Abstract
To study plasma arachidonic acid (AA) and docosahexaenoic acid (DHA) status in Tunisian very low birth weight (VLBW) infants and their association with selected neonatal morbidities. A total of 709 VLBW infants and 339 term infants were included. Plasma fatty acids were analyzed using capillary gas chromatography. VLBW infants had significantly (p < 0.001) lower plasma AA (9.44 ± 2.12 vs. 10.8 ± 2.10) and DHA (2.56 ± 0.89 vs. 3.46 ± 1.09) levels, but higher n-6:n-3 ratio (5.58 ± 1.22 vs. 5.17 ± 1.46) than term infants. In VLBW infants, plasma AA and DHA were related to gestational age (r = 0.156; p = 0.001 and r = 0.134; p = 0.003, respectively), birthweight (r = 0.242; p < 0.001 and r = 0.181; p < 0.001, respectively) and head circumference (r = 0.138; p = 0.005 and r = 0.108; p = 0.027, respectively). Infants with respiratory distress syndrome have decreased plasma AA and DHA and those with intraventricular hemorrhage have decreased plasma AA and n-6:n-3 ratio. Sepsis was associated with decreased DHA levels. Plasma long chain polyunsaturated fatty acids status is low in VLBW infants. These deficits may enhance the risk of common neonatal morbidities, rendering their prevention and correction greatly warranted.
Highlights
Long chain-polyunsaturated fatty acids (LCPUFAs) arachidonic acid (AA, C20:4 n-6) and docosahexaenoic acid (DHA, C22:6 n-3) are critical for neural, visual and vascular development [1, 2]
Fetal needs in these LCPUFAs are mainly covered by placenta transfer, which substantially increases during the third trimester of pregnancy with little synthesized into fetus [1, 5]
This study showed lower plasma AA and DHA levels in Tunisian very low birth weight (VLBW) neonates compared to term infants
Summary
Long chain-polyunsaturated fatty acids (LCPUFAs) arachidonic acid (AA, C20:4 n-6) and docosahexaenoic acid (DHA, C22:6 n-3) are critical for neural, visual and vascular development [1, 2]. The development and maturation of the nervous system in Humans begins in utero and extends over the two first years of life, period during which the needs of the fetus and newborn in AA and DHA are elevated [3, 4] Fetal needs in these LCPUFAs are mainly covered by placenta transfer, which substantially increases during the third trimester of pregnancy with little synthesized into fetus [1, 5]. Preterms may be in disadvantage compared to term infants regarding PUFAs status due to a shortened gestation [4, 6] and low activity of enzymes responsible of endogen synthesis of LCPUFAs [7,8,9]
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