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Case Description :

Introduction: Respiratory Distress Syndrome (RDS) is a common cause of morbidity and mortality in preterm neonates. Levels of minor phospholipids and lecithin in amniotic fluid are significantly influenced by lipid metabolism.

Aim: To evaluate umbilical cord lipid profile of preterm infants with RDS and normal preterm group without RDS.

Materials and Methods: This was a hospital based cross-sectional study carried out in neonatal unit of at a Tertiary Care Centre at SMS Medical College, Jaipur, from June 2017 to May 2018. Out of total 80 preterm infants, 40 developed RDS and 40 infants served as controls. Umbilical cord blood lipid profile of neonates were done in both the groups and compared. Chi-Square test and unpaired Student’s t-test were used for statistical analysis. Probability was considered significant if less than 0.05


Mean weight of babies was 1494.75±201.66 grams in normal preterm group and 1450.25±233.23 grams in preterm with RDS group (p=0.364). Mean gestational age was 31.45±1.36 weeks in normal preterm group and 30.98±1.49 weeks in preterm with RDS group p=0.140). Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL) were higher in male babies in both the groups as compared to female babies (p>0.05). Mean cord blood Triglyceride (TG), Total Cholesterol (TC), Very Low Density Lipoprotein (VLDL), LDL and HDL levels were significantly lower in preterms with RDS as compared to normal preterms without RDS which was statistically significant (p<0.05). Mean cord blood TG, TC, VLDL and HDL levels in all gestational age were higher in normal preterm as compared to preterm with RDS (p<0.05), except for LDL on 34-36 weeks age.


Lower serum cord lipids of newborns may develop RDS. The cord blood, which is easily available, can be used for lipid levels at birth to predict RDS.


Preterm birth is one of the leading causes of infant morbidity and mortality worldwide [1]. The rate of preterm births has been increasing over the last several decades [2]. In extremely preterm newborns with respiratory distress, RDS is by far the most common diagnosis. RDS is one of the most common causes of morbidity and mortality associated with premature delivery [3]. RDS is a developmental disorder rather than a disease process per se. Surfactant deficiency which increases surface tension in alveoli, resulting in micro atelectasis and low lung volumes is the primary cause of RDS [4].
Pulmonary surfactant is a complex mixture of 90% lipids and 10% proteins [5]. Levels of lecithin and phospholipids in amniotic fluid, use of cholesterol for hormone synthesis, fetal growth and development during late gestation are significantly affected by lipid metabolism [6,7].
Umbilical Cord Serum Lipid Profile of Normal Preterm Neonates and Preterm Neonates with Respiratory Distress Syndrome: A Hospital-Based Cross-sectional Study
Lung cholesterol metabolism is regulated by both LDL and HDL. In addition, several factors significantly affect neonatal serum lipids, especially gestational age and birth weight. Maternal lipoproteins provide the free fatty acid substrate required for fetal surfactant synthesis in vivo [8]. Reduced transport of essential and long chain polyunsaturated fatty acids could inhibit normal fetal growth and maturation including delayed development of fetal lungs, which could lead to the RDS [9].
The purpose of the study was to compare umbilical cord lipid profile of preterm infants with RDS and normal preterm infants without RDS.


This hospital-based cross-sectional study was carried out at Neonatal Units of Department of Paediatrics, SMS Medical
Ram Narain Sehra1, Ankus h Garg 2, Sun iti Verma3 Ram Narain Sehra et al., Umbilical cord blood lipid profile in RDS and normal preterm.
Indian Journal of Neonatal Medicine and Research. 2020 Oct, Vol-8(4): PO34-PO38
College Jaipur from June 2017 to May 2018, after getting ethical clearance from research review board of the institute (IRB No. 57673/2017)
Sample size calculation was done using the formula:
(n) =(Z1-α/2)2 (σ)2/(d)2, where n= desired no of samples, Z1-α/2= Standardised value for corresponding level of confidence (At 95% CI, it is 1.96 in two tailed and 1.64 in one tailed test), d= Margin of error or rate of precision, σ=SD which is based on previous study, n=(1.96)2 (6.6)2/(2)2 = 42, two tailed = (1.64)2 (6.6)2/(2)2=29, one tailed, alpha error 0.05% . Sample size was rounded off to 40 cases and 40 controls with expected HDL values 34.2 mg/dL with SD±6.60 and weight [10]. Total 80 newborns were included in study, 40 newborns were normal at birth and 40 newborns developed RDS.
All newborn that fulfilled inclusion criteria were divided in two subsets on the basis of development of RDS. Preterm babies who developed RDS were included as preterm with RDS study group B and who did not develop RDS as healthy preterm control group A. Silverman and Andersen scoring was used for assessment of respiratory distress [11].

Inclusion criteria:

Inclusion criteria at admission was neonates with gestational age ≥ 28 weeks to ≤ 36 weeks and birth weight ranging from 980 grams to 2260 grams. For preterm with RDS (group B) clinical signs suggestive of RDS used in the study were cyanosis, retractions, evidence of acidosis or hypoxemia or hypercarbia on blood gas, diffuse alveolar atelectasis on X-ray. For healthy preterm neonates (group A) with the same gestational age were enrolled as controls.

Exclusion criteria: Exclusion criteria was history of maternal hypertension either before or during pregnancy, paternal or maternal hyperlipidemia, maternal cardiovascular disease and diabetes mellitus or gestational diabetes, any history of maternal drug use during or before pregnancy (except for vitamins, folic acid, and iron), maternal history of smoking, neonates with congenital malformations, hypoxic ischemic encephalopathy, sepsis, small for gestation age.
Predesign structured proforma, devised by investigators, was used for history and data collection. After taking written consent from all parents/attendants detailed antenatal and natal history was taken. The mothers were analysed for maternal age, maternal membrane ruptured >24 hours, antenatal steroid administration, Pregnancy Induced Hypertension (PIH), and parity. Newborn examination included birth weight, assessment of gestational age by Modified Ballard score [12], Apgar score at 1 and 5 minutes, and complete clinical examination. Information of subjects was entered in separate proforma for each baby.

Sample collection: Primary investigator collected the cord blood sample. Cord blood samples of 3 mL were obtained from umbilical vein immediately after delivery. Samples were taken with all aseptic precautions in plain dry test tube and allowed to clot at room temperature for 20 minutes. Serum was separated by centrifugation (20 min, 2500 rpm) and kept at -20°C in hospital blood bank until the analysis. Serum was used for estimation of lipid profile using enzymatic colorimetric method. Serum LDL was estimated using Friedewald’s Formula [13].

Statistical analysis was performed with Statistical Package for the Social Sciences (SPSS), version 21 for windows statistical software package (SPSS inc, Chicago, IL, USA). The categorical data was presented as numbers (percentage) and were compared among groups using Chi-square test. The quantitative data was presented as mean and standard deviation and were compared by student’s t-test and continuous non-parametric data were compared by Pearson correlation coefficient test. Probability was considered to be significant if less than 0.05.

The study groups consisted of 80 preterm infants with gestational ages ranging from 28 weeks to less than 36 weeks and birth weights from 980 g to 2260 g. Of these neonates 40 developed RDS and 40 served as controls.
As regard the clinical characteristics of the studied infants in the present study, Apgar scores at 5 min were significantly higher in preterm with RDS as compared to the normal preterm group (p<0.001) and no significant differences of mean birth weight (p=0.364), mean gestational age (p=0.140), mean Apgar score at 1 minute (p=0.280), mode of delivery (p>0.05), parity (p=0.749) and premature rupture of membranes ≥ 24 hours (p=1.00) were observed between the groups [Table/Fig-1].
In the present study, mean cord lipid levels in relation to gender were observed statistically nonsignificant in both the groups (p>0.05), except for TC, which was significantly lesser (p<0.05) in females than males in group A. The male to female ratio was 1.2:1 and 0.91:1 in normal preterm group and preterm with RDS group, respectively [Table/Fig-2].
Mean cord blood TG, TC, VLDL, LDL and HDL levels were significantly lower in preterms with RDS as compared to normal preterms without RDS which was statistically significant (p<0.05) [Table/Fig-3].
Mean cord blood levels of TG, TC, HDL and VLDL were found to have significant differences in all gestational age subgroups in both RDS and non-RDS group (p< 0.05) except LDL which was nonsignificant in 34-36 weeks (p>0.05) [Table/Fig-4].
In preterm with RDS babies, there was a poor positive correlation between gestational age and cord blood TG (r=0.077, p=0.635), TC (r=0.145, p=0.369), VLDL (r=0.0792, p=0.627), LDL (r=0.1702, p=0.293) and HDL (r=0.0546, p=0.737) levels.


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