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BMC Pregnancy and Childbirth logoLink to BMC Pregnancy and Childbirth
. 2026 Jan 24;26:245. doi: 10.1186/s12884-026-08678-1

Prevalence and maternal-fetal outcomes of early-onset versus late-onset of preeclampsia: a prospective cohort study at Wallaga university compressive specialized hospital

Debissa Kefiyalew 1,✉, Abebaye Aragaw 2, Kejela Bula 3, Guluma Etana 4
PMCID: PMC12973849  PMID: 41580670

Abstract

Background

Preeclampsia is a multisystem disorder and is one of the leading causes of maternal and perinatal morbidity and mortality worldwide, particularly in developing countries like Ethiopia. Therefore, this study aim to asses the prevalence and feto-maternal outcome of early onset of preeclampsia and late onset of Preeclamsia in selected hospitals in Nekemte City.

Materials and Methods

A Facility-based prospective cohort study was conducted at Wallaga University compressive specialized Hospital from December 2024 to June 2025. A total of 104 pregnant women with Preeclampsia were recruited for this study. Data were entered into Epi Info version 3.1, transferred, and analyzed using SPSS version 27.0. Categorical variables are presented as frequencies and percentages. Differences between the early-onset and late-onset groups were assessed using the Chi-square test. For tables with small expected cell counts (<5), Fisher’s Exact test was employed. P-value < 0.05 was considered statistically significant.

Result

Late-onset preeclampsia was significantly more prevalent than early-onset (70.2% vs. 29.8%, p<0.001). Infants in the early-onset group had significantly lower birth weights and poorer Apgar scores at 1 and 5 minutes (all p<0.05). Gestational age at delivery was a critical factor for neonatal survival (p<0.001), with all cases of intrauterine and neonatal death occurring in the early-onset group. The mode of delivery and rates of major maternal complications did not differ significantly between the two groups. Most women in both groups showed improvement and were discharged.

Conclusion

This study confirms that early-onset preeclampsia, though less common, carries significantly higher risks of adverse neonatal outcomes, including mortality, compared to late-onset preeclampsia. We recommend enhanced fetal monitoring and delivery planning at advanced care facilities for early-onset cases to improve survival.

Keywords: Preeclampsia, Early-onset of preeclampsia, Late-onset of preeclampsia, Pregnancy outcome, Ethiopia, Cohort study

Introduction

Maternal deaths are significantly impacted by complications, in that 75% of the deaths are attributed to severe bleeding, infection, hypertension, delivery delays, and unsafe abortions [1]. preeclampsia (PE) and gestational hypertension are the deadly triad of interrelated contributors to maternal morbidity and mortality, with population-level changes in risk factors over the last few decades [2].These complications affect 4–5% of all pregnancies worldwide [3].

PE is characterized by new-onset hypertension (blood pressure ≥ 140/90 mmHg) and proteinuria (≥ 300 mg in a 24-hour urine sample) after the 20th week of gestation [3]. The updated classification excludes proteinuria in the presence of other end-organ damage, and severe features include blood pressure ≥ 160/110 mmHg on two occasions [4]. While PE’s etiology remains unclear, proposed mechanisms include immunological dysregulation, endothelial damage, and genetic factors [5, 6]. Risk factors span primiparity, PE history, hypertension, anemia, and blood group incompatibility [7].

The disease is divided into two subtypes: early onset(EOPE) (< 34 + 0 weeks of gestation) and late onset (LOPE) (≥ 34 + 0 weeks) [8]. LOPE is more common than EOPE, with an incidence of 2.7 versus 0.3% in a population-based study [4].

Although EOPE and LOPE share the same diagnostic criteria, their maternal and fetal outcomes differ. EOPE carries higher risks for both mother and baby [9], while LOPE often has milder symptoms [10]. However, uncertainties remain about the exact differences in outcomes [11, 12].

Although EOPE and LOPE share a clinical presentation, they are thought to arise from distinct pathophysiological pathways [13]. The prevailing theory posits that EOPE is primarily a disorder of placentation, characterized by inadequate remodeling of the maternal spiral arteries in the first trimester. This is hypothesized to lead to placental ischemia, oxidative stress, and subsequent release of anti-angiogenic factors and inflammatory mediators into the maternal circulation, often resulting in fetal growth restriction [14, 15], In contrast, LOPE is theorized to originate from a later-onset dysfunction of the syncytiotrophoblast (the placental barrier), exacerbated by the increasing metabolic demands of late pregnancy and pre-existing maternal endothelial vulnerability (e.g., due to obesity, chronic hypertension, or diabetes) [15–17]). This model suggests LOPE involves a significant angiogenic imbalance (e.g., high sFlt-1, low PlGF) without the profound early spiral artery defects seen in EOPE [15]. It is important to recognize that these leading theories, while providing a useful model, describe pathways that have not been fully proven in human pregnancy.

Despite the clinical significance of distinguishing between EOPE and LOPE, Ethiopia lacks local data on their prevalence and associated maternal-neonatal outcomes. No published studies have specifically examined EOPE/LOPE differences and their impacts in the Ethiopian context. This study therefore, aims to assess the prevalence and feto-maternal outcomes of EOPE and LOPE in selected hospitals in Nekemte city.

Materials and methods

Study area and period

This study was conducted at Wallaga University Comprehensive Specialized Hospital (WUCSH), located in Nekemte city. Nekemte city is the administrative center of the East Wollega Zone in the Oromia Region, Ethiopia. It is located about 331 km west of Addis Ababa, the capital city of Ethiopia, and is one of the major urban centers in western Ethiopia. The city has an estimated population of 120,000-150,000 people and serves as a critical hub for healthcare services for both urban and rural residents of the surrounding areas. WUCSH is the Governmental Hospitals found in Nekemte city and act as the referral centers for medical services within the region by providing a full range of healthcare services to more than 2.1 million people living in East Wollega Zone, parts of West Wollega Zone, Horroo guduru Wollega Zone, and West Shoa Zone. These services also include obstetrics and gynecology, emergency care, specialized maternal health, and WUCSH offers services as a teaching hospital. The study was conducted from December 2024 to June 2025. Data collection and maternal-neonatal follow-up are now complete.

Study design and population

Study design and populationA Facility-based prospective cohort study was conducted at WUCSH, located in Nekemte city. All pregnant women who were attending the antenatal clinic and delivery units at these hospitals during the study period were the source population. Pregnant women at Nekemte hospitals diagnosed with PE, were our study population. Each individual pregnant woman diagnosed with PE met inclusion criteria during study period were study unit.

Eligibility criteria

Inclusion criteria

The study included pregnant women aged between 18 and 48 years and who completed the written informed consent and pregnant women with PE, which was diagnosed after 20 weeks of gestation.

Exclusion criteria

Pregnant women with gestational age of less than 20 weeks, Postpartum PE.

Sample size determination

The sample size was calculated to compare the proportion of Low Birth Weight (LBW) (< 2500 g) between groups. Using Open Epi software with an allocation ratio of 1:2.3 [18]. 80% power, α = 0.05, and expected proportions of 65% (EOPE) vs. 35% (LOPE) [18, 19], the minimum required sample was 96. We enrolled 104 participants to account for incomplete data. A post-hoc calculation for the observed LBW rates (71.0% vs. 15.1%) confirmed power > 80%.

Sampling techniques and procedure

This hospital-based study employed a consecutive sampling method to recruit 104 pregnant women diagnosed with preeclampsia from ANC of WUCSH. Participants were classified as early-onset preeclampsia (EOPE, n = 31) if diagnosed between 20 and 34 weeks of gestation, or late-onset preeclampsia (LOPE, n = 73) if diagnosed after 34 weeks. All eligible women meeting the inclusion criteria were invited to participate consecutively until the predetermined sample size for each group was fulfilled.

Study variables

The dependent variables were feto-maternal outcomes, while the independent variables were socio-demographic: age, marital status, residence, occupation, educational status, socioeconomic status, and onset of preeclampsia.

Data collection techniques and instruments

Socio-demographic characteristics, obstetric characteristics, assessment criteria for diagnosing PE, lifestyle, and maternal and neonatal outcomes were collected using a structured questionnaire. The questionnaire was translated into the local language and back to English for data entry and analysis. Data were collected by trained nurses, midwives, and obstetrics and Gynecology residents.

Blood pressure measurement

Blood pressure was measured by using an aneroid sphygmomanometer and a stethoscope from the upper right arm for consistency. A trained nurse/midwife working at ANC, patients took SBP and DBP measurements after a 10-minute rest. The participants sit comfortably, with their back supported, legs uncrossed, feet on the ground, and their upper arms positioned at heart level during blood pressure measurement.

Operational definitions

Preeclampsia

Is a hypertensive disorder in pregnancy characterized by new-onset hypertension (systolic blood pressure ≥ 140 mm Hg or diastolic blood pressure ≥ 90 mm Hg) after 20 weeks of gestation, in combination with proteinuria (≥ 300 mg in a 24-hour urine sample) or other signs of organ dysfunction (e.g., thrombocytopenia, renal impairment, liver involvement, or pulmonary edema) [20].

Early onset of preeclampsia

Preeclampsia diagnosed with onset before 34 + 0weeeks of gestation.

Late onset of preeclampsia

Preeclampsia diagnosed with onset at or after 34 + 0weeeks of gestation.

Fetal outcomes of preeclampsia

Pregnancy outcome including stillbirth, growth restriction (IUGR), respiratory distress syndrome (RDS), low birth weight, < 7 APGAR score at 1st and 5th minutes of life, neonatal death [21]. Assessed from birth until hospital discharge for all infants.

Intra uterine growth restriction (IUGR)

A rate of fetal growth that is less than normal in light of the growth potential of that specific infant [22].

Respiratory distress syndrome (RDS)

Life-threatening condition characterized by poor oxygenation and non-compliant or “stiff” lungs [23].

Spontaneous vaginal delivery (SVD)

Vaginal delivery of a cephalic-presenting fetus without instrumental assistance (forceps or vacuum), regardless of whether labor began spontaneously or was medically induced.

Intra uterine fetal death (IUFD)

Fetal death in womb after 20week of gastation [24].

Maternal outcomes of preeclampsia

Are the health effects on the mother resulting from this condition, such as severe hypertension, Eclampsia, HELLP Syndrome (Hemolysis, Elevated Liver enzymes, and a Low Platelet count), renal failure, pulmonary edema, placental abruption, and maternal death [25].

Maternal mortality ratio

Defined as the number of maternal deaths per 100,000 live births during a given period [1].

Data quality assurance and management

To ensure high-quality data, a structured protocol was followed. The questionnaire was translated into Afaan Oromo and back-translated for consistency, then pre-tested. Data collectors received two-day training on standardized procedures. Blood pressure was measured using calibrated automated devices by trained staff to ensure reliability. Data underwent daily supervisory review and was entered into EpiData software, where validation rules were applied to check consistency and identify outliers, with discrepancies resolved by referring to source documents. Missing data were minimal (< 2%) and handled by list wise exclusion in relevant analyses; no data imputation was performed.

Data entry and analysis

Data were entered into Epi Info version 3.1, transferred, and analyzed using the Software Package for the Social Sciences (SPSS version 27.0). To analyze the variable differences between cases and controls, Categorical variables are presented as frequencies and percentages. Differences between the early-onset and late-onset groups were assessed using the Chi-square test. For tables with small expected cell counts (< 5), Fisher’s Exact test was employed. P-value < 0.05 was considered statistically significant.

Result

Socio-demographic characteristics

This study included 104 women with preeclampsia, comprising 31 (29.8%) with early-onset preeclampsia (EOPE) and 73 (70.2%) with late-onset preeclampsia (LOPE).

Age distribution revealed that among women aged 25–34 years, LOPE cases 43 (68.3%) vs. EOPE cases 20 (31.7%). Notably, all 6(100%) cases in the 35–48 age group were LOPE, while among younger women (18–24 years), 24(68.6%) cases were LOPE compared to 11(34.4%) EOPE cases (Fig. 1).

Fig. 1.

Fig. 1

Distribution of early-onset and late –onset of preeclampsia across maternal age group among pregnant women

The socio-demographic characteristics did not differ significantly between the early-onset and late-onset preeclampsia groups (all p-values > 0.05) (Table 1).

Table 1.

Socio-demographic characteristics of the study participants

Variables Categories Onset of Preeclampsia p-value
EOPE N (%) LOPE N (%)
Age 18–24 11(35.5) 24(32.9) 0.259
25–34 20(64.5) 43(58.9)
35–48 0 6(8.2)
Religion Orthodox 6(19.4) 17(23.3) 0.732
Protestant 20(64.5) 48(65.8)
Muslim 5(16.1) 8(11.0)
Residence Urban 13(41.9) 44(60.3) 0.086
Rural 18(58.1) 29(39.7)
Marital status Married 31(100) 73(100) 0.155
Occupation House wife 27 (87.1) 58(79.5) 0.658
Employee 4(12.9) 12(16.4)
Student 0 1 (1.4)
Others 0 2(2.7)
Educational status Not attend formal education 3(9.7) 9(12.3) 0.37
Write and read 13(41.9) 24(32.9)
Complete primary school 6(19.4) 7 (9.6)
High school 5(16.1) 23(31.5)
Higher level education 4(12.9) 10(13.7)

EOPE Early-onset preeclampsia, LOPE Late-onset preeclampsia

Association between onset of preeclampsia and neonatal outcome

The distribution of neonatal outcomes differed significantly according to gestational age at diagnosis. As anticipated, birth weight showed a clear inverse relationship with earlier diagnosis (p < 0.001). Reduced weights were higher at 20–34 weeks (< 1000 g: 1(100%) vs. 0(0%); 1000–1499 g: 2(100%) vs. 0(0%); 1500–2499 g: 19(63.3%) vs. 11(36.7%)), while increased weights (2500–3999 g) were higher after 34 weeks (61(87.1%) vs. 9(12.9%)). One baby weighed > 4000 g (> 34 weeks).

A similar pattern was observed for Apgar scores. Both 1st minute and 5th minute Apgar scores p < 0.001). showed lower values at 20–34 weeks (1st: 0–3 = 3(100%) vs. 0(0%); 4–6 = 22(55%) vs. 18(45%); 5th: 0–3 = 5(100%) vs. 0(0%); 4–6 = 10(71%) vs. 4(29%)), with increased scores [7–10] were higher after 34 weeks (1st: 55(90.1%); 5th: 69(81.2%)). Adverse perinatal outcomes were significantly concentrated in the earlier gestational age group (p < 0.001). With worse outcomes at 20–34 weeks (IUFD: 2(100%) vs. 0(0%); neonatal death: 4(100%) vs. 0(0%)), though preterm deliveries were similar (19(47.5%) vs. 21(52.5%)) (Table 2).

Table 2.

Association between onset of preeclampsia and neonatal outcome (N = 104)

Variable Categories Onset of Preeclampsia p-value
EOPE N (%) LOPE N (%)
Neonatal weight < 1000gm 1(3.2) 0 0.001
1000-1499gm 2(6.5) 0
1500-2499gm 19(61.3) 11(15.1)
2500-3999gm 9(29.0) 61(83.6)
> 4000gm 0 1(1.4)
1st minute APGAR score 0–3 3(9.7) 0 0.001
4–6 22(71) 18(24.7)
7–10 6(19.3) 55(75.3)
5th minute APGAR score 0–3 5(16.1) 0 0.001
4–6 10(32.3) 4(5.5)
7–10 16(51.6) 69(94.5)
Neonatal outcome Preterm 19(61.3) 21(28.8) 0.001
IUFD 2(6.5) 0
Early neonatal death 4(12.9) 0
Survived to discharge 6 (19.4) 52 (71.2)

EOPE Early-onset preeclampsia, LOPE Late-onset preeclampsia, IUFD Intrauterine fetal death, APGAR Appearance, Pulse, Grimace, Activity, and Respiration; *P-value < 0.05

Association between onset of preeclampsia and maternal outcome

The majority of maternal outcomes did not differ significantly between women with EOPE and LOPE. There were no statistically significant associations between onset of preeclampsia and pregnancy outcome, mode of delivery, occurrence of specific maternal complications, or final discharge status (all p-values > 0.05).

Most women experienced no major maternal complications (68 (70.1%) late-onset vs (29). 29.9% early-onset) (70.1% of LOPE vs. 29.9% of EOPE cases). Severe complications such as Eclampsia and placental abruption occurred infrequently, with no statistically significant difference in their distribution between the two groups. (Table 3).

Table 3.

Association of preeclampsia with maternal outcomes

Variables Categories Onset of preeclampsia p-value
EOPE N (%) LOPE N (%)
pregnancy termination Yes 27(87.1) 63(86.3) 0.913
No 4 (12.9) 10(13.7)
Mode of delivery SVD 20(64.5) 36(49.3) 0.713
Breech D. 2(6.5) 2(2.7)
Instrumental 0(0) 4(5.5)
C/S 9(29.0) 31(42.5)
Maternal complication No complication 29(93.5) 68(93.2) 0.456
Placenta abruption 0 2(2.7)
Thrombocytopenia 0 1(1.4)
Eclampsia 2(6.5) 1(1.4)
PPH 0 1(1.4)
Maternal outcome Improved and discharged 31(30.1) 72(69.9) 0.513
Referred 0 1(100)

EOPE Early-onset preeclampsia, LOPE Late-onset preeclampsia, SVD Spontaneous Vaginal Delivery (non-instrumental vaginal delivery of cephalic fetus), C/S Caesarean section, D Delivery; *P-value < 0.05

Discussion

The present study found that late-onset preeclampsia (LOPE, > 34 weeks) was significantly more prevalent than early-onset preeclampsia (EOPE, < 34 weeks), consistent with [16, 26, 27]. may stem from differing etiologies: EOPE is often described as primarily driven by placental dysfunction, specifically inadequate spiral artery remodeling due to impaired trophoblast invasion [28–30], whereas LOPE is more frequently associated with maternal metabolic and vascular stressors (obesity, preexisting hypertension, diabetes) and age-related placental senescence [30]. Consequently, low-dose aspirin prophylaxis (initiated before 16 weeks) reduces EOPE incidence but shows no efficacy against LOPE [31].

It is important to note that the primary distinguishing factor between groups is gestational age at diagnosis, which inherently influences fetal maturity and outcomes. In our cohort, no significant differences were observed in composite maternal outcomes between EOPE and LOPE [32, 33] (Table 3). However, it is noteworthy that EOPE cases exhibited more severe antepartum manifestations [28, 34], which reported more severe maternal symptoms in early-onset cases. The discrepancy between may stem from key methodological differences. While our study focused on composite clinical outcomes (e.g., ICU admission, mortality), previous studies have emphasized symptom severity (e.g., hypertension, proteinuria), which is typically more acute in early-onset preeclampsia due to its abrupt placental pathology. Retrospective designs may overemphasize documented symptoms, while prospective studies. Furthermore, Geographic or demographic variations (e.g., obesity rates, access to care) could also contribute to different findings across studies.

Regarding neonatal outcomes, our findings show a clear distinction driven by gestational age. LOPE was associated with better neonatal prognosis, including higher birth weights, improved APGAR scores, and lower mortality [8, 35]. No significant differences were observed in composite maternal outcomes between EOPE and LOPE [32, 33] (Table 2). This aligns with the pathophysiological model that LOPE arises later in gestation, allowing for greater fetal maturation, whereas EOPE’s early placental dysfunction is associated with growth restriction and preterm complications [16].

In summary, our descriptive epidemiologic observations confirm that late-onset preeclampsia (LOPE, > 34 weeks) is associated with significantly better neonatal outcomes compared to early-onset cases (EOPE, < 34 weeks), including higher birth weights, improved APGAR scores, and greater survival rates [8, 35]. The prevailing theoretical framework suggests this dichotomy stems from their distinct pathophysiological origins: EOPE results primarily from defective placental development, particularly inadequate spiral artery remodeling leading to placental insufficiency, hypoxia, and subsequent fetal growth restriction [28, 32]. In contrast, LOPE is more frequently linked to maternal metabolic and vascular stressors (e.g., obesity, pre-existing hypertension) rather than profound placental pathology [1, 27]. Ultimately, the timing of disease manifestation is a key factor, as EOPE’s early onset often necessitates preterm delivery, while LOPE’s later onset permits greater fetal maturation [36].

Limitation of the study

While our sample (N = 104) met power requirements, larger multi-center studies are needed.

The findings may lack generalizability to broader populations. Furthermore, study design and selection biases, if any, restrict us from establishing causality. Finally, partial follow-up of neonatal outcomes could have underestimated the actual impact of preeclampsia on infant health. These restrictions indicate the necessity for carefulness in applying these results to clinical practice and offer directions for future research.

Strength

This study has important strengths, employed prospectively gathered primary data, which yielded strong and stable estimates of clinical measures. Furthermore, assessment of both maternal and neonatal outcomes offers a comprehensive view regarding the impact of preeclampsia.

Conclusion

This study confirms that while LOPE is more common, EOPE carries a significantly greater risk of severe neonatal complications, including mortality, making gestational age a critical prognostic indicator. Consequently, management must be risk-stratified, prioritizing enhanced monitoring and delivery at facilities with advanced neonatal care for EOPE cases to improve outcomes. Future research should investigate the long-term health implications for both mother and child, as the higher prevalence of LOPE likely stems from maternal metabolic factors, whereas EOPE is driven by placental dysfunction.

Acknowledgements

Our gratitude goes to data collectors, supervisors, and pregnant women who participated in this study their cooperation was invaluable and clinical directors and heads of the respective departments of each hospital that permits this study to be conducted.

Abbreviations

EOPE

Early onset of preeclampsia

PE

Preeclampsia

IUFD

Intrauterine Fetal Death

APGAR

Appearance, Pulse, Grimace, Activity, and Respiration

HELLP

Hemolysis, Elevated Liver Enzymes, And Low Platelet Count

DIC

Disseminated Intravascular Coagulation

LOPE

Late onset of preeclampsia

PPH

Postpartum Hemorrhage

IUGR

Intra-Uterine Growth Restriction

WUCSH

Wallaga University Comprehensive Specialized Hospital

ANC

Antenatal Clinic

BP

Blood Pressure

CI

Confidence Interval

SPSS

Statistical Package for Social Sciences

ID

Identification

Authors' contributions

DK **:** Led conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, supervision, validation, visualization, wrote original draft, wrote manuscript. AA **:** Contributed to conceptualization, data curation, software, formal analysis, methodology, validation, reviewed & edited manuscript. KB: Participated in conceptualization, data curation, software, formal analysis, methodology, validation GE: Participated in conceptualization, data curation, software, formal analysis, methodology, validation. All authors read and approved the final manuscript.

Funding

The author(s) declare that no financial support was received for the research and/or publication of this article.

Data availability

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

Declarations

Ethics approval and consent to participate

Ethical approval was obtained from the institutional review board (IRB) of the Department of Medical Physiology, School of Biomedical and Laboratory Sciences, College of Health Sciences, Addis Ababa University. The IRB does not issue approval reference number. Permission was obtained from the clinical directors of NSH and WUCSH and the heads of the respective departments to authorize the actual study. The purpose of the study was explained to study participants, and written informed consent was obtained from each participant. The confidentiality of participant data was ensured by assigning unique ID numbers to each questionnaire, and personal identifying information was not included in analysis. The study was conducted in accordance with the ethical principles of the declaration of Helsinki.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Footnotes

Publisher’s note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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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 analyzed during the current study are available from the corresponding author on reasonable request.


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