Effects of postnatal hydrocortisone on cytokine profile in extremely preterm infants

Kentaro Tamura1, Mitsuhide Nagaoka1, Satomi Inomata1

  • 1Division of Neonatology, Maternal and Perinatal Center, Toyama University Hospital, Toyama, Japan.

Insights

Systemic hydrocortisone in preterm infants did not prevent bronchopulmonary dysplasia (BPD), but it may suppress interleukin-6 (IL-6) overproduction. This study examined cytokine profiles in extremely preterm infants receiving hydrocortisone.

Area of Science:

  • Neonatal Medicine
  • Pediatric Pulmonology
  • Immunology

Background:

  • Systemic hydrocortisone is used in preterm infants at risk for bronchopulmonary dysplasia (BPD).
  • The impact of hydrocortisone on cytokine profiles in this population is not well understood.
  • Investigating these effects is crucial for optimizing treatment strategies.

Purpose of the Study:

  • To examine the effects of postnatal hydrocortisone treatment on serum cytokine levels in extremely preterm infants.
  • To compare cytokine profiles between infants who received hydrocortisone and those who did not.
  • To assess the relationship between hydrocortisone use and BPD development.

Main Methods:

  • Retrospective study of 29 infants born before 28 weeks gestational age.
  • Serum cytokine levels measured in early (5-20 days) and late (28-60 days) phases.
  • Analyzed proinflammatory, Th1, Th2, Th17 cytokines, and chemokines, comparing steroid vs. non-steroid groups.

Main Results:

  • 45% of infants received hydrocortisone for respiratory deterioration.
  • BPD incidence was higher in the hydrocortisone group (P=0.008).
  • Hydrocortisone group showed a significantly lower late-to-early phase ratio of IL-6 (P=0.04); other cytokines were unchanged.

Conclusions:

  • Postnatal hydrocortisone for respiratory issues did not prevent BPD in this cohort.
  • Hydrocortisone treatment may suppress interleukin-6 (IL-6) overproduction in extremely preterm infants.
  • Further research is needed to clarify hydrocortisone's role in neonatal inflammatory responses.
Abstract

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