Fetal-placental inflammation, but not adrenal activation, is associated with extreme preterm delivery.

Trivedi S, Joachim M, McElrath T, Kliman HJ, Allred EN, Fichorova RN, Onderdonk A, Heitor F, Chaychi L, Leviton A, Majzoub JA; ELGAN study investigators.

Journal	Am J Obstet Gynecol.	Year	2011
Species	Human	Volume
Analytes Measured	CRP, E-Selectin, I-TAC, ICAM-1, ICAM-3, IGFBP-1, IL-1β, IL-6, IL-6R, IL-8, MCP-1, MCP-4, MIP-1β, MMP-1, MMP-9, Myeloperoxidase, RANTES, SAA, TNF-α, TNF-RI, TNF-RII, VCAM-1, VEGF, VEGFR-1 (sFlt-1), VEGFR-2 (KDR)	Page #
Matrix Tested	Dried blood spots	Category	Cytokines & Chemokines

Abstract

OBJECTIVE: Spontaneous labor at term involves the activation of placental corticotropin-releasing hormone and the fetal adrenal axis, but the basis for extreme preterm labor is unknown. Our objective was to determine whether placental corticotropin-releasing hormone is activated in extreme preterm labor.

STUDY DESIGN: One thousand five hundred six mothers delivering at less than 28 weeks' gestation were enrolled. Each mother/infant pair was assigned to the category that described the primary reason for hospitalization. Observers who had no knowledge of patient categorization assessed placenta microbiology, histology, and corticotropin-releasing hormone expression. These were correlated with the primary reason for hospitalization.

RESULTS: Among infants delivered at less than 28 weeks' gestation, spontaneous (vs induced) delivery was associated with less placental corticotropin-releasing hormone expression and more frequent signs of placental inflammation and infection.

CONCLUSION: Inflammation and infection, rather than premature activation of the fetal adrenal axis, should be the major focus of research to prevent extremely preterm human birth.