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. 2025 Aug 6;8(8):e71133. doi: 10.1002/hsr2.71133

Psychological Distress and Maternal Outcomes in Women With Pre‐eclampsia: A Retrospective Case‐Control Study

Fatemeh Esmaeilpour Gangi 1, Mahbobeh Faramarzi 2, Zinatossadat Bouzari 3,, Soraya Khafri 2, Maedeh Rezaie Bazgir 4, Mehrzad Netadj 5
PMCID: PMC12326432  PMID: 40772116

ABSTRACT

Background and Aims

Pre‐eclampsia (PE) is a significant pregnancy complication associated with adverse maternal and neonatal outcomes. This study aimed to explore the relationship between anxiety and depression symptoms and PE, as well as maternal and neonatal outcomes.

Methods

This retrospective case‐control cohort study included 2184 pregnant women enrolled in the Pregnant Women's Mental Health Registry between 2022 and September 2024, among whom PE was diagnosed. Based on the inclusion criteria, 196 women with PE were selected. A control group of 366 women without PE, matched for age and number of pregnancies, was included. Statistical analyses were performed using Chi‐square, Mann‐Whitney, and Kruskal‐Wallis tests.

Results

Women with PE exhibited significantly higher frequencies of depressive symptoms (26.5% vs. 16.7%, p = 0.004), anxiety symptoms (34.2% vs. 16.7%, p < 0.001), and psychological distress (46.9% vs. 26%, p < 0.001) compared to women without PE. Additionally, women with PE experienced more frequent adverse maternal outcomes, including shorter pregnancy duration, higher rates of emergency cesarean sections, bleeding, and postpartum infections (p < 0.001). Similarly, neonatal outcomes were worse in the PE group, with higher rates of NICU admission, low birth weight, birth trauma, and hospitalization within 6 weeks post‐birth (including measurements of height and head circumference) (p < 0.001). However, anxiety and depression scores did not significantly affect maternal and neonatal outcomes, except in women with PE whose infants were hospitalized within 6 weeks of birth, where higher anxiety scores and psychological distress were observed.

Conclusion

The increased prevalence of anxiety and depression symptoms in women with PE, along with their association with adverse maternal and neonatal outcomes, underscores the need to address psychological factors in the management of PE. Incorporating psychological support alongside medical care is recommended for obstetricians and healthcare providers.

Keywords: anxiety, depression, maternal outcomes, neonatal outcomes, pre‐eclampsia

1. Introduction

Pre‐eclampsia (PE) is a significant and common cause of morbidity and mortality for both mothers and fetuses. According to the American College of Obstetrics and Gynecology (ACOG), it is characterized by hypertension (HTN‐Preg) and proteinuria after the 20th week of pregnancy [1]. The incidence of PE ranges from 2% to 8% of pregnancies worldwide [2, 3] and is responsible for over 70,000 maternal deaths and 500,000 fetal deaths annually across the globe. In the United States, the leading causes of maternal mortality are severe maternal complications, ICU admissions, cesarean sections, and preterm births [4]. Studies in Eastern countries show the lowest incidence of PE in Vietnam (1.0%–1.9%) and the highest in the Philippines (3.3%–3.6%). In Western countries, Spain reports the lowest incidence (0.7%–1.6%), while Finland shows the highest (1.8%–3.6%). In the Middle East, Saudi Arabia has the lowest incidence (1.3%–3.9%), while Iran has the highest (3.3%–7.8%), and Jordan demonstrates significant variation in incidence (0.9%–6.8%) [5]. PE is associated with adverse pregnancy outcomes for both the mother and fetus, including acute kidney failure, cerebral hemorrhage, disseminated intravascular coagulation, and vascular collapse in pregnant women, as well as intrauterine growth restriction (IUGR), preterm birth, intraventricular hemorrhage, low Apgar score at 5 min, neonatal seizures, and respiratory distress syndrome [6, 7, 8].

The etiology of PE remains unclear, though its risk factors are well‐documented. These include a history of PE, chronic hypertension, pregestational diabetes, antiphospholipid syndrome, and obesity, as well as rarer factors such as a family history of PE and maternal trisomy 13 [4]. Other contributing factors include maternal and paternal race, genetics, maternal age, singleton versus multiple pregnancies, maternal education, climate, and air pollution [9]. Some studies highlight the role of psychiatric factors in the development of high blood pressure during pregnancy [10]. Many risk factors for PE are related to lifestyle habits (e.g., diet, sleep, physical activity, weight management, and smoking), psychological factors, high hemoglobin levels, and sleep disorders [11]. These findings suggest a potential link between depression and PE. Increased activity of the central and autonomic nervous systems may contribute to PE, a condition that occurs exclusively during pregnancy [10].

Depression and anxiety are common disorders during pregnancy, associated with an increased risk of adverse maternal and neonatal outcomes [12, 13, 14]. Depression is linked to functional impairments and health‐damaging behaviors, such as self‐medication, substance abuse, smoking, poor nutrition, inadequate weight gain, suicide, and delayed prenatal care [15]. Furthermore, placental corticotrophin‐releasing hormone (CRH), which is predominantly secreted in the second half of pregnancy, may influence adverse maternal and neonatal outcomes, such as preterm labor and low birth weight, in the context of depression [16, 17, 18]. These psychological factors, by stimulating the autonomic nervous system—an established risk factor for PE—lead to excessive activation of the sympathetic nervous system (SNS). Previous studies have shown that depressive symptoms are associated with adverse pregnancy outcomes, such as preterm birth, low birth weight (< 2500 g), and small head circumference at birth. Several studies have reported a positive relationship between maternal psychological factors and PE [11, 19]. Research by Malakuti and Basharpour found a positive correlation between the psychological status of pregnant women and PE, noting that higher anxiety levels were observed in women with PE [20, 21]. According to a study by Kutki and colleagues in Finland, the rates of depression and anxiety among 623 primiparous women, 28 of whom were diagnosed with PE, were 30% and 16%, respectively. This study found a significant association between PE and both anxiety and depression [22]. However, studies on the relationship between maternal depression and pregnancy outcomes have yielded contradictory evidence, particularly concerning its connection to adverse delivery outcomes, such as preterm birth, low birth weight, fetal growth restriction, and hypertension [18, 23, 24, 25, 26, 27]. Research in Iran indicates that approximately 30.6% of pregnant women experience depressive symptoms, most of whom do not receive adequate treatment or care [28].

Several studies have specifically examined the relationship between PE and depression, reporting mixed results. For example, Kurki et al [22]. found that both depression and anxiety were associated with an increased risk of PE among Finnish women. Similarly, Qiu et al [29]. observed a positive correlation between depression and the risk of developing PE. However, Vollebregt et al. [30] demonstrated that depression during pregnancy was not associated with PE or pregnancy‐induced hypertension.

The role of psychological factors, such as anxiety and depression, in PE and their relationship to maternal and neonatal outcomes remains underexplored, with existing studies presenting contradictory findings. To clarify this relationship, studies across different ethnic and racial populations are necessary. Although studies in Iran have examined the relationship between psychological factors, such as depression and anxiety [22, 31], and the occurrence of PE [11, 19], a systematic review and meta‐analysis by Shay et al. [32] reported a higher prevalence of pregnancy‐related hypertension in women with depression or anxiety. However, no recent studies were found examining maternal and neonatal outcomes in PE patients related to depression and anxiety in both Iran and other countries. Existing studies report a relatively high prevalence of PE in Iran, with regional differences in its occurrence [33]. Given the high prevalence of depression and anxiety among pregnant women in Iran [28, 34, 35] and the significant impact of psychological factors on maternal and infant health, our study aims to investigate the relationship between maternal and neonatal outcomes in PE patients and the occurrence of anxiety and depression symptoms among pregnant women in Babol County, Iran.

2. Material and Methods

2.1. Study Design and Setting

his retrospective case‐control cohort study was conducted on pregnant women registered in the Babol Pregnancy Mental Health Registry (http://register.mubabol.ac.ir) [36] between 2023 and September 2025. During this period, 2184 pregnant women who gave birth were enrolled, and their data were recorded at 4–6 weeks postpartum.

2.2. Sample Size Calculation

The sample size was determined using G‐Power software (version 3.1), based on a 95% confidence level and the incidence rate of adverse pregnancy outcomes (preterm birth) in women with anxiety (2.52) and the probability of preterm birth in anxious women (0.8). The analysis indicated that at least 196 women with pre‐eclampsia were required for sufficient power. To enhance the study's robustness, a 2:1 ratio of non‐Pre‐eclampsia controls was planned.

2.3. Inclusion and Exclusion Criteria

The inclusion criteria for both groups (pre‐eclampsia and non‐pre‐eclampsia) required that the women were at least 18 years old, had a singleton pregnancy, and had completed demographic information questionnaires and the Brief Symptom Inventory‐18 (BSI‐18) questionnaire. Additionally, data on labor outcomes and follow‐up between 4 and 6 weeks postpartum were available in the registry system. The exclusion criteria included incomplete delivery data in the registry system, pregnancies ending before 28 weeks for medical or nonmedical reasons (e.g., miscarriage, ectopic pregnancy, hydatidiform mole), and women who received counseling or medication during pregnancy.

2.4. Case and Control Selection

Women diagnosed with pre‐eclampsia after 20 weeks of gestation were classified as the case group, based on the diagnostic criteria established by the International Society for the Study of Hypertension in Pregnancy [37, 38]. From an initial pool of 236 eligible women with pre‐eclampsia identified in the registry, 40 individuals were excluded due to not meeting inclusion criteria or meeting one or more exclusion criteria. Ultimately, 196 women with pre‐eclampsia were retained in the study as the case group.

The control group was drawn from a total of 948 pregnant women without any clinical diagnosis of pre‐eclampsia during the same period. All control participants were screened using the same inclusion and exclusion criteria applied to the case group. Additionally, a frequency matching procedure was implemented based on maternal age and number of pregnancies (parity) to enhance comparability between groups. Following this process, 582 women were excluded due to unmatched characteristics or incomplete data, and a final sample of 366 women without pre‐eclampsia was included as the control group.

The process of group selection and matching was conducted a priori, before any outcome analyses, to minimize selection bias and preserve internal validity.

2.5. Data Collection Instruments

Three questionnaires were used to assess the study variables: demographic information, BSI‐18 for depression/anxiety, and maternal and neonatal outcomes. The demographic questionnaire included questions on age, education level, place of residence, and parity. If necessary, incomplete data were completed through follow‐up phone calls. The demographic questionnaire included questions on age, education level, place of residence, and parity.

2.6. Ethical Considerations

This study was approved by the Ethics Committee of Babol University of Medical Sciences (Ethical code: IR.MUBABOL.REC.1403.077). Written informed consent was obtained from all participants for the inclusion of their data. All personal and medical information was handled in strict confidentiality by the research team.

2.7. Measurement

  • Brief Symptom Inventory (BSI‐18)

    Psychological symptoms were assessed using the Persian version of the Brief Symptom Inventory‐18 (BSI‐18), a widely used self‐report screening tool for mental distress. The BSI‐18 is a shortened version of the BSI‐53, comprising 18 items across three subscales: somatization, depression, and anxiety, with six items each. Each item is rated on a 4‐point Likert scale (1 = not at all to 4 = extremely), with higher scores reflecting greater symptom severity. The total score ranges from 18 to 72. A cutoff score of ≥ 13 for women suggests clinically significant psychological distress and indicates the need for psychosocial intervention [39, 40].

    The psychometric validity and reliability of the Persian version have been previously established, with a Cronbach's alpha of 0.90 and test‐retest reliability of 0.81, confirming strong internal consistency and stability over time [41].

  • Assesses maternal and neonatal outcomes

    This questionnaire also assesses maternal and neonatal outcomes during labor and up to 4–6 weeks postpartum. Pregnancy outcomes include gestational age (based on the last menstrual period or ultrasound), type of delivery (vaginal or cesarean), perineal tears, bleeding, and post‐delivery infections. Neonatal outcomes include the newborn's condition at birth, including the need for ICU care or resuscitation, gender, length, weight, head circumference, birth injuries, and hospitalization status.

2.8. Data Analysis

Descriptive statistics were used to summarize the data: means, standard deviations (SD), and ranges were reported for continuous variables, and frequencies and percentages for categorical variables. The normality of continuous variables was assessed using the Shapiro‐Wilk test. Based on the distribution of data, chi‐square tests were used for categorical variable comparisons. For non‐normally distributed continuous variables, the Mann‐Whitney U test (two‐group comparison) and Kruskal‐Wallis test (more than two groups) were applied. Spearman's rank correlation was used to explore associations between non‐normally distributed continuous or ordinal variables. All hypothesis tests were two‐sided, and a p < 0.05 was considered statistically significant. All statistical analyses were performed using IBM SPSS Statistics 25.0.

Descriptive statistics were used to summarize the data: means and standard deviations (SD) were reported for both normally and non‐normally distributed continuous variables, and mean rank was use for only non‐normally distributed continuous variables. The normality of continuous variables was assessed using the Shapiro‐Wilk test. Based on the distribution of data, chi‐square tests were used for categorical variable comparisons. For non‐normally distributed continuous variables, the Mann‐Whitney U test (two‐group comparison) and Kruskal‐Wallis test (more than two groups) were applied. Spearman's rank correlation was used to explore associations between non‐normally distributed continuous or ordinal variables. All hypothesis tests were two‐sided, and a p < 0.05 was considered statistically significant. All statistical analyses were performed using IBM SPSS Statistics 25.0.

3. Results

The mean age of the women was 31.60 ± 45.6 years, with a median age of 32 years, ranging from a minimum of 16 years to a maximum of 49 years. To facilitate analysis, participants' ages were divided into two groups based on the median age (32 years): those aged 32 years or younger and those older than 32 years. Except for the parity variable, no significant correlation was observed between demographic characteristics in women with and without pre‐eclampsia (All p > 0.05) (Table 1).

Table 1.

Comparison of demographic characteristics in women with and without pre‐eclampsia.

Demographic characteristics Without Pre‐eclampsia (n = 366) Frequency (%) With Pre‐eclampsia (n = 196) Frequency (%) p value
Maternal age (years) 0.08
≤ 32 202 (55.2%) 95 (48.5%)
> 32 164 (44.8%) 101 (51.5%)
Maternal education level
Below high school 77 (21%) 9 (25%) > 0.99
High school diploma 144 (39.3%) 76 (38.8%)
University degree 145 (39.6%) 71 (36.2%)
Place of residence > 0.99
Rural 143 (39.5%) 76 (40%)
Urban 219 (60.5%) 114 (60%)
Gravidity > 0.99
≤ 2 261 (71.3%) 131 (66.8%)
> 2 105 (28.7%) 65 (33.2%)
Parity 0.001
≤ 2 310 (84.7%) 184 (93.9%)
> 2 56 (15.3%) 12 (6.1%)

Note: Data are presented as frequency (%). Categorical variables were compared using chi‐square or Fisher's exact tests, as appropriate.

Based on the results of Table 2, the mean scores for depression, anxiety, somatization symptoms, and the psychological distress index were significantly higher in women with pre‐eclampsia compared to those without pre‐eclampsia (All p < 0.001).

Table 2.

Comparison of mean of anxiety and depression scores in women with and without pre‐eclampsia.

BSI‐18 subscales Without pre‐eclampsia, Mean ± SD With pre‐eclampsia, Mean ± SD p value
Depressive symptoms 1.66 ± 2.95 2.99 ± 4 < 0.001
Anxiety symptoms 3.33 ± 2.78 4.88 ± 3.82 < 0.001
Somatization symptoms 2.34 ± 2.24 3.65 ± 3.04 < 0.001
Psychological Distress Index 0.40 ± 0.35 0.64 ± 0.5 < 0.001

Note: All comparisons were performed using Mann‐Whitney U tests (two‐tailed).

Based on the results of Table 3, in women with pre‐eclampsia compared to those with normal pregnancies, the frequency of depression symptoms (26.5% vs. 16.7%, p = 0.004), anxiety symptoms (34.2% vs. 16.7%, p < 0.001), and the psychological distress index (46.9% vs. 26%, p < 0.001) were significantly higher.

Table 3.

Comparison of the prevalence of Depression, Anxiety, and Psychological Distress Index in women with and without pre‐eclampsia.

Variables Without Pre‐eclampsia Frequency (%) With pre‐eclampsia frequency (%) OR (CI) p value
Depressive symptoms

1.80 (1.18, 2.74)

0.006

≤ 4 305 (83.3%) 144 (73.5%)
> 4 61 (16.7%) 52 (26.5%)
Anxiety symptoms

2.59 (1.73, 3.88)

< 0.001

≤ 6 305 (83.3%) 129 (65.8%)
> 6 61 (16.7%) 67 (34.2%)
Somatization symptoms

3.20 (2.12, 4.85)

< 0.001

≤ 5 313 (85.5%) 127 (64.8%)
> 5 53 (14.5%) 69 (35.2%)
Psychological Distress Index

2.52 (1.75, 3.63)

< 0.001

≤ 0.5 271 (74%) 104 (53.1%)
> 0.5 95 (260.0%) 92 (46.9%)

Note: All comparisons were performed using chi‐square tests (two‐tailed). The reference group for each OR calculation is the lower symptom category.

Table 4 shows that the frequency of cesarean sections, postpartum hemorrhage, and postpartum infections, were significantly higher in women with pre‐eclampsia compared to those without pre‐eclampsia. Regarding neonatal outcomes, the mean birth weight, birth length, and head circumference of newborns from mothers with pre‐eclampsia were significantly lower than those from non‐preeclamptic mothers. Additionally, other adverse neonatal outcomes, such as the frequency of preterm delivery, NICU admission, birth injuries, and hospital admissions, were significantly higher in women with pre‐eclampsia compared to those without pre‐eclampsia. However, the gender distribution (female/male) in women with and without pre‐eclampsia showed no significant difference (p > 0.05).

Table 4.

Comparison of maternal and neonatal outcomes in women with and without pre‐eclampsia.

Maternal outcomes Without pre‐eclampsia frequency (%) With pre‐eclampsia frequency (%) p value
Maternal outcomes Gestational age (weeks) < 0.001 a
≥ 37 173 (47.3%) 84 (66.1%)
< 37 193 (52.7%) 43 (33.9%)
Mode of Delivery 0.005 a
Vaginal Delivery 103 (28.1%) 23 (16.3%)
Elective Cesarean 152 (41.5%) 57 (40.4%)
Emergency Cesarean 111 (30.3%) 61 (43.3%)
Postpartum hemorrhage < 0.001 a
No 289 (79%) 186 (94.9%)
Yes 77 (21%) 10 (5.1%)
Postpartum infection < 0.001 a
No 141 (38.6%) 142 (72.4%)
Yes 224 (61.4%) 54 (27.6%)
Neonatal outcomes Need for ICU or resuscitation <0.001 a
No 287 (79.7%) 96 (65.3%)
Yes 73 (20.3%) 51 (34.7%)
Gender > 0.99
Male 187 (51.1%) 84 (55.6%)
Female 179 (48.9%) 67 (44.4%)
Birth weight (grams%) 0.002 a
≥ 2500 276 (75.4%) 91 (61.1%)
< 2500 90 (24.6%) 58 (38.9%)
Birth injuries < 0.001 a
No 336 (91.8%) 135 (68.9%)
Yes 30 (8.2%) 61 (31.1%)
Hospital admission < 0.001a
No 177 (48.4%) 75 (58.6%)
Yes 189 (51.6%) 48 (37.5%)
Neonatal death 5 (3.9%)
Neonatal length (cm) 49.02 ± 3.33 (250.87) 48.04 ± 3.92 (219.34) 0.03b
Head circumference (cm) 33.78 ± 2.66 (205.34) 33.39 ± 3.35 (237.13) 0.03 b

Note: Data are presented as Mean ± Standard Deviation (SD). Bold indicates significance at α = 0.05 (two‐tailed).

a

p values were calculated using Chi‐square,

b

p values were calculated using Fisher's Exact Test.

Table 5 compares maternal and neonatal outcomes in women with pre‐eclampsia based on the mean scores of depression and anxiety. The results indicated that the mean scores for depression, anxiety, somatization, and psychological distress in women with re‐eclampsia did not significantly correlate with maternal outcomes (e.g., gestational age, type of delivery, postpartum hemorrhage, or postpartum infection) (all p > 0.05). However, the mean somatization score was significantly higher in women who underwent elective cesarean sections compared to those who had emergency cesarean sections (p < 0.05). Additionally, the mean scores for depression, anxiety, somatization, and psychological distress in women with pre‐eclampsia showed no significant correlation with neonatal outcomes (e.g., birth weight, birth injuries, or need for NICU admission) (all p > 0.05). However, the mean scores for anxiety and psychological distress were significantly higher in mothers whose infants required hospitalization within 6 weeks after birth compared to those whose infants did not require hospitalization (p = 0.002 and p = 0.015, respectively) (Table 5).

Table 5.

Relation of scores of depression and anxiety with maternal and neonatal outcomes in women with pre‐eclampsia.

Subscales Depression Mean ± SD (Mean Rank) Anxiety Mean ± SD (Mean Rank) Somatization Mean ± SD (Mean Rank) Psychological Distress Index Mean ± SD (Mean Rank)
Maternal outcomes Gestational age (weeks)
≥ 37 2.3 ± 74.59 (65.90) 4.3 ± 75.55 (65.83) 3.07 ± 2.99 (60.88) 0.58 ± 0.45 (65.11)
< 37 2.4 ± 70.08 (60.29) 4.3 ± 37.72 (60.43) 3.58 ± 2.71 (70.09) 0.59 ± 0.50 (61.84)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Mode of delivery
Vaginal delivery 3.48 ± 4.55 (78.15) 5.13 ± 3.37 (77.35) 3.70 ± 2.89 (74.39) 0.68 ± 0.49 (77.50)
Elective cesarean 2.37 ± 3.79 (63.54) 4.58 ± 3.81 (67.29) 4.09 ± 2.85 (80.55) 0.61 ± 0.48 (70.20)
Emergency cesarean 2.82 ± 3.23 (75.27) 4.9 ± 3.77 (72.07) 2.89 ± 3.01 (60.80) 0.58 ± 0.44 (69.30)
p value b > 0.99 > 0.99 > 0.99 > 0.99
Postpartum hemorrhage
No 2.99 ± 3.99 (98.13) 4.87 ± 3.85 (98.04) 3.66 ± 3.07 (98.41) 0.63 ± 0.51 (98.10)
Yes 3.00 ± 4.32 (105.35) 5.10 ± 3.24 (107.05) 3.50 ± 2.55 (100.20) 0.64 ± 0.46 (105.85)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Postpartum infection
No 3.01 ± 3.92 (100.48) 4.88 ± 3.70 (99.17) 3.64 ± 3.16 (97.25) 0.64 ± 0.50 (99.39)
Yes 2.94 ± 4.24 (93.30) 4.89 ± 4.15 (96.75) 3.69 ± 2.73 (101.79) 0.63 ± 0.52 (96.17)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Neonatal outcomes Fetal gender
Male 2.43 ± 3.36 (73.70) 4.75 ± 3.74 (74.41) 3.17 ± 2.93 (71.61) 0.57 ± 0.43 (72.13)
Female 3.27 ± 4.40 (78.88) 5.13 ± 3.94 (77.99) 3.76 ± 2.93 (81.50) 0.67 ± 0.53 (80.86)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Birth weight (grams)
≤ 2500 2.40 ± 2.55 (79.16) 4.84 ± 3.58 (75.72) 3.05 ± 2.96 (68.62) 0.57 ± 0.38 (75.99)
> 2500 3.00 ± 4.48 (72.35) 4.96 ± 4.02 (74.54) 3.67 ± 2.90 (75.99) 0.64 ± 0.53 (74.37)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Need for ICU or resuscitation
No 2.97 ± 4.36 (72.16) 5.02 ± 4.02 (73.92) 3.52 ± 2.98 (75.60) 0.63 ± 0.53 (72.88)
Yes 2.39 ± 2.72 (77.47) 4.80 ± 3.54 (74.15) 3.20 ± 2.88 (70.99) 0.57 ± 0.38 (76.11)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Birth injuries
No 3.59 ± 4.58 (105.44) 5.00 ± 3.97 (100.37) 4.10 ± 3.17 (106.76) 0.70 ± 0.57 (104.12)
Yes 2.73 ± 3.69 (95.36) 4.83 ± 3.76 (97.66) 3.45 ± 2.97 (94.77) 0.61 ± 0.47 (95.96)
p value a > 0.99 > 0.99 > 0.99 > 0.99
Hospitalization
No 2.05 ± 3.05 (57.59) 4.17 ± 3.68 (54.15) 3.25 ± 2.87 (69.33) 0.52 ± 0.43 (55.76)
Yes 3.48 ± 4.48 (68.90) 6.02 ± 3.93 (74.27) 3.58 ± 2.93 (64.63) 0.72 ± 0.51 (71.75)
p value a 0.08 0.002 > 0.99 > 0.99

Note: Data are presented as Mean ± Standard Deviation (SD). Mean Rank values represent the average ranks assigned to each group in nonparametric comparisons (Mann‐Whitney U/Kruskal‐Wallis tests). Higher ranks indicate greater values in the psychological symptom scales. Bold indicates significance at α = 0.05 (two‐tailed).

a

p values were calculated using Chi‐square and Fisher's Exact Test.

b

p values were calculated using the Mann‐Whitney test.

4. Discussion

The findings of this study revealed that the frequency of symptoms such as depression, anxiety, and psychological distress in women with pre‐eclampsia was approximately 1.5–2 times higher compared to pregnant women without pre‐eclampsia. Although limited studies have explored the relationship between depression, anxiety during pregnancy, and pre‐eclampsia, the results are mixed. A systematic review by Abadibavil et al. indicated that the likelihood of developing pre‐eclampsia was three times higher in individuals with anxiety and depression [42] Similarly, Shay et al. found that women experiencing depression or anxiety during pregnancy had a higher prevalence of pre‐eclampsia compared to their nondepressed or non‐anxious counterparts [32]. According to Kharaghani et al., women without depression had a 1.81‐fold greater risk of developing pre‐eclampsia compared to those with mild depression, while moderate to severe depression was associated with a 2.52‐fold increased risk [19]. In contrast, Moafi et al. concluded that depression did not affect the incidence of pre‐eclampsia [43]. Moreover, Roberts et al. found no significant association between depression, anxiety, and pre‐eclampsia after multivariate adjustment [44].

The increased frequency of mental health disorders in preeclamptic patients can be explained by studies showing that psychological factors such as high pregnancy‐related stress, which triggers excessive sympathetic activity by stimulating the autonomic nervous system, are considered risk factors for the development of pre‐eclampsia [45]. To explain these contradictions, it can be suggested that differences in the classification of pregnancy‐related hypertension disorders and the temporal and geographic variability of the disease may contribute to varying reports of pre‐eclampsia incidence. Consequently, the frequency of depression and anxiety in women with pre‐eclampsia may also vary. The results of this study indicated that Pre‐eclampsia is associated with an increased risk of adverse maternal and neonatal outcomes. Specifically, the prevalence of preterm birth, cesarean delivery, postpartum hemorrhage, and postpartum infection was significantly higher in individuals with pre‐eclampsia compared to those without the condition. Additionally, adverse neonatal outcomes, including lower mean birth weight, birth length, and head circumference, as well as a higher need for NICU admission, birth injuries, and hospital admission, were significantly more prevalent among neonates born to preeclamptic mothers than those of non‐preeclamptic mothers.

Several studies have reported findings consistent with these results. Regarding adverse maternal outcomes, increased rates of hemorrhage and infection [46, 47], preterm birth [48, 49, 50, 51, 52], and cesarean delivery [53] were more frequently observed in women with pre‐eclampsia compared to non‐preeclamptic women. pre‐eclampsia develops due to endothelial dysfunction, severe inflammatory responses, and hyperactivity of the sympathetic nervous system, which can lead to complications such as preterm birth, postpartum hemorrhage, and an elevated risk of infection [54]. Furthermore, elevated blood pressure and reduced placental blood flow in pre‐eclampsia contribute to fetal hypoxia, increasing the risk of preterm birth and the necessity for cesarean delivery [55]. Additionally, heightened sympathetic nervous system activity and hypothalamic‐pituitary‐adrenal (HPA) axis dysfunction in women with pre‐eclampsia may exacerbate these complications [56].

Regarding adverse neonatal outcomes, findings from multiple studies have demonstrated that a history of pre‐eclampsia in pregnant women is associated with an increased risk of adverse neonatal outcomes, including low birth weight [48, 49, 50, 52, 57, 58], NICU admission [48, 49, 50], intrauterine growth restriction (IUGR) [51], perinatal mortality [51, 57], and asphyxia [57]. Check's study revealed that highly preterm infants born to mothers with pre‐eclampsia and fetal growth restriction had smaller head circumferences at 24 months, a reduction linked to delayed neuropsychological development and impaired brain growth [59]. Additionally, Khan et al. found that pre‐eclampsia was associated with an increased risk of adverse neonatal outcomes such as preterm birth and low birth weight [52]. pre‐eclampsia disrupts placental function and reduces fetal blood supply, thereby increasing the risk of IUGR and low birth weight [55]. Oxidative stress and excessive sympathetic nervous system activity further contribute to reduced oxygen delivery and placental vascular constriction, which may result in preterm birth and placental abruption [54, 60]. Furthermore, these conditions are linked to restricted brain growth and reduced neonatal head circumference [61]. Beyond short‐term complications, intrauterine exposure to pre‐eclampsia has been associated with an increased risk of metabolic and cardiovascular diseases later in life [62].

The results of this study revealed that the depression and anxiety scores in women with pre‐eclampsia did not have a significant exacerbating effect on adverse maternal and neonatal outcomes, except in the case of women whose infants required hospitalization within the first 6 weeks after birth. While no specific studies exclusively focusing on preeclamptic pregnant women were found, research on pregnant women with hypertension has indicated that the co‐occurrence of hypertension and depression during pregnancy can increase the risk of maternal complications such as pre‐eclampsia and preterm birth, as well as adverse neonatal outcomes, including low birth weight and NICU admission [63]. Additionally, Horsley's study demonstrated that more severe symptoms of depression and anxiety in hypertensive mothers were associated with a greater reduction in gestational age at birth [64]. Studies by Gumusoglu and Raina further reported that both maternal hypertension and maternal psychiatric disorders (including anxiety and depression) were independently associated with an increased risk of adverse neonatal outcomes such as preterm birth, low birth weight, and NICU admission [65, 66]. In preeclamptic women, psychological distress can rapidly escalate the condition from mild to severe, exacerbating hypertension and increasing the risk of eclampsia [67]. Moreover, preeclamptic women are inherently predisposed to adverse maternal and neonatal outcomes [68]. Psychological distress, through chronic activation of the HPA axis and increased inflammation, may exacerbate the severity of pre‐eclampsia and adverse pregnancy outcomes. This association is supported by both the allostatic load theory and empirical evidence [69, 70].

This aspect of our study yielded limited significant findings, which may be attributed to the complex interplay between pre‐eclampsia, psychiatric symptoms, and maternal and neonatal outcomes in pregnant women. Recent studies show that obstructive sleep apnea in pregnancy is linked to lower Apgar scores, highlighting how other medical conditions may also affect neonatal outcomes [71]. Additionally, the assessment tools used for evaluating anxiety and depression might not have been sensitive enough to detect subtle associations between these symptoms and maternal and neonatal outcomes. Demographic characteristics (maternal age, educational level, place of residence, gravidity, and parity) were matched between the two groups, a measure that may have reduced the influence of confounding factors and consequently diminished statistically significant differences. Therefore, further comprehensive studies are required to elucidate better the relationship between pre‐eclampsia, psychiatric disorders, and maternal and neonatal outcomes.

5. Limitation

This study has several limitations. First, the screening system for perinatal mental health disorders was limited to a single county in one country, and therefore, its findings may not be generalizable to all pregnant women. Additionally, the diagnosis of mental disorders was based solely on questionnaires, which may not be as accurate as clinical interviews. Future studies should be based on data from multiple systems and incorporate diagnoses made through clinical interviews, which have higher diagnostic accuracy. Although this study adjusted for key demographic variables (e.g., age, education, parity), unmeasured confounding factors—such as socioeconomic status, lifestyle factors, and medical comorbidities—may influence the observed association between psychological symptoms and pre‐eclampsia outcomes.

Despite these limitations, this study carries significant clinical implications. Given the high prevalence of mental health symptoms in women with pre‐eclampsia and the associated adverse maternal and neonatal outcomes, obstetricians, gynecologists, and healthcare providers must focus not only on immediate medical treatments but also on screening for mental health issues. Timely psychological interventions should also be provided. A deeper understanding of the psychological outcomes following pre‐eclampsia, especially concerning depression, anxiety, and psychological distress, is essential. Women who experience pre‐eclampsia and are at an increased risk for mental health issues must be accurately diagnosed. Implementing targeted screening during the perinatal and postpartum periods could lead to earlier referrals, more timely treatment, and a reduction in adverse maternal and neonatal outcomes.

6. Conclusions

The results of this study indicate that the frequency of symptoms such as depression, anxiety, somatization, and psychological distress is higher in women with pre‐eclampsia compared to those without the condition. Additionally, the incidence of adverse maternal and neonatal outcomes is significantly higher in women with pre‐eclampsia compared to those with normal blood pressure. However, depression and anxiety did not exacerbate maternal and neonatal outcomes in preeclamptic mothers. Given the substantial impact of these outcomes on both maternal and neonatal health, preventive measures are essential. These measures should focus on identifying women at risk and addressing contributing factors through routine psychological screening before pregnancy and at regular intervals throughout pregnancy (every 3 months).

Author Contributions

Fatemeh Esmaeilpour Gangi: investigation, data curation. Mahbobeh Faramarzi: conceptualization, writing – original draft, methodology. Zinatossadat Bouzari: conceptualization, funding acquisition, supervision. Soraya Khafri: methodology, formal analysis. Maedeh Rezaie Bazgir: methodology, data curation. Mehrzad Netadj: writing – review and editing.

Conflicts of Interest

The authors declare no conflicts of interest.

Transparency Statement

The lead author Zinatossadat Bouzari affirms that this manuscript is an honest, accurate, and transparent account of the study being reported; that no important aspects of the study have been omitted; and that any discrepancies from the study as planned (and, if relevant, registered) have been explained.

Acknowledgments

All authors have read and approved the final version of the manuscript. The corresponding author Zinatossadat Bouzari had full access to all of the data in this study and takes complete responsibility for the integrity of the data and the accuracy of the data analysis. The authors would like to sincerely thank the Research Deputy of Babol University of Medical Sciences throughout the study. They also wish to thank the patients for their cooperation and participation, which were crucial to successfully completing this study. The present Project was financially supported by Babol University of Medical Sciences supported the funding (Grant Number: 724135383). The funder had no role in study design; collection, analysis, and interpretation of data; writing of the report; the decision to submit the report for publication.

Fatemeh Esmaeilpour Gangi and Mahbobeh Faramarzi contributed equally to this study.

Data Availability Statement

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.


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