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Serum lactate dehydrogenase level in preeclampsia and its correlation with disease severity, maternal and perinatal outcomes

BMC Women's Health volume 25, Article number: 108 (2025) Cite this article

Abstract

Background

Preeclampsia is a rapidly progressing pregnancy-specific multi-systemic syndrome that is the leading cause of maternal and neonatal morbidity and mortality. Lactate dehydrogenase (LDH) is a valuable and potential biomarker for predicting the severity of Preeclampsia.

Objectives

To assess the level of LDH in women with preeclampsia and to correlate its level with the severity of the disease and maternal/perinatal outcomes.

Patients and methods

This prospective case-control study was conducted at Sulaimani Maternity Teaching Hospital, Sulaimaniyah, Iraq, from March 1st, 2021, to June 30th, 2022, on 150 pregnant women in 3rd trimester of their pregnancy. Patients (n = 100) were diagnosed with mild and severe Preeclampsia. Serum LDH level was measured and correlated with the severity of the disease and maternal/perinatal outcomes.

Results

LDH was significantly (p = 0.001) elevated in preeclampsia groups compared to the control group. The mild preeclampsia group had a mean LDH level of 302.9 ± 138.5 IU/L, while the severe preeclampsia group had a mean level of 488.6 ± 223.4 IU/L. Also, maternal complications, stillbirth rate, and neonatal intensive Care Unit (NICU) admission were higher in women with high LDH levels.

Conclusions

The serum LDH level is high in women with preeclampsia and correlated with the disease severity as well as maternal and perinatal outcomes. So, serum LDH may be a valuable biomarker for predicting the severity of preeclampsia.

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Introduction

Preeclampsia is a multi-systemic disorder specific to pregnancy that is characterized by a new onset of hypertension and end-organ dysfunction, mostly with proteinuria after 20 weeks of gestation. Preeclampsia is the leading cause of maternal and fetal morbidity and mortality, especially when the condition is of early onset due to its severity [1, 2].

Preeclampsia is identified in 5–8% of all pregnancies, and its incidence is influenced by age, race, ethnicity and genetic predisposition, and it is 1.5–2 fold higher in the first pregnancy [3]. Preeclampsia is less common before 34 weeks of gestation. In one population-based study, the incidence before and after 34 weeks was 0.3 and 2.7%, respectively [4]. The leading cause of preeclampsia is still debated; clinical and pathological studies suggest that the placenta is central to the pathogenesis of this syndrome [5]. In placentas destined to develop preeclampsia, cytotrophoblasts fail to transform from the proliferative epithelial subtype to the invasive endothelial subtype, which causes incomplete remodelling of the spiral artery, leading to narrow maternal vessels and relative placental ischemia. The narrow spiral arteries are prone to atherosis—characterized by lipid-laden macrophages within the lumen, fibrinoid necrosis of the arterial wall, and a mononuclear perivascular infiltrate, leading to further compromise in placental flow. Accordingly, significant impairment of diastolic flow with a characteristic notch in the waveform indicates clinical signs and symptoms of preeclampsia. Thus, a diseased placenta releases soluble toxic factors in the maternal circulation that result in inflammation, endothelial dysfunction, and maternal systemic disease [5]. Atherosclerotic changes in maternal radial arteries that supply the decidua as opposed to the spiral arteries are also observed in preeclampsia. Decidual vasculopathy (DV) is a lesion common to disorders of placental insufficiency, including intrauterine growth restriction and preeclampsia, and combines acute atherotic lesions with medial hypertrophy and perivascular lymphocytes. Within preeclampsia phenotypes, the presence of DV is associated with worse clinical outcomes, higher diastolic BP, worse renal function, and perinatal fetal death [6].

The abnormal placentation early in the first trimester, followed by a maternal syndrome in the later second and third trimesters increases release of anti-angiogenic markers from placenta to maternal circulation, such as soluble fms-like tyrosine kinase-1 (sFT-1) and soluble endoglin (sENG) play a significant role in the pathogenesis of preeclampsia [7]. sFLT-1 is a soluble splice variant of the membrane-bound receptor VEGFR1 that binds to the proangiogenic proteins VEGF and placental growth factor (PlGF); therefore, sFLT1 acts as a ligand trap and antagonizes ligand-mediated angiogenic signalling via the cell surface receptors. High plasma sFLT1:PlGF ratios also strongly predict disease severity and adverse clinical outcomes. On the other hand, the sENG inhibits transforming growth factor-β (TGFβ) signalling and is expressed at high levels in pre-eclampsia and eclampsia [8]. Even though PIGF and the sFlt-1/PlGF ratio show prognostic promise for adverse outcomes in preeclampsia, study heterogeneity limits their clinical utility [9].

Genetic and immunological theories are interlinked to explain the cause of preeclampsia. Several genes may exist for preeclampsia that interact with the hemostatic and cardiovascular systems and the inflammatory response [10]. Preeclampsia can be perceived as an impairment of the maternal immune system that prevents it from recognizing the fetoplacental unit [11].

Primary criteria for the diagnosis of preeclampsia, according to the National Institute for Health and Care Excellence (NICE) guideline, includes the new onset of hypertension (> 140 mmHg systolic or > 90 mmHg diastolic) after 20 weeks of pregnancy and the coexistence of one or more new-onset conditions such as proteinuria, renal insufficiency, liver insufficiency, neurological disorders, hematological problems, and uteroplacental dysfunction with or without right upper quadrant or epigastric abdominal pain [12]. The underlying vascular manifestations, oxidative stress, and endothelial damage can lead to fetal growth restriction (FGR) with underlying hypoxia and acidosis [13]. The presence of hypoxia in preeclampsia and the frequent associations with FGR lead to an increase in the incidence of fetal distress before or during labour [14]. The risk of intrauterine fetal death (IUFD) varies widely depending on the severity of preeclampsia, hypoxia, placental insufficiency/abruption, and FGR [15]. Preeclampsia is the primary indication for iatrogenic preterm delivery, and the underlying disease processes may increase the risk of spontaneous preterm birth [16]. Also, preeclampsia might affect renal, hepatic, nervous and coagulation system, thus leading to cellular death and significantly raised lactate dehydrogenase LDH levels [17]. In this regard, serum LDH enzyme level is a useful biomarker for cellular injury which may reflect the severity of preeclampsia and its level might be a guide for management of patients and can be considered a potential marker of severe preeclampsia [18]. Therefore, this study aimed to assess the level of LDH in women with preeclampsia and correlate it with the severity of the disease. It also aimed to determine the maternal and perinatal outcomes in relation to serum LDH levels.

Patients and methods

Study setting, design, and participants

This prospective case-control study was conducted at Sulaimani Maternity Teaching Hospital, Sulaimaniyah, Iraq, from March 1st, 2021 to June 30th, 2022. The participants were 150 pregnant women in the 3rd trimester (from 28 weeks) of their pregnancy. They were divided into three groups: Group A comprised 50 pregnant women diagnosed with mild Preeclampsia, Group B comprised 50 pregnant women diagnosed with severe preeclampsia, and Group C comprised 50 healthy pregnant women (control group).

Diagnosis of preeclampsia

Preeclampsia was diagnosed in pregnant women as mild when systolic BP was 140–159 mmHg and diastolic BP was 90–109 mmHg after 20 weeks of gestation without abnormalities in laboratory tests [12, 19]. On the other hand, severe preeclampsia was considered when there was sustained systolic BP of ≥ 160 mmHg or diastolic BP of ≥ 110 mmHg and had either thrombocytopenia (platelet count < 100000/µL), renal insufficiency (serum creatinine concentration > 1.02 mg/100 mL, hepatic dysfunction (alanine transaminase (ALT) > 70 IU/L, or two times higher than the upper limit of typical), new onset of visual symptoms or headache, convulsion, proteinuria (≥ 3.0 g in 24 h urine specimen), or signs of impending pulmonary edema [12, 19].

Inclusion criteria

Pregnant women in 3rd trimester (from 28 weeks) of their pregnancy, regardless of age, ethnicity, and residency.

Exclusion criteria

Pregnant women with multiple gestations and those with a history of chronic hypertension, history of diabetes mellitus, history of renal disease, cardiac disease, liver disease, and neurological disorders were not enrolled in the study.

Data collection

A complete history was taken from all participants, including maternal age, gravity, height/weight (to determine body mass index; BMI), parity, last menstrual period, gestational age (calculated by the ultrasound before 20 weeks), past obstetrical history, past medical history, drug history, and family history. The complete examination was done for all patients, including general examination, vital signs, fundal height, fetal heart rate, and laboratory investigation. Then, 2.0 mL of blood was taken from the patient, centrifuged, frozen, and sent to a private laboratory to determine the LDH level without isoenzymes. The LDH level of 135–214 IU/L is considered normal, and higher than that amount is deemed elevated [20].

For cases with mild preeclampsia, the blood sample was taken at the time of diagnosis (hospital admission); however, if she developed severe preeclampsia, another sample was taken, and she was transferred to the severe group. Follow-up of the patients was done till delivery. Any maternal complications (intrapartum and postpartum) were recorded, and a neonatologist diagnosed the respiratory distress syndrome (RDS) through a combination of clinical assessments and chest X-rays. The three groups were compared in correlation with serum LDH levels.

Statistical analysis

The Statistical Package for the Social Sciences (SPSS, IBM, Chicago, USA) was used for data analysis. The chi-square test was employed to compare the categorical data between groups. Variables are described by mean and standard deviation (SD). The statistical significance of the difference in means between the two groups was assessed using an independent sample t-test. In comparison, an ANOVA test was used between more than two groups. P values of 0.05 were used as a cut-off point for the significance.

Results

Sociodemographic and clinical characteristics

The mean age of the patients with severe preeclampsia was 31.48 ± 5.79 years, compared to 30.98 ± 6.31 years for those with mild preeclampsia and 30.29 ± 5.61 years for the control group. Most patients with mild Preeclampsia (n = 39) and severe Preeclampsia (n = 46) were aged 34–41 years old, and the lowest numbers in both groups were aged 17–26 years. There was no significant difference in the age between the study groups (p = 0.15). The multipara women in the preeclampsia group were 70/100, and primipara cases were 30/100. The multiparous women were more frequent in the control group (38/50) than the primipara women (12/50). There was no significant difference in the parity between the study groups (p = 0.82). Most patients were overweight in all groups, with a mean BMI of 27.5 kg/m2 in control (54%), 27.2 kg/m2 in mild preeclampsia (42%) and 26.9 kg/m2 in severe preeclampsia (50%) patients. No significant difference was seen in the BMI among three groups (p = 0.71) (Table 1). Additionally, most women with severe preeclampsia (46/50) delivered preterm, with a mean gestational age of 33.04 ± 3.4 weeks compared to 18/50 of mild preeclampsia (37.12 ± 1.78 weeks). On the other hand, most women in the control group (47/50) delivered at term with a mean gestational age of 38.36 ± 1.40 weeks. There was a highly significant difference in the gestational age between study groups (p = 0.001) (Table 2).

Table 1 Sociodemographic characteristics of the study groups
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Table 2 Distribution of the study groups according to their gestational age at birth
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Serum LDH level

The mean serum LDH level in the preeclampsia groups (both mild and severe) was 395.8 ± 231.8 IU/L, which was significantly higher (p˂0.001) than the mean LDH level in the control group (149.3 ± 42.4 IU/L). The preeclampsia women with a high LDH level was 75%, which is significantly higher (p˂0.001) than in the control group (2.0%) (Table 3).

Table 3 Serum LDH level in the study groups
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Serum LDH level in the preeclampsia groups (mild and severe)

Women with high LDH levels were significantly higher (p˂0.001) in the severe preeclampsia group (88%) compared to the mild preeclampsia group (62%). Also, the mean level of LDH was significantly higher (p˂0.001) in the severe preeclampsia group compared to the mild preeclampsia group (488.6 ± 267.9 versus 302.9 ± 138.5) (Table 4).

Table 4 LDH level in the mild and severe preeclampsia groups
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Maternal complications due to preeclampsia

Maternal complications developed in 17 cases of severe preeclamptic women in which eclampsia was the most recorded complication (8/50), followed by Hemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome (7/50), then each pulmonary oedema (1/50) and cerebrovascular complications (CVA) (1/50) (Fig. 1).

Fig. 1
figure 1

Frequency of complications in the pregnant women diagnosed with severe preeclampsia. CVA: Cerebrovascular complication

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Serum LDH level in correlation with maternal complications

The mean LDH level among preeclamptic women who developed complications was 700.5 ± 356.8 IU/L, while in those without complications was 414.2 ± 182.7 IU/L. The difference in the mean LDH level among preeclamptic women with and without complications was significant (p = 0.01) (Table 5).

Table 5 The difference in LDH level among preeclampsia cases in relation to maternal complications
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LDH level and perinatal outcome

The most common adverse perinatal outcomes were RDS, 33.3% in newborn whose mothers had high LDH levels, compared to 12% in the newborn whose mothers had normal LDH (p = 0.07). Both intrauterine growth restriction (IUGR; 4.0%) and perinatal death (13.3%) were only seen in babies whose mothers had high LDH levels. There was no significant association between the level of LDH in preeclamptic women and the development of IUGR in their newborns (p = 0.14). The NICU admission rate was significantly (p = 0.001) higher in babies whose mothers had elevated LDH levels (40%) (Table 6).

Table 6 Perinatal complications based on different LDH levels in the preeclampsia cases
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Discussion

New-onset hypertension, along with evidence of maternal organ failure, is defined as preeclampsia. Its rate has steadily increased over the past 30 years, causing a high economic burden [21]. Thus, in this study, for the first time in our locality, we aimed to correlate LDH level and the severity of preeclampsia and maternal/perinatal outcomes.

In the current study, most patients with preeclampsia were aged 34–41 years (42.5%), multipara (70%) and overweight (46%). These indicate that middle-aged pregnant women are more vulnerable to preeclampsia, especially those with multipara and overweight. However, another study in Switzerland by Purde et al. stated that most pregnant women (36.7%) with preeclampsia were aged 30–34 years, primiparous (23.3%), and had average body weight (53.3%) [22], which is not agreed with the outcomes of this study.

Moreover, most women with severe preeclampsia (92%) delivered preterm, with a mean gestational age of 33.04 ± 3.4 weeks at delivery, which is not in line with that of Purde et al. who found only 30% of preeclamptic women to have preterm delivery [22]. Our results indicate that preeclampsia is directly related to preterm delivery and immature neonate, which might lead to NICU admission and neonatal death.

Also, in this study, maternal complications developed in 17 cases (8.5%) of the severe preeclamptic women in which eclampsia was the most recorded complication (8 cases), followed by HELLP syndrome (7 cases), then pulmonary edema and CVA (1 case each). However, another study reported that only four preeclampsia patients developed eclampsia (0.31%). In contrast, three patients (0.23%) progressed to HELLP syndrome, and one pregnancy did not result in the birth of a living baby [22]. These variations might be related to the sample size, ethnicity, race, gestational age, maternal age, and environmental factors.

Biomarkers for the early detection of preeclampsia are essential for risk stratification and testing therapies to prevent the disease [23]. Thus, in this study, the LDH level was used as a biomarker, and we found that the mean LDH level was high in preeclampsia patients, which was correlated with the severity of the disease. These findings are in agreement with the results of Mary et al. in a case-control study on 400 pregnant women, of which 121 had mild preeclampsia and 79 had severe preeclampsia. They observed a significant rise in the LDH levels with increasing disease severity (p < 0.001) [18]. Also, our study results follow an observational study in Pakistan by Kasraeian et al., who found that high LDH levels were significantly correlated with the severity of preeclampsia [24]. Similarly, Gupta et al. study on 51 cases of mild preeclampsia and 49 cases of severe preeclampsia observed higher levels of LDH (627.38 ± 230.04 IU/L) than the control group (224.43 ± 116.61 IU/L) [25]. However, other biomarkers might be used as predictors for the detection of preeclampsia, such as eosinophil-based complete blood cell indices [26], increased platelet counts and lower aspartate aminotransferase to platelet ratio index (APRI), were found to be valuable indices for predicting of early onset of preeclampsia, but with relatively low sensitivity and specificity [27].

Furthermore, this study showed a significant difference in LDH enzyme levels between preeclampsia with and without maternal complications. Similarly, Dev et al. in India found a higher rate of maternal complications when the LDH level is high (> 800 IU/L) [28]. Kozic et al., in a prospective cohort study for assessing predictors of preeclampsia and its correlation with maternal outcome, found that a high LDH level had a moderate predictive value for developing maternal complications in preeclampsia patients [29].

Regarding the neonatal outcomes, RDS among neonates born from high LDH enzyme mothers with preeclampsia was significantly higher than in neonates born from mothers with normal LDH level. This outcome is similar to that of Jha et al., who found an increase in the risk of RDS among infants born from preeclampsia mothers with high LDH levels [30]. The incidence of IUGR was not significantly different among babies with preeclampsia mothers, whether they have normal or high LDH levels. These results were against the findings of Jaiswar et al. [31] and Dacaj et al. [32], who found a significant increase in the number of fetal IUGRs in patients with high LDH. Extensive cohort studies must elucidate these dissimilarities to clarify the association between maternal LDH levels and fetal IUGR.

High maternal LDH levels in preeclampsia were associated with a significantly high frequency of perinatal death. These findings agree with Qublan et al.‘s study of 49 cases of mild preeclampsia and 62 cases of severe preeclampsia. They found an increase in the incidence of perinatal death among women with high LDH levels [33]. The need for a NICU was significantly higher for babies born from preeclamptic women with high LDH levels than those born from women with normal LDH levels. These results align with Prajapati et al.‘s observational study on 90 cases of preeclampsia. They showed a strong association between high LDH levels and adverse perinatal outcomes [34].

Conclusions

The LDH level is high among women with preeclampsia, and it correlates with the severity of the disease as well as the maternal and perinatal outcomes. LDH can be a valuable biomarker for predicting the severity of preeclampsia. Preeclampsia women with elevated LDH need to be closely monitored, and a large cohort study is recommended to clarify the association between maternal LDH and maternal/perinatal outcomes.

Data availability

No datasets were generated or analysed during the current study.

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Acknowledgements

The authors would like to thank the Sulaimani Maternity Teaching Hospital authorities for their help and support to this study.

Funding

The study is self-funded; no grant or fund was obtained from national/international agencies, organizations, or Universities.

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Authors and Affiliations

  1. Department of Clinical Medical Sciences, College of Medicine, University of Sulaimani, Sulaimaniyah, Iraq

    Sallama Kamel Nasir, Rozhan Yassin Khalil & Maryam Bakir Mahmood

  2. Sulaimani Maternity Teaching Hospital, Sulaimani Directorate of Health, Sulaimaniyah, Iraq

    Sallama Kamel Nasir, Rozhan Yassin Khalil, Maryam Bakir Mahmood & Aveen Saadi Dawd

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  1. Sallama Kamel Nasir
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Contributions

Sallama Kamel Nasir: Methodology, data collection, data analysis, edit, revise, and correct the original manuscript. Rozhan Yassin Khalil: Conceptualization, study registration, written the original manuscript. Maryam Bakir Mahmood: Supervision, resources, study administration. Aveen Saadi Dawd: Methodology, written the original manuscript. All authors agreed to submit the manuscript.

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Correspondence to Sallama Kamel Nasir.

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Ethical approval

The Scientific and Ethical Committees of the College of Medicine, University of Sulaimani, Sulaimaniyah, Iraq (No. 43/21/04/2024-UoS) revised and approved the study protocol. Additionally, patient-informed consent forms were filled out for all participants, and the study protocol was explained to them thoroughly. All parameters were done based on the Declaration of Helsinki.

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The authors declare no competing interests.

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Nasir, S.K., Khalil, R.Y., Mahmood, M.B. et al. Serum lactate dehydrogenase level in preeclampsia and its correlation with disease severity, maternal and perinatal outcomes. BMC Women's Health 25, 108 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12905-025-03622-5

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  • Published:

  • DOI: https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12905-025-03622-5

Keywords

BMC Women's Health

ISSN: 1472-6874

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