The Journal of Maternal-Fetal & Neonatal Medicine

ISSN: 1476-7058 (Print) 1476-4954 (Online) Journal homepage: http://www.tandfonline.com/loi/ijmf20

Association between serum 25 (OH) vitamin D

level at birth and respiratory morbidities among
preterm neonates

Adham Mohamed El Tahry Hegazy, Dina Mohamed Shinkar, Noha Refaat

Mohamed & Hala Abdalla Gaber

To cite this article: Adham Mohamed El Tahry Hegazy, Dina Mohamed Shinkar, Noha Refaat
Mohamed & Hala Abdalla Gaber (2017): Association between serum 25 (OH) vitamin D level
at birth and respiratory morbidities among preterm neonates, The Journal of Maternal-Fetal &
Neonatal Medicine, DOI: 10.1080/14767058.2017.1350162

To link to this article: http://dx.doi.org/10.1080/14767058.2017.1350162

Accepted author version posted online: 02

Jul 2017.

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Download by: [Cornell University Library] Date: 04 July 2017, At: 03:44
 Association between serum 25 (OH) vitamin D level at
birth and respiratory morbidities among preterm
neonates

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Prof. Dr. Adham Mohamed El Tahry Hegazy M.D.
Professor of Pediatrics.

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Faculty of Medicine-Ain Shams University-Cairo-Egypt.

Dr. Dina Mohamed Shinkar M.D.

Lecturer of Pediatrics.

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Faculty of Medicine-Ain Shams University-Cairo-Egypt.

Dr. Noha Refaat Mohamed .M.D.

Lecturer of Clinical Pathology-Cairo-Egypt.
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Faculty of Medicine-Ain Shams University- Cairo-Egypt

Hala Abdalla Gaber M.B.B.CH.

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Ministry of health- Egypt.

Correspondent author: Dr. Dina Mohamed Shinkar M.D.

62 Dr.Abdel Shafie Mohamed Street-7 th district-Nasr City-Cairo-Egypt.
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Tel: +201112636097
Email: drdodi28@gmail.com.
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Short title: Vitamin D level at birth and respiratory morbidities.

Key words: Vitamin D; Prematurity; Respiratory distress syndrome; Bronchopulmonary
dysplasia.

There is no financial assistance or potential conflicts of interest.

Abstract:
Objectives:

To determine the association between 25-hydroxyvitamin D [25(OH)D] levels on first

day of life with respiratory distress syndrome (RDS), need and duration of mechanical

ventilation and subsequent development of bronchopulmonary dysplasia (BPD) among

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preterm neonates.

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Study design:

In this case control study, serum 25(OH)D was measured on first day of life in 65

preterm neonates < 34 weeks: 40 with RDS and 25 without RDS and compared between

insufficiency: (20- 30 ng/mL),

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them. Serum 25(OH)D levels were categorized into; normal : above 30 ng/mL ,

moderate deficiency (10 – 20 ng/mL) and severe

deficiency (< 10 ng/mL). Neonates with different 25(OH)D levels were compared as
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regard grade of RDS, initial pH, initial CO2, need and duration of mechanical ventilation,
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development of BPD and mortality.

Results:

Only one of 65 studied preterm neonates had normal vitamin D level. Neonates with RDS
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had significantly lower mean serum 25(OH)D level than controls (10.6 ng/dl vs 13.9

ng/dl) (P value =0.028). Neonates with severe 25(OH)D deficiency developed more BPD

than those with moderate deficiency (29.4% vs 8.7%) but did not reach significant level
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(P value =0.08). There is no correlation between serum 25(OH)D level and duration of

mechanical ventilation. Logistic regression analysis shows that low serum 25(OH)D level

is an independent risk factor for RDS.

Conclusion:
Low 25(OH)D level is far frequent among Egyptian preterm neonates. Vitamin D

deficiency is an independent risk factor for development of RDS in preterm neonates.

Key words: Vitamin D; Prematurity; Respiratory distress syndrome; Bronchopulmonary

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dysplasia.

Abbreviations: [25(OH)D]:25-hydroxyvitamin D; RDS: Respiratory distress syndrome;

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BPD: bronchopulmonary dysplasia; VDR:Vitamin D receptor; AT2C :Alveolar type 2

cell; nCPAP :Nasal continuous positive air pressure; VDRE:vitamin D response

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elements.

Introduction:
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Respiratory distress syndrome (RDS) is leading cause of mortality and mortality in
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premature babies (1).

Bronchopulmonary dysplasia (BPD) is the most prevalent long-term morbidity among

surviving extremely preterm infants (2) .BPD affects ~20% of preterm infants, and up to
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60% of extremely preterm infants who are born before 26 completed weeks of gestation

(3).Early preterm infants are likely at risk of low vitamin D status because of high

prevalence of vitamin D deficiency in pregnancy, lack of sunlight exposure during

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hospitalization and difficulty in ensuring adequate enteral nutrition (4).

Animal and laboratory studies showed substantial positive effects of vitamin D on the

alveolar type II cell, fibroblast proliferation, surfactant synthesis and alveolarization (5).

Vitamin D and the vitamin D receptor (VDR) have important roles inperinatal lung

development (6,7).
Vitamin D may play a role in the embryogenesis and in cellular growth and

differentiation, including lung development and regulation of lung maturation in the fetus

(8, 9).

Vitamin D has anti-inflammatory properties and modulates lung growth. It directly

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increase fetal alveolar type 2 cell (AT2C) growth by 26% And enhanced AT2C growth

by 73% (10).Several epidemiological studies have described an association between

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maternal vitamin D deficiency and the development of early childhood respiratory

infections, wheezing, and asthma later in life (11,12).

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The impact of vitamin D on early lung development and maturation and lung diseases of

early life is an emerging field of research.

We aimed at determining the association between 25-hydroxyvitamin D [25(OH) D]

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levels at birth with RDS and subsequent development of BPD in Egyptian preterm
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neonates.

Patients and methods:

This prospective case control study was carried out in the level III Neonatal Intensive
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Care Unit of Ain Shams University Maternity and Children Hospital, Cairo, Egypt. It was

conducted in the period between November 2015 and May 2016.

Study Population:
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A total of 65 preterm neonates < 34 weeks gestational age were enrolled in the study, 40

preterm neonates with RDS and 25 preterm neonates without RDS. The required sample

size has been calculated using the G*Power software version 3.1.7 (Universitat

Dusseldorf, Germany). The sample size was calculated as 60 for α = 0.05 and power

0.90.Neonates whose mothers have parathyroid hormone and/or calcium metabolism

problems, those with major congenital abnormalities and/or chromosomal disorder and

babies with blood culture proven sepsis were excluded.

Methods:

The study protocol was approved by Ain Shams University NICU Ethical Committee.

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Informed consent was taken from mother or legal guardians of included neonates in the

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study. Detailed history was taken for all neonates including maternal history of PROM,

diabetes mellitus, preeclampsia, antenatal steroid use and history and doses of maternal

intake of vitamin D during pregnancy. Also Apgar score was recorded (13).Diagnosis of

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RDS was based on presence of respiratory distress in conjugation with chest X ray.

Grading of respiratory distress was done by Downes score (14).

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Capillary blood gases analysis was done on admission and repeated as needed. Serum
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level of vitamin D (25(OH)D) was measured in venous blood sample in all included

neonates on day one of life using 25(OH) D ELISA kit Immundiagnostik AG, Germany.

Serum Ca was measured on first day of life.

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We considered vitamin D “deficiency” if 25(OH) D value below 20 ng/ml and

“insufficiency” if 25(OH) D value between 20 and 30 ng/ml.

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Vitamin D deficiency was further classified as severe deficiency < 10 ng/ mL and

moderate deficiency10 – 20 ng/mL (15).

All included neonates were followed up for need and duration of mechanical ventilation,

development of BPD using the National Institutes of Health consensus definition of BPD

(16) and fate (died or alive).

Management strategy:

All infants were followed on nasal continuous positive air pressure (nCPAP) as an initial

respiratory support and mechanical ventilation was started if fraction of inspired oxygen

of > 0.4 and mean airway pressure > 7 cm H2O. Surfactant was given as early rescue if

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mechanical ventilation was needed.

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Outcome measures:

The primary outcome was to determine the association between 25-hydroxyvitamin D

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[25(OH)D] levels on day one of life with RDS and subsequent development of BPD.

Statistical analysis:
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Data were analyzed using SPSS version 20 computer software (SPSS, Chicago, IL). The
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qualitative data were presented as number and percentages while quantitative data were

presented as mean, standard deviations, and ranges when parametric and presented as

median with interquartile ranges (IQR) when non parametric. The comparison between
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groups regarding qualitative data were done by using Chi-square test and/or Fisher exact

test when the expected count in any cell found less than 5.
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The comparison between two groups regarding quantitative data with parametric

distribution were done by using Independent t-test while the comparison between two

groups regarding quantitative data with non parametric distribution were done by using

Mann-Whitney test.
The comparison between more than two groups regarding quantitative data with

parametric distribution were done by using One Way ANOVA while the comparison

between more than two groups regarding quantitative data with non parametric

distribution were done by using Kruskall-Wallis test. Spearman correlation coefficients

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were used to assess the correlation between two quantitative parameters in the same

group.

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Logistic regression analysis was used to assess the risk factors of RDS. A two-tailed p

value was considered significant if < 0.05.

Results:
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From November 2015 to May 2016, we enrolled 65 preterm infants in this study; 40

neonates with RDS and 25 control neonates. The mean gestational age of neonates with
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RDS was 31.4 ± 2.25 wks versus 32.4 ± 1.76 wks in control group and mean birth weight

was 1.55 ± 0.63 kg in RDS group versus 1.72 ± 0.52 kg in control group(non- significant

difference). There was no significant difference between neonates in RDS group and Commented [M1]: There is no significant difference .
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control group as regard sex, mode of delivery, maternal age, antenatal steroid intake,

vitamin D supplementation during pregnancy ,PROM, DM and preeclampsia (Table 1).

47.5% of mothers of RDS neonates received vitamin D supplementation during

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pregnancy while 60% of control neonates received vitamin D supplementation( P =

0.326). Most of these mothers reported that their vitamin D intake was not regular and the

dose was not fixed due to lack of adherence to antenatal care. Although mean S.Ca level

in neonates in RDS group was lower than in the control group (8.7 mg/dl vs 9.0 mg/dl),

this difference is statistically non-significant (P=0.07).

Only one out of 65 studied preterm neonates had normal serum 25(OH)D level. None of

RDS neonates had 25(OH)D insufficiency, 23 (57.5%) had moderate 25(OH)D

deficiency and 17 (42.5%) had severe deficiency while, 3 (12.0%) of control group had

25(OH)D insufficiency, 12 (48.0%) had moderate deficiency and 10 (40.0%) had severe

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deficiency

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Neonates in RDS group had significantly lower mean serum 25(OH)D level than the

control group (10.6 ng/dl Versus 13.9 ng/dl; P = 0.028) (Figure 1).

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Five out of 17 neonates with severe 25(OH)D deficiency developed BPD (29.4%) while 2

out of 23 neonates with moderate deficiency developed BPD (8.7%) (P value =0.08)

(Figure 2).
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As regard demographic and maternal clinical data, there is no significant difference
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between neonates with moderate and severe 25(OH)D deficiency in RDS group. Males

had significantly more severe 25(OH)D deficiency than females (64.7% versus 35.3%; P

= 0.015) (Table 2).

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Also, there is no significant difference between neonates with moderate and severe

vitamin D deficiency in RDS group as regard Apgar score, grade of RDS, initial pH,
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initial CO2 and maximum PIP. Although neonates with severe 25(OH)D deficiency had

longer days on mechanical ventilation (16.53 ± 13.46 versus 12.09 ± 9.46 days; P=

0.227) and higher mortality (23.5% versus 8.7%; P=0.194), these differences are

statistically non-significant (Table 3 ). There is no statistically significant correlation

between serum 25(OH)D level and birth weight (r =,-0.013; P=0.935) and gestational age

(r =0.042 ; P=0.797) and serum Ca level (r =-0.013; P=0.935). Also, There is no Commented [M2]: There is no correlation with birth weight and
gestational ae
statistically significant correlation between serum 25(OH)D level and duration of

mechanical ventilation (r = 0.061; P = 0.710) (Table 4).

Logistic regression analysis shows that low serum 25(OH)D level on first day of life is

an independent risk factor for RDS (P=0.036), Odds

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ratio (OR) : 0.904, 95% CI (0.82- 0.94) .As we chose both our groups gestational age

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matched, gestational age was not the independent risk factor in our patients (Table 5) .

Discussion:

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Preterm infants have increased risk of developing vitamin D deficiency compared with

full-term infants (17) as they miss the late gestation transfer of vitamin D from mother to

fetus (18).
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The impact of vitamin D on early lung development and maturation and lung diseases of
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early life is an emerging field of research.

The purpose of our study was to assess the relation between vitamin D status at birth and

development of RDS and subsequent BPD in Egyptian preterm neonates.

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In our study, only one of 65 studied Egyptian preterm neonates had normal serum

25(OH)D level. This reflects poor vitamin D status of Egyptian women due to poor diet
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lacking sources of vitamin D as Fish, more prevalence of dark skin colored skin,

multiparity and lack of adequate supplementation during pregnancy.

Vitamin D freely crosses the placenta during pregnancy. Thus, levels of neonates at birth

depend entirely on that of the mother ()(19). Neonatal serum 25(OH)D level differed

significantly between the groups of mothers with different serum 25(OH)D levels
(P<0.001). Maternal 25(O.H) D level is positively correlated with neonatal vitamin D

level (r=0.914, P<0.001) (20). This occurs as the fetus has no endogenous production of

25(OH)D and depends on transplacental transfer (21). Maternal vitamin D level can help

to predict neonatal vitamin D deficiency.

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Transplacental transfer occurs mainly in the third trimester and therefore, preterm infant s

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are at increased risk of vitamin D deficiency (22).

In our study, neonates in RDS group had significantly lower mean serum25(OH)D level

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than the control group (10.6 ng/dl vs 13.9 ng/dl) (P value =0.028). Logistic regression

analysis shows that low day 1 serum 25(OH)D level is independent risk factors for RDS.
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It was demonstrated that in type 2 pneumocytes, 1,25(OH)D increased surfactant

synthesis by increasing intracellular phosphatidylcholine and phosphatidylglycerol and

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increased surfactant secretion by providing migration of newly formed osmophilic

lamellar bodies to the apex of the cell (8).

Sakurai et al. (2009) stated that 1,25(OH)D and its metabolite C-3 epimer play key role
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in alveolar epithelial–mesenchymal interaction, lipofibroblast proliferation, and apoptosis

of lung fibroblasts, which have critical roles in perinatal lung maturation (5).
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It has been demonstrated in experimental studies that vitamin D receptors are found in

type II pneumocytes, and that vitamin D plays a role in the morphogenesis of lung and

surfactant production (23).

Data from human and animal studies suggest that vitamin D may have a role in lung

development. The biological effects of metabolically active form of vitamin D,

1,25(OH)2D3, are mediated by the vitamin D receptor (VDR), It has been reported that

over 3000 genes have VDRE, many of which are involved in lung development. Vitamin

D pathway genes have been reported to be upregulated during the pseudoglandular and

saccular stages of lung development where proximal and distal airways are formed,

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respectively (24).

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We could not demonstrate any correlation between gestational age and vitamin D status.

Also, Park et al. reported that the serum 25-OHD concentrations were not significantly

correlated to gestational age (r=-0.034, P=0.573). There were no significant differences in

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serum 25-OHD concentrations and incidence of severe vitamin D deficiency among

early, moderate, and late preterm infants (19).

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Also Ataseven et al, in their study demonstrated that Vitamin D status was not correlated

with gestational age [r = 0.039; p = 0.634](25). Commented [M3]: another study showing no correlation with
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gestational age.
Ataseven F, Aygun C ,Okuyucu A ,im Bedir A, Kucuk Y, and
Kucukoduk S: Is Vitamin D Defi ciency a Risk Factor for
In RDS group, 57.5% had moderate 25(OH)D deficiency and 42.5% had severe 25(OH)D Respiratory
Distress Syndrome?
Int. J. Vitam. Nutr. Res. 83 (4)
deficiency. In control group, 12% of neonates had 25(OH)D insufficiency, 48% had
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moderate 25(OH)D deficiency, and 40% had severe 25(OH)D deficiency.

In study on 278 preterm infants, the incidence of vitamin D deficiency or insufficiency

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was 91.7% and 7.2%, respectively, and 51.1% of preterm infants were classified as

having severe vitamin D deficiency. Only 3 preterm infants were on sufficient vitamin D

status (26).

BPD is the most prevalent long-term morbidity among surviving extremely preterm

infants and has a multifactorial etiology. BPD is associated with later risk of reactive
airways disease, such as asthma, post neonatal mortality and adverse neuro-

developmental outcomes (27).

In our study more neonates with severe 25(OH)D deficiency developed BPD than those

with moderate deficiency (29.4% vs 8.7%) but the difference is not significant (P value

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=0.08). The lack of statistically significant relation between vitamin D status and

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development of BPD may be explained by genetic predisposition to BPD in addition to

oxygen toxicity, barotrauma and volutrauma. A study by Koroglu et al. examined the role

of the VDR variant Fok 1 in BPD risk among 109 preterm neonates but did not find a

significant relation (28).

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Fettah et al. reported that 36.8% were diagnosed with BPD in vitamin D deficient group,
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and 8.3% were diagnosed with BPD in neonates with normal vitamin D level (P 0.014)
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(23).

Cetinkaya et al. reported that by univariate analysis lower cord blood 25(OH) levels were

associated with BPD in a cohort of 100 preterm infants (32 weeks) (29) .In contrary,
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Joung et al., reported that among 44 infants born before 29 weeks, median 25(OH)D

levels at birth were 30.4 ng/ ml in preterm infants who subsequently died or developed

BPD and 33.8 ng ml in infants who survived without BPD, and there were no statistically
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significant differences between these two groups (P= 0.6) (27).

There is no statistically significant correlation between serum 25(OH)D level and

duration of mechanical ventilation . In a study by Onwuneme et al., low 25OHD level

(<30 nmol/L) in preterm infants at birth was associated with increased oxygen

requirement (P=.008), increased duration of intermittent positive-pressure ventilation

during resuscitation at delivery (P=.032), and greater need for assisted ventilation

(P=.013) (30).

On contrary, Fettah et al. reported that when groups with deficient and normal vitamin D

levels were compared, duration of mechanical ventilation did not differ between both

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groups.

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Vitamin D supplementation during pregnancy in the United States (31) and Europe (32)

showed trends but no significant decreases in the incidence of childhood wheezing and

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asthma in the first 3 years of life among the offspring. However, these studies did not

analyze the role of vitamin D status in RDS or BPD among preterm infants.

American Academy of Pediatrics guidelines recommend vitamin D intake of 400 IU per

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day for all infants (33). Fort et al. suggested that vitamin D deficiency among preterm
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infants can be prevented by supplementation with 800 units of vitamin D daily (34).

At Ain Shams University Hospital, we provide 400 IU vitamin D daily for exclusively

human milk-fed infants. For infants with a combination of human milk and formula also
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400 units is added until the infant is consuming a volume adequate to provide 400 units

per day.
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We conclude that that low 25(OH)D level is universal among Egyptian preterm neonates

at birth and it is independent risk factor for development of RDS . However, we did not

detect a statistically association between vitamin D status and BPD.

Limitations in our study included small sample size, risk and lack of data on prenatal

maternal 25(OH)D levels. Further studies on larger population of preterm neonates are
needed to assess the relation of maternal and neonatal vitamin D status with subsequent

development of BPD. Interventional trials of vitamin D supplementation are also needed.

We recommend regular supplementation of Egyptian pregnant women with vitamin D to

avoid development of RDS.

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Serum 25(OH)D (ng/ml)
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13.92

10.65
14
12
10
8
ST

6
4
2
0
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RDS group Control group

Fig. (1): Comparison between neonates in RDS group and control group as regard mean
serum 25(OH)D level.
 D
TE
Moderate deficiency Severe deficiency

91.30%

EP
100%
70.60%
80%

60%
29.40%
40%
8.70%
C
20%

0%
AC

Negative Positive
BPD

Fig. (2): Comparison between neonates with moderate and severe 25(OH)D deficiency in
ST

RDS group as regards BPD.

JU
 D
Table (1): Descriptive demographic data of neonates of RDS group and

TE
control group:
RDS group Control group Independent t-test
No. = 40 No. = 25 t/X²* P-value

EP
Gestational age (weeks) Mean ± SD 31.4 ± 2.25 32.44 ± 1.76 -1.964 0.054

Birth weight(kg) Mean ± SD 1.55 ± 0.63 1.72 ± 0.52 -1.121 0.267

C
Sex no (%) Female 23 (57.5) 13 (52) 0.188* 0.664
Male 17 (42.5) 12 (48)
AC

Mode Of delivery no (%) LSCS 33 (82) 19 (76) 0.406* 0.524

VD 7 (17.5) 6 (24)
IUGR no (%) Negative 34 (85) 23 (92) 0.698* 0.403
Positive 6 (15) 2 (8)
Maternal age (years) Median (IQR) 29 (24 – 31.5) 27 (26 – 29) -1.258 0.208
Range 18 – 36 19 – 33
ST

Antenatal steroid no (%) Negative 36 (90) 23 (92) 0.073* 0.786

Positive 4 (10) 2 (8)
Vitamin D Negative 21 (52.5) 10 (40) 0.964* 0.326
supplementation
Positive 19 (47.5) 15 (60)
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during pregnancy no (%)

PROM no (%) Negative 21 (52.5) 8 (32) 2.616* 0.106
Positive 19 (47.5) 17 (68)
DM with pregnancy no Negative 38 (95) 25 (100) 1.290* 0.256
(%) Positive 2 (5) 0 (0)
Preeclampsia no (%) Negative 34 (85) 24 (96) 1.937* 0.164
Positive 6 (15) 1 (4)

*: Chi-square test
 D
TE
Commented [M4]: Table deleted as it is mentioned in results

EP
C
AC
ST
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Table (2): Comparison between neonates with moderate and severe

25(OH)D deficiency in RDS group as regards demographic and maternal
clinical data:
Moderate Severe Independent t-
 deficiency(No=23) deficiency(No=17) test
t/X²* P-value

Birth weight (kg) Mean ± 1.49 ± 0.51 1.64 ± 0.78 -0.771 0.446 Commented [M5]: This demonstrate that the degree of vitamin
SD D deficiency is not related to birth weight

Range 0.8 – 2.8 0.94 – 4

Gestational age Mean ± 31.43 ± 2.29 31.35 ± 2.26 0.112 0.911 Commented [M6]: This demonstrate that that the degree of
(weeks) SD vitamin D deficiency is not related to gestational age

D
Range 26 – 34 26 – 34
Mode of delivery no LSCS 20 (87) 13 (76.5) 0.744* 0.388

TE
(%) VD 3 (13) 4 (23.5)
Sex no (%) Female 17 (73.9) 6 (35.3) 5.966* 0.015
Male 6 (26.1) 11 (64.7)
Vitamin D Negative 11 (47.8) 10 (58.8) 0.474* 0.491
supplementation Positive 12 (52.2) 7 (41.2)

EP
during pregnancy no
(%)
Antenatal steroid no Negative 21 (91.3) 15 (88.2) 0.102* 0.749
(%) Positive 2 (8.7) 2 (11.8)
Preeclampsia no (%) Negative 19 (82.6) 15 (88.2) 0.243* 0.622
C
Positive 4 (17.4 2 (11.8)
DM no (%) Negative 22 (95.7) 16 (94.1) 0.048* 0.826
Positive 1 (4.3) 1 (5.9)
AC

PROM no (%) Negative 12 (52.2) 9 (52.9) 0.002* 0.962

Positive 11 (47.8) 8 (47.1)

*: Chi-square test
ST
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Table (3) Comparison between neonates with moderate and severe

25(OH)D deficiency in RDS group as regard respiratory parameters:
 Moderate Severe Mann-Whitney
deficiency(No=23) deficiency(No=17) test
Z/t*/X²• P-
value
Apgar 1 Median 5 (4 – 6) 5 (4 – 6) -0.155 0.877
(IQR)
Range 0–7 2–6

D
Apgar 5 Median 7 (6 – 7) 7 (7 – 7) -0.032 0.975
(IQR)
2–9 5–9

TE
Range
Grade of RDS Grade I-2 9 (39.1) 7 (41.2) 0.017• 0.896
no (%) Grade 3-4 14 (60.9) 10 (58.8)
Initial pH Mean ± SD 7.32 ± 0.09 7.30 ± 0.10 0.746* 0.460
7.15 – 7.48 7 – 7.46

EP
Range
Initial CO2 Mean ± SD 47.94 ± 14.37 51.89 ± 15.94 -0.819* 0.418
Range 26.4 – 80.3 26.8 – 91.6
Mechanical Negative 1 (4.3) 0 (0) 0.758 0.384
ventilation Positive 22 (95.7) 17 (100)
C
no (%)
Maximum PIP (Cm Mean ± SD 12.74 ± 8.05 13.12 ± 9.23 -0.138* 0.891
H2O) Range 0 – 20 0 – 25
AC

Duration of Mean ± SD 12.09 ± 9.46 16.53 ± 13.46 -1.227* 0.227

mechanical
Range 2 – 40 2 – 40
ventilation (days)
Days of NICU Mean ± SD 25.83 ± 17.29 28.53 ± 13.69 -0.532* 0.598
admission (days) Range 7 – 52 3 – 46
Mortality no (%) Alive 21 (91.3) 13 (76.5) 1.687 0.194
ST

Died 2 (8.7) 4 (23.5)

*: Independent t-test
•
: Chi-square tes
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 Commented [M7]: New table
Table (4): Correlation between serum vitamin D level and demographic,
respiratory and laboratory parameters of neonates in RDS group:

Serum vitamin D (ng)

D
r P-value

Gestational age -0.013 0.935

TE
Birth weight 0.042 0.797

Apgar 1 -0.020 0.904

EP
Apgar 5 -0.009 0.958

Initial pH -0.269 0.093

Initial CO2 0.072 0.658

C
Maximum PIP 0.047 0.774
AC

Days of mechanical ventilation (days) -0.061 0.710

Days of NICU admission (days) -0.161 0.320

Serum Ca (mg/dl) -0.013 0.935

ST
JU
Table (5): Logistic regression analysis of risk factors of RDS in our
patients:

D
B S.E. Wald Sig. Odds 95% CI for OR
ratio (OR)
Lower Upper

TE
Gestational age (weeks) -0.261 0.138 3.550 0.060 0.770 0.587 1.011

Serum vitamin D (ng/dl) -0.101 0.048 4.375 0.036 0.904 0.822 0.994

birth is independent risk factor for RDS. EP

Logistic regression analysis shows that low serum vitamin D level at
Commented [M8]: Added this table to highlight that low vitamin
D level independently from low gestational age a risk factor for RDS
in our patients as both our groups are almost gestational age
C
matched.

28
AC
ST
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