TY - JOUR
T1 - Delayed villous maturation of the placenta
T2 - Quantitative assessment in different cohorts
AU - Treacy, Ann
AU - Higgins, Mary
AU - Kearney, John M.
AU - McAuliffe, Fionnuala
AU - Mooney, Eoghan E.
PY - 2013/3
Y1 - 2013/3
N2 - Placental villous maturation is maximal in the 3rd trimester, with an abundance of terminal villi. Delayed villous maturation (DVM) of the placenta is associated with chromosomal abnormalities, gestational diabetes, and an adverse outcome. This study compares quantitative assessment of vasculo-syncytial membranes (VSM) in cases of liveborn infants, perinatal deaths, and controls. Cases were selected as follows: (1) liveborn infants with a qualitative diagnosis of DVM ( n = 15); (2) controls matched for gestational age whose placentas did not have DVM (n = 15); (3) stillbirths (SB)/neonatal deaths (NND) showing DVM (n = 13); and (4) SB from autopsies in which DVM was felt to be the cause of death (COD) (n = 12). Vasculo-syncytial membranes were counted in 10 terminal villi in each of 10 consecutive high-power fields on 3 slides. Data analysis was carried out using SPSS. Liveborn cases with DVM showed statistically significantly less VSM than controls (mean 1.01 vs 2.42, P < 0.0001). The SB/NND group also showed significantly less VSM than the control group (mean 0.46 vs 2.42, P < 0.0001) and less than the liveborn DVM group (mean 0.46 vs 1.01, P = 0.001). The COD group was significantly different from the control group (mean 0.42 vs 2.42, P < 0.0001) and the liveborn DVM group (mean 0.42 vs 1.01, P < 0.0001) but not significantly different from the SB/NND group. There is a quantitative reduction in VSM in cases of DVM compared to controls.
AB - Placental villous maturation is maximal in the 3rd trimester, with an abundance of terminal villi. Delayed villous maturation (DVM) of the placenta is associated with chromosomal abnormalities, gestational diabetes, and an adverse outcome. This study compares quantitative assessment of vasculo-syncytial membranes (VSM) in cases of liveborn infants, perinatal deaths, and controls. Cases were selected as follows: (1) liveborn infants with a qualitative diagnosis of DVM ( n = 15); (2) controls matched for gestational age whose placentas did not have DVM (n = 15); (3) stillbirths (SB)/neonatal deaths (NND) showing DVM (n = 13); and (4) SB from autopsies in which DVM was felt to be the cause of death (COD) (n = 12). Vasculo-syncytial membranes were counted in 10 terminal villi in each of 10 consecutive high-power fields on 3 slides. Data analysis was carried out using SPSS. Liveborn cases with DVM showed statistically significantly less VSM than controls (mean 1.01 vs 2.42, P < 0.0001). The SB/NND group also showed significantly less VSM than the control group (mean 0.46 vs 2.42, P < 0.0001) and less than the liveborn DVM group (mean 0.46 vs 1.01, P = 0.001). The COD group was significantly different from the control group (mean 0.42 vs 2.42, P < 0.0001) and the liveborn DVM group (mean 0.42 vs 1.01, P < 0.0001) but not significantly different from the SB/NND group. There is a quantitative reduction in VSM in cases of DVM compared to controls.
KW - Delayed villous maturation
KW - Diabetes mellitus
KW - Distal villous immaturity
KW - Perinatal mortality
KW - Vasculo-syncitial membranes
UR - http://www.scopus.com/inward/record.url?scp=84877755426&partnerID=8YFLogxK
U2 - 10.2350/12-06-1218-OA.1
DO - 10.2350/12-06-1218-OA.1
M3 - Article
C2 - 23137099
AN - SCOPUS:84877755426
SN - 1093-5266
VL - 16
SP - 63
EP - 66
JO - Pediatric and Developmental Pathology
JF - Pediatric and Developmental Pathology
IS - 2
ER -