Cross-sectional description of early postnatal fatty acid patterns in delivered preterm infants.

Preterm birth prematurely interrupts maternal fatty acid supply, yet gestational age-specific serum fatty acid profiles and perinatal determinants remain incompletely defined. In this prospective cohort, serum samples of very preterm infants (<32 weeks) collected within 24 h of birth were analyzed by gas chromatography-mass spectrometry. Fatty acids were classified as SCFAs, MCFAs, LCFAs, MUFAs, and PUFAs. Associations with gestational age, maternal comorbidities, antenatal medications, and infant sex were assessed using multivariable linear regression. A total of 105 very preterm infants were included. Lower gestational age was associated with greater fatty acid insufficiency. Total SCFAs increased with gestational age (p = 0.003), driven by rising butyric acid (C4:0) and caproic acid (C6:0). SFAs and MUFAs increased significantly (p = 0.005 and 0.04) with gestational age. Although total LCFAs and PUFAs did not differ significantly, the proportion of linoleic acid increased with gestational age (C18:2n6c) (p = 0.01). Maternal hypertension was associated with higher proportions of C18:2n6c (p = 0.001) and decreased levels of eicosatrienoic acid (C20:3n6, p = 0.04) and arachidonic acid (ARA, C20:4n6; p = 0.05). Infants of diabetic mothers showed an elevated ARA/DHA (docosahexaenoic acid, C22:6n3) ratio (p = 0.003). In multiple gestation, the C18:2n6c proportion increased (p = 0.0007), and the DHA proportion decreased (p = 0.005). Male infants had lower levels and proportions of C20:3n6 than females (p = 0.009 and 0.003). Antenatal corticosteroids were associated with reduced levels and proportions of C6:0 (both p = 0.02), decreased C18:2n6c proportion (p = 0.003), and higher levels of ARA (p = 0.03) and DHA (p = 0.05). Antenatal magnesium sulfate exposure was linked to decreased levels and proportions of C16:1n7 (p = 0.04 and 0.05). Serum fatty acid profiles in preterm infants exhibit gestational age-dependent patterns and are associated with maternal comorbidities, antenatal medication exposure, and infant sex, providing new insights into early postnatal fatty acid status in this population.