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.