Female foetus was reported as a potential risk
factor, which is supported by the population-based Norwegian study among
1,691,053 singleton pregnancies38 and a nested
case-control study of 216 preeclamptic women39. A
systematic review and meta-analysis reported that male foetal sex was
associated with increased maternal risk of PE in the non-Asian
population40. Also, foetal sex might influence
maternal immunological function which could be the likely mediator
between foetal sex and PE. A recent finding proved the presence of a
higher concentration of spermine metabolite N1,N12-diacetylspermine
(DiAcSpm) in placenta, and serum of women pregnant with a female foetus,
which eventually increased the risk of
PE41.
Twin pregnancy (referred to multiple gestations in the current study) is
a risk factor for PE with a reported incidence of 2-3 times higher than
singleton pregnancy42.Likewise, nulliparity, increased
maternal BMI and chronic hypertension were risk factors for PE in twin
pregnancies, while monochorionicity, ethnicity, and assisted
reproductive techniques are not. In common with singleton pregnancies,
twin pregnancies complicated by PE are at greater risk of an adverse
pregnancy outcome43.In contrast with our findings,
some studies suggest that IVF is significantly associated with a higher
incidence of PE. Also,severe PE was more prevalent in the singleton
IVF-PE group than in the singleton SC-PE group44–46.
The prediction of PE is challenging and predicting the same among
high-risk pregnant women has not been attempted so far given the
complexity associated with its aetiology. Due to the multifactorial
aetiology of PE, the value of maternal characteristics and maternal
clinical factors can remain as one of the best ways to screen the
high-risk pregnant women susceptible to PE.