Iodine Status of Preterm Infants Born in an Area of Iodine Sufficiency: Are They at Risk of Iodine Deficiency?

ObjectiveTo the assess the iodine status of preterm infants born in an area of iodine sufficiency using the urinary iodine concentration (UIC) and thyroid-stimulating hormone (TSH) levels and compare these values across different feeding practices during the first 7 days of life.MethodsIn this cross-sectional study, 88 preterm infants born at 30 to 34 weeks of gestation and admitted to the neonatal intensive care unit of a referral hospital in Tehran (Iran) were included. The infant UIC and TSH levels and breast milk iodine concentration in mothers who were exclusively breastfeeding were measured.ResultsMedian (interquartile range [IQR]) UIC and TSH levels in the study population were 81 (39-189) μg/L and 1.60 (0.80-2.85) mIU/L, respectively. When preterm infants were stratified by the type of feeding, the median (IQR) UICs were 64 (42-126) μg/L in parenteral nutrition, 125 (41-195) μg/L in exclusively breastfeeding, 57 (28-123) μg/L in formula feeding, and 45 (35-132) μg/L in mixed feeding, with no statistically significant difference between the groups (P = .31). The median (IQR) breast milk iodine concentration was 271 (177-521) μg/L in preterm infants exclusively fed their mothers’ own milk. There was no significant difference in the proportion of the TSH levels of >5 mIU/L between preterm infants who received enteral and parenteral nutrition (P = .27).ConclusionPreterm infants are at risk of iodine deficiency even in an area where the general population has adequate iodine. Only the preterm infants who received exclusively their mothers’ own milk had marginally adequate iodine status. Further studies are warranted to determine the necessity of iodine supplementation for this vulnerable group.     

Transient Improvement of Cerebellar Oligodendroglial Development in a Neonatal Hyperoxia Model by PDGFA Treatment

In preterm infants, the changes from fetal life to ex‐utero conditions often coincide with reduced growth and white matter damage of the cerebellum. The premature increase in arterial oxygen tension caused by preterm birth may dysregulate cerebellar development. In a hyperoxia rat model of white matter damage to mimic a steep increase in oxygen levels by 24 h exposure to 80% O₂ from postnatal day 6 (P6) to day 7, we analyzed growth factor (GF) synthesis of cerebellar astrocytes. Determination of GF production was performed in astrocytes after Magnetic‐activated cell sorting (MACS) isolation from cerebelli after hyperoxia exposure ex vivo, and also in astroglial cultures. Oligodendrocyte progenitor cell (OPC) function was analyzed in cerebellar OPCs isolated by MACS after hyperoxia. Administration of PDGFA from P6 to P11, during hyperoxia and during 4 days recovery, was finally tested for protection of oligodendroglia and myelination. As a result, expression of the GFs Pdgfa, Fgf2, and Bdnf was diminished in cerebellar astrocytes in vitro and in vivo. Gene expression of Olig1, Olig2, Sox9, Sox10, and Cnp was reduced in OPCs in vivo. Nasal PDGFA application improved oligodendroglial proliferation after hyperoxia at P7. However, this treatment effect vanished until P9. Impaired MBP expression after hyperoxia was attenuated by PDGFA treatment until P11, but not beyond when PDGFA supply was stopped. In this study on neonatal cerebellar injury, it is documented for the first time that improvement of oligodendroglial proliferation and of myelination can be achieved by PDGFA treatment. However, the treatment benefit is not maintained long term.     

20-αHydroxycholesterol,an oxysterol in human breast milk,reverses mouse neonatal white matter injury through Gli-dependent oligodendrogenesis

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5-Hydroxyeicosatetraenoic acid and human parturition

5-Hydroxyeicosatetraenoic acid (5-HETE) is an arachidonic acid (AA) metabolite derived from the lipoxygenase pathway which is capable of inducing uterine contractions. The purpose of this study was to determine a). whether 5-HETE concentrations in amniotic fluid increase before or after the onset of labor and b). whether acetylsalicylic acid (ASA) could modulate the production of 5-HETE by human amnion cells. 5-HETE concentrations are increased in amniotic fluid before the onset of labor. Furthermore, ASA treatment as expected inhibited PGE₂, but also significantly increased 5-HETE production by amnion cells. 5-HETE concentrations on average increased by greater than 2.5 fold (p < 0.001) in amniotic fluid prior to spontaneous labor when compared with samples obtained from the same patients earlier in gestation and therefore may be important in mechanisms regulating the onset of labor. ASA provokes an increase in 5-HETE biosynthesis by amnion cells: control media 2.60 ± 1.5, ASA treatment alone 5.17 ± 0.20, IL-1β alone 6.39 ± 2.1, and ASA + IL-1β 8.95 ± 1.2 (mean ± SEM) picograms per microgram protein per 16 hours. These findings may explain in part why cyclooxygenase inhibitors are not always successful in treating women with preterm labor.     

Synthesis of 5- and 7-hydroxy indolizidin-2-one prostaglandin-F2α modulators and activity on myometrial contractility towards development of agents for delaying preterm birth

In pursuit of more effective-labor delaying tocolytic agents, the prostaglandin F2α (PGF2α) receptor (FP) modulator PDC113.824 [(6S)- 2 ] represents a potent lead for developing therapy to treat preterm birth. Derivatives of FP modulator (6S)- 2 were synthesized, possessing respectively 5- and 7-hydroxyl groups on the indolizidin-2-one amino acid (I²aa) residue. The effects of the alcohol substituents were examined in a PGF2α-induced myometrial contraction assay. Based on knowledge of dihedral angle values of model I²aa peptides from X-ray analyses, the results of the study indicate respectively encouraging and limited potential for creating improved tocolytic agents by modifications at the 5- and 7-positions.     

Is a foetus developing in a sterile environment?

Novel findings in microbiology question the long‐standing paradigm that a healthy pregnancy implies a sterile uterus. It now seems that the placenta is frequently colonized with bacteria, and a placental microbiome has been identified. Recent literature findings are summarized here, and an attempt is made to separate pathological bacterial presence from a naturally occurring microbiome.