06 septembre 2017

L'association entre l'histopathologie placentaire et le "trouble du spectre de l'autisme"

Aperçu: G.M.
La recherche suggère que le trouble du spectre de l'autisme (TSA) a son origine dans l'utérus. Cette étude examine l'association entre la preuve de l'histopathologie placentaire et le TSA.
Une inflammation placentaire aiguë, quel que soit le type, a été associée à un risque accru de TSA (odds ratio [OR] = 3,14, IC 95% = 1,39, 6,95). 
Dans les sous-analyses parmi l'ensemble des inflammations aiguës des placentas masculins, la réponse inflammatoire fœtale dans les vaisseaux de la cororie et la pathologie de la malpérité vasculaire maternelle est restée significativement associée à un risque accru de TSA alors que l'œdème de villosité placentaire est resté associé à une diminution du risque de TSA.  

Placenta. 2017 Sep;57:183-188. doi: 10.1016/j.placenta.2017.07.006. Epub 2017 Jul 8.

The association between placental histopathology and autism spectrum disorder

Author information

1
Department of Public Health Sciences, Henry Ford Hospital, 1 Ford Place, Suite 3E, Detroit, MI 48202, USA. Electronic address: jstraug1@hfhs.org.
2
Department of Family Medicine and Public Health Sciences, Wayne State University, 6135 Woodward Avenue, Detroit, MI 48202, USA. Electronic address: dmisra@med.wayne.edu.
3
Department of Public Health Sciences, Henry Ford Hospital, 1 Ford Place, Suite 3E, Detroit, MI 48202, USA. Electronic address: gdivine1@hfhs.org.
4
Placental Modulation Laboratory, Institute for Basic Research in Developmental Disabilities, 1550 Forest Hill Road, Staten Island, NY 10314, USA. Electronic address: ruchit.shah27@gmail.com.
5
Placental Analytics LLC, 187 Overlook Circle, New Rochelle, NY 10804, USA. Electronic address: gaby15785@gmail.com.
6
Placental Analytics LLC, 187 Overlook Circle, New Rochelle, NY 10804, USA; Department of Women's, Gender, & Sexuality Studies & Bioethics, Emory University, 201 Dowman Drive, Atlanta, GA 30322, USA. Electronic address: samantha.vanhorn@emory.edu.
7
Department of Obstetrics and Gynecology, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: vonbreyt@gmail.com.
8
Department of Pediatrics, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: bdygulska@outlook.com.
9
Department of Pediatrics, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: rebeccaschmitt427@gmail.com.
10
Department of Obstetrics and Gynecology, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: sal9047@nyp.org.
11
Department of Pediatrics, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: prn9001@nyp.org.
12
Placental Modulation Laboratory, Institute for Basic Research in Developmental Disabilities, 1550 Forest Hill Road, Staten Island, NY 10314, USA; Placental Analytics LLC, 187 Overlook Circle, New Rochelle, NY 10804, USA; Department of Obstetrics and Gynecology, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA; Department of Pediatrics, New York Presbyterian Brooklyn Methodist Hospital, 550 6th Street, Brooklyn, NY 11215, USA. Electronic address: carolyn.salafia@gmail.com.

Abstract

INTRODUCTION:

Research suggests that autism spectrum disorder (ASD) has its origins in utero. This study examines the association between evidence of placental histopathology and ASD.

METHODS:

Administrative claims data and medical records data were used to identify ASD cases (N = 55) and matched controls (N = 199) born at New York Methodist Hospital between 2007 and 2014 and subsequently seen in affiliated pediatrics clinics. Placentas from all births during this time period were reviewed as part of routine care. Data were analyzed using conditional logistic regression to account for the matched (gender, gestational age, and birth weight) design.

RESULTS:

Acute placental inflammation, regardless of type was associated with an increased risk of ASD (odds ratio [OR] = 3.14, 95% CI = 1.39, 6.95). Chronic uteroplacental vasculitis (OR = 7.13; 95% CI = 1.17, 43.38), the fetal inflammatory response in the chorionic plate vessels (OR = 5.12; 95% CI = 2.02, 12.96), and maternal vascular malperfusion pathology (OR = 12.29; 95% CI = 1.37, 110.69) were associated with an increased risk of ASD. Placental villous edema was associated with a decreased risk of ASD (OR = 0.05; 95% CI = 0.0005, 0.42). In subanalyses among male placentas acute inflammation overall, fetal inflammatory response in the chorionic plate vessels, and maternal vascular malperfusion pathology remained significantly associated with an increased risk of ASD whereas placental villous edema remained associated with a decreased risk of ASD.

DISCUSSION:

Histologic evidence of placental inflammation and maternal vascular malperfusion pathology are associated with ASD.
PMID:28864010
DOI:10.1016/j.placenta.2017.07.006

Aucun commentaire: