|
Gathwala G, Aggarwal R. Selenium supplementation for the preterm Indian neonate. Indian J Public Health 2016;60:142-4
|How to cite this URL:|
Gathwala G, Aggarwal R. Selenium supplementation for the preterm Indian neonate. Indian J Public Health [serial online] 2016 [cited 2020 Apr 10];60:142-4. Available from: http://www.ijph.in/text.asp?2016/60/2/142/184571
| Introduction|| |
Selenium is a constituent of the antioxidant enzyme glutathione peroxidase (GPX) and therefore, is vital to antioxidant defense. Several diseases of the neonate have been shown to be caused at least in part by oxygen-free radicals. These include bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), necrotizing enterocolitis, periventricular leukomalacia, and neuronal injury of hypoxic ischemic encephalopathy. Antioxidant capacities are inadequate in preterm newborns, both because of placental-fetal transfer interruption of antioxidant molecules and insufficient endogenous production. Selenium intake in mothers is generally from food, the selenium content of which depends on soil selenium and plant accumulation. The selenium content of soils can vary widely and is low in India. Since Indian mothers are undernourished themselves, fetal concentrations may be still lower. Selenium supplementation in the Indian neonates, especially preterm, may be expected to positively impact neonatal survival.
| Role of Selenium|| |
Selenium is a trace element considered to be essential in neonates due to its participation in major metabolic functions - antioxidant defense, immune system, and thyroid hormone metabolism.
The role of selenium in the body as the prosthetic group of the selenium enzyme GPX is firmly established. There are cellular (classical GPX and phospholipid hydroperoxide GPX) and extracellular GPXs. The cellular form is found within all cells and the extracellular form is found in plasma, breast milk, and lung lavage fluid. GPXs are primary antioxidant enzymes and function to reduce hydroperoxides according to the following general reaction:
The reaction has special significance in the protection of the polyunsaturated fatty acids located within the cell membranes where the enzyme functions as a part of a multicomponent antioxidant defense system within the cell. The selenium regulation of GPX activity is mediated by selenium regulation of GPX messenger RNA (mRNA).
Type I: Iodothyronine 5'Deiodinase
This is a selenoprotein that is found to have the highest activity in the liver and kidney and its primary role is considered to be the supply of plasma T3.
A greater hypothyroid stress is reported in combined selenium and iodine deficiencies than in iodine deficiency alone.
Selenium and immune system
Selenium also plays an important role in immune competence. Neutrophils and macrophages from selenium-deficient animals have low GPX concentrations and impaired antimicrobial properties. Selenium causes direct reversible inhibition of nuclear factor-êB binding to DNA, decreasing synthesis of proinflammatory cytokines. Se-enriched probiotics have been shown to strongly inhibit the growth of pathogenic E coli. 
| Selenium Levels in the Indian Mother and Neonate|| |
Selenium transfer through the placenta is limited, and fetal concentrations are approximately 65% of maternal serum levels. The plasma selenium concentrations of the majority of healthy neonates at birth and up to 3 months of age are within the range of 45-90 μg/L while the normal level in adults is 75-120 μg/L.  Selenium levels in full-term Indian neonates were reported to be 54.17 ± 3.4 μg/L.  Se levels in preterm neonates with a mean gestational age of 31.7 ± 0.6 weeks and a mean birth weight of 1464.22 ± 50.14 g were 31.1 ± 14.8 μg/L.  The mean plasma selenium level in full-term Indian mothers was 70.63 ± 1.62 μg/L and in preterm mothers, it was 63.28 ± 2.31 μg/L. 
| Selenium Supplementation Improves Neonatal Outcomes|| |
Premature very low birth weight (VLBW) infants are inherently susceptible to selenium deficiency.
In a study of 38 preterm infants receiving parenteral nutrition, 19 were randomized to selenium supplements (3 μg/kg/day) and 19 to placebo. The mean birth weight was 1,129 (±42) g in the selenium group and 1,211 (±65) g in the placebo group. The mean gestational age was 29.0 (±0.5) weeks in the selenium group and 28.0 (±0.5) weeks in the placebo group. Those receiving 3 μg/kg/d of selenium had a lower incidence of sepsis than nonsupplemented infants (42%, n = 8 vs 79%, n = 15, P < 0.05). 
In another study a total of 529 infants were studied, 268 being randomized to selenium supplements and 261 to placebo. The mean birth weight was 1,047 (±255) g in the selenium group and 1,039 (±270) g in the placebo group. The mean gestational age was 28.0 (±2.3) weeks in the selenium group and 27.8 (±2.5) weeks in the placebo group. Infants randomized to treatment received 7 μg/kg/d of sodium selenate added to the amino acid solution when fed parenterally and 5 μg/kg/d of sodium selenite when fed enterally. Fewer infants in the selenium group had an episode of nosocomial sepsis after the first week of life (25.1% vs 33.3%; P = 0.038). The study also found that lower maternal and infant selenium concentrations before randomization were associated with an increased risk of oxygen dependency at 28 days. 
In a recent study, preterm VLBW neonates (mean birth weight of 1464.22 ± 50.14 g and mean gestational age of 31.7 ± 0.6 weeks) were found to be Se-deficient at birth with mean (SD) Se levels of 31.1 ± 14.8 μg/L. Se supplementation at 10 μg/day increased serum Se levels significantly [63.9 ± 13.9 μg/L on day 28 in selenium vs. 40.9 ± 17.3 μg/L on day 28 in placebo; P < 0.01]. The incidence of the first episode of culture proven late-onset sepsis was significantly lower in the selenium group than in the placebo group [0/45 (0%) in selenium vs 6/45 (13.3%) in placebo; P = 0.033]. The incidence of probable sepsis was also found to be significantly lower in the selenium group [7/45 (15.55%)] than in the placebo group [16/45 (35.55%)]; P = 0.02. The total incidence of any late-onset sepsis (i.e., culture-proven plus probable sepsis) was also significantly reduced by selenium supplementation [7/45 (15.55%) in Se vs 22/45 (48.88%) in placebo; P = 0.001]. 
Yang et al. reported that the serum selenium levels in preterm infants with ROP were also much lower compared to controls.  Papp et al. conducted a study on 60 oxygen-treated premature infants weighing less than 2,000 g (1,529 ± 302 g) and their mothers. The concentrations of free sulfhydryl groups in the plasma and the blood Se levels were significantly lower in the premature infants suffering from moderate retinopathy (n = 5) than in the other oxygen-treated premature infants without retinopathy (n = 27). 
| Selenium Supplementation|| |
According to the National Health and Medical Research Council (NHMRC) in 2006, the daily recommended oral dose of selenium for the neonate is 12-15 μg. For parenteral nutrition, the European Society for Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN, 2005) has recommended the administration of 2-3 μg/kg/day. The addition of selenium to oral, enteral, and parenteral infant formulas is not a routine practice in many countries including India.
| Conclusion|| |
For reasons of compromised antioxidant defense and the fact that much of neonatal morbidity is oxygen-free radical-mediated, selenium supplementation in preterm infants is likely to have beneficial effects on their outcomes. Neonatal mortality continues to be a significant problem in the Indian setting, especially in premature neonates. Two major causes of newborn deaths in India are prematurity (35%) and neonatal infections (33%). Selenium supplementation can impact both these outcomes positively and contribute to improved neonatal survival. Good selenium nutrition therefore, makes good sense. However, more research is needed to better define the impact of Se supplementation of preterm infants on their morbidity and mortality.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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