Am J Perinatol 2015; 32(03): 247-250
DOI: 10.1055/s-0034-1383849
Original Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Is Higher 25-Hydroxyvitamin D Level Preventive for Respiratory Distress Syndrome in Preterm Infants?

Nurdan Dinlen Fettah
1   Neonatal Intensive Care Unit, Dr. Sami Ulus Maternity and Children Research and Training Hospital, Ankara, Turkey
,
Ayşegül Zenciroğlu
1   Neonatal Intensive Care Unit, Dr. Sami Ulus Maternity and Children Research and Training Hospital, Ankara, Turkey
,
Dilek Dilli
1   Neonatal Intensive Care Unit, Dr. Sami Ulus Maternity and Children Research and Training Hospital, Ankara, Turkey
,
Serdar Beken
1   Neonatal Intensive Care Unit, Dr. Sami Ulus Maternity and Children Research and Training Hospital, Ankara, Turkey
,
Nurullah Okumuş
1   Neonatal Intensive Care Unit, Dr. Sami Ulus Maternity and Children Research and Training Hospital, Ankara, Turkey
› Author Affiliations
Further Information

Publication History

28 February 2014

08 May 2014

Publication Date:
13 September 2014 (online)

Abstract

Objective The objective of this study was to investigate the relationship between cord blood 25-hydroxyvitamin D (25(OH)D) levels and respiratory distress syndrome (RDS) development in preterm infants.

Study Design Between January 2012 and January 2013, 81 preterm infants, gestational age below 32 weeks, were prospectively enrolled into the study. Cord bloods of these newborns were tested for 25(OH)D levels. Low level was defined as ≤ 15 ng/mL (Group 1) and normal level as > 15 ng/mL (Group 2). Patients in Group 1 were also divided further into two subgroups as severe deficiency (Group 1a, ≤ 5 ng/mL) and mild deficiency (Group 1b, 5–15 ng/mL).

Results In this study, 57 infants had low 25(OH)D levels (Group 1, median 8.0 ng/mL [interquartile range, IQR, 5–10]; Group 2, median 21 ng/mL [IQR, 19–24.7]). RDS rate was significantly higher in Group 1a (n = 18, 32.7%) and Group 1b (n = 34, 61.8%) compared with Group 2 (n = 3, 5.4%) (p = 0.001). There were no difference of having RDS between Group 1a (94.7%) and Group1b (89.5) (p = 0.512). Multivariate analysis showed that higher 25(OH)D level can be preventive for the development of RDS (odds ratio, 0.6; 95% confidence interval (0.5–0.8); p = 0.001).

Conclusion Lower cord blood 25(OH)D levels might be associated with increased risk of RDS in preterm infants with very low birth weight.

Note

The clinical trials registration number of this study is NCT01812681.


 
  • References

  • 1 Özkan B, Döneray H. Non-skeletal effects of vitamin D. Çocuk Sağılığı ve Hastalıkları Dergisı 2011; 54: 99-119
  • 2 Thandrayen K, Pettifor JM. Maternal vitamin D status: implications for the development of infantile nutritional rickets. Endocrinol Metab Clin North Am 2010; 39 (2) 303-320
  • 3 Rodriguez RJ. Management of respiratory distress syndrome: an update. Respir Care 2003; 48 (3) 279-286 , discussion 286–287
  • 4 Mendelson CR. Role of transcription factors in fetal lung development and surfactant protein gene expression. Annu Rev Physiol 2000; 62: 875-915
  • 5 Nguyen TM, Guillozo H, Marin L, Tordet C, Koite S, Garabedian M. Evidence for a vitamin D paracrine system regulating maturation of developing rat lung epithelium. Am J Physiol 1996; 271 (3 Pt 1) L392-L399
  • 6 Misra M, Pacaud D, Petryk A, Collett-Solberg PF, Kappy M. Drug and Therapeutics Committee of the Lawson Wilkins Pediatric Endocrine Society. Vitamin D deficiency in children and its management: review of current knowledge and recommendations. Pediatrics 2008; 122 (2) 398-417
  • 7 Sakurai R, Shin E, Fonseca S , et al. 1alpha,25(OH)2D3 and its 3-epimer promote rat lung alveolar epithelial-mesenchymal interactions and inhibit lipofibroblast apoptosis. Am J Physiol Lung Cell Mol Physiol 2009; 297 (3) L496-L505
  • 8 Marin L, Dufour ME, Tordet C, Nguyen M. 1,25(OH)2D3 stimulates phospholipid biosynthesis and surfactant release in fetal rat lung explants. Biol Neonate 1990; 57 (3-4) 257-260
  • 9 Phokela SS, Peleg S, Moya FR, Alcorn JL. Regulation of human pulmonary surfactant protein gene expression by 1alpha,25-dihydroxyvitamin D3. Am J Physiol Lung Cell Mol Physiol 2005; 289 (4) L617-L626
  • 10 Ballard PL, Ertsey R, Gonzales LW, Gonzales J. Transcriptional regulation of human pulmonary surfactant proteins SP-B and SP-C by glucocorticoids. Am J Respir Cell Mol Biol 1996; 14 (6) 599-607
  • 11 Beers MF, Shuman H, Liley HG , et al. Surfactant protein B in human fetal lung: developmental and glucocorticoid regulation. Pediatr Res 1995; 38 (5) 668-675
  • 12 Nguyen M, Trubert CL, Rizk-Rabin M , et al. 1,25-Dihydroxyvitamin D3 and fetal lung maturation: immunogold detection of VDR expression in pneumocytes type II cells and effect on fructose 1,6 bisphosphatase. J Steroid Biochem Mol Biol 2004; 89-90 (1-5) 93-97
  • 13 Zasloff M. Fighting infections with vitamin D. Nat Med 2006; 12 (4) 388-390
  • 14 Burris HH, Van Marter LJ, McElrath TF , et al. Vitamin D status among preterm and full-term infants at birth. Pediatr Res 2014; 75 (1-1) 75-80
  • 15 Yorifuji J, Yorifuji T, Tachibana K , et al. Craniotabes in normal newborns: the earliest sign of subclinical vitamin D deficiency. J Clin Endocrinol Metab 2008; 93 (5) 1784-1788
  • 16 Hollis BW, Wagner CL. Assessment of dietary vitamin D requirements during pregnancy and lactation. Am J Clin Nutr 2004; 79 (5) 717-726
  • 17 Salle BL, Delvin EE, Lapillonne A, Bishop NJ, Glorieux FH. Perinatal metabolism of vitamin D. Am J Clin Nutr 2000; 71 (5, Suppl): 1317S-1324S