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Markers of placental insufficiency: etiology and the risk of cerebral palsy:Population based studies of preeclampsia, low birth weight, and abnormal placental weight

Strand, Kristin Melheim
Doctoral thesis
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URI
http://hdl.handle.net/11250/2372382
Date
2015
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  • Institutt for klinisk og molekylær medisin [2008]
Abstract
Placental insufficiency may be defined as a placenta not able to perform its central tasks;

namely, delivery of sufficient oxygen and nutrients to the developing fetus. In this thesis,

preeclampsia, fetal growth restriction (FGR), and abnormal placental weight were applied as

markers of placental insufficiency.

Abnormal interaction between fetal and maternal tissues during placentation, leading to

shallow placentation, may be the commencing step of placental insufficiency.

Cytomegalovirus (CMV), a virus capable of infecting the placenta, has been suggested to

potentially harm placentation and thereby initiate the pathophysiological cascade leading to

preeclampsia. However, results from epidemiological studies assessing maternal CMV

antibodies in pregnancy and development of preeclampsia have been inconclusive.

At the other end of placental insufficiency, is its potential to compromise the fetus by limiting

oxygen supply and ultimately cause fetal death. The etiology of cerebral palsy (CP), a

disorder often considered to be an intermediate outcome between a healthy infant and

neonatal death, remains largely unknown. The placenta has recently been highlighted as an

area of major interest in CP etiology.

The aim of this thesis was to assess CMV infection as a potential etiological factor in

preeclampsia (paper I) and to study the association between markers of placental insufficiency

and CP (papers II and III).

Paper I was a case control study based on the Norwegian Mother and Child Cohort Study and

included 1500 women with preeclampsia (cases) and 1000 women without preeclampsia

(controls). Maternal antibodies to CMV were analyzed in plasma samples collected at 17-18

weeks of gestation. The proportion of women seropositive for CMV antibodies did not differ

between cases and controls. Thus, this study could not find evidence of CMV infection as a

potential etiological factor in preeclampsia pathogenesis.

Data for papers II and III were obtained by linkage of the Cerebral Palsy Register of Norway

(CPRN) and the Medical Birth Registry of Norway (MBRN). The CPRN contains detailed

clinical data about children with CP, and pregnancy and perinatal data were available in the

MBRN.

In Paper II, the association between preeclampsia and cerebral palsy was assessed, and

singleton children that survived the first week of life in Norway during 1996-2006 were

included. Preeclampsia was associated with an increased risk of CP. This association was

mainly mediated through the children being born preterm and/or small for gestational age

(SGA- a proxy for FGR). Children exposed to preeclampsia and born at term with normal

birth weight had no excess risk of CP, indicating that preeclampsia may not have a direct

effect on the risk of CP.

In Paper III, we analyzed the association between low or high placental weight and CP, and

included all singleton infants born alive in Norway during 1999-2008. Low placental weight,

low placental weight/birth weight ratio, and low placental weight/birth length ratio were

associated with an increased risk of CP. Regarding CP subtypes, the most consistent finding

was a high risk of spastic bilateral CP associated with low placental weight and low placental

weight/birth length ratio. These results warrant further study of poor placental reserve as a

potential cause of CP.

Thus, the main conclusions of this thesis are that CMV infection in early pregnancy unlikely

is a major contributing factor in the pathogenesis of preeclampsia, and that placental

insufficiency may play a significant role in the etiology of CP, in particular through its effect

on fetal growth and preterm delivery.
Publisher
NTNU
Series
Doctoral thesis at NTNU;2015:172

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