Preeclampsia constitutes a pregnancy-specific multisystem disorder characterized by new-onset hypertension accompanied by proteinuria or evidence of end-organ dysfunction after 20 weeks of gestation [1]. This condition represents one of the most significant complications of pregnancy, affecting approximately 3-8% of pregnancies globally and contributing substantially to maternal and perinatal morbidity and mortality [2]. The burden is disproportionately higher in low- and middle-income countries, where preeclampsia accounts for approximately 10-15% of direct maternal deaths [3]. The pathophysiological mechanisms underlying preeclampsia are complex and multifactorial, originating from abnormal placentation during early pregnancy [4]. Inadequate trophoblastic invasion and remodeling of maternal spiral arteries result in placental hypoperfusion and ischemia, triggering the release of anti-angiogenic factors, pro-inflammatory cytokines, and oxidative stress mediators into maternal circulation [5]. These circulating factors induce widespread endothelial dysfunction, leading to characteristic manifestations including hypertension, proteinuria, thrombocytopenia, hepatic dysfunction, renal impairment, and neurological complications [6]. The clinical spectrum of preeclampsia ranges from mild disease with minimal symptoms to severe life-threatening conditions including eclampsia, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets), acute renal failure, cerebrovascular accidents, and placental abruption [7]. Fetal complications encompass intrauterine growth restriction, preterm birth, oligohydramnios, and stillbirth, contributing to substantial neonatal morbidity and mortality [8]. The unpredictable progression from mild to severe disease necessitates reliable methods for early identification of high-risk women to enable intensified surveillance and timely intervention. Serum uric acid elevation represents one of the earliest biochemical abnormalities in preeclampsia, resulting from multiple mechanisms including decreased renal clearance secondary to reduced glomerular filtration, increased tubular reabsorption, and enhanced production from placental tissue undergoing oxidative stress [9]. Hyperuricemia contributes to endothelial dysfunction through multiple pathways, including oxidative stress generation, inflammatory response activation, and impairment of nitric oxide bioavailability [10]. Previous investigations have demonstrated associations between elevated uric acid levels and adverse pregnancy outcomes, though controversy persists regarding whether hyperuricemia represents a causative factor or merely a marker of disease severity [11]. Lactate dehydrogenase, a ubiquitous intracellular enzyme involved in anaerobic glycolysis, is released into circulation following cellular injury and tissue damage [12]. In preeclampsia, elevated LDH levels reflect widespread cellular dysfunction affecting multiple organ systems, including hepatocytes, endothelial cells, erythrocytes, and placental tissue [13]. Furthermore, LDH elevation serves as a diagnostic criterion for HELLP syndrome, indicating hemolysis and hepatocellular injury [14]. Several studies have identified LDH as a potential predictor of disease severity and adverse outcomes in hypertensive disorders of pregnancy [15]. Despite extensive research on preeclampsia biomarkers, most promising candidates including angiogenic factors (PlGF, sFlt-1) and novel proteins remain expensive, require specialized laboratory facilities, and are unavailable in many resource-limited settings where preeclampsia burden is highest [16]. In contrast, serum uric acid and LDH measurements are widely available, inexpensive, and routinely performed in most healthcare facilities, making them attractive candidates for risk stratification in diverse clinical settings. However, existing literature presents conflicting evidence regarding their predictive utility, with variations in threshold values, outcome definitions, and study populations limiting clinical applicability [17]. The primary objective of this study was to comprehensively evaluate the association between serum uric acid and lactate dehydrogenase levels with disease severity in women diagnosed with preeclampsia. Secondary objectives included assessment of their predictive utility for maternal complications and adverse perinatal outcomes, determination of optimal threshold values for risk stratification, and evaluation of their correlation with established severity indicators. We hypothesized that elevated levels of both biomarkers would demonstrate significant associations with severe preeclampsia and predict increased risk of adverse maternal and perinatal outcomes.

Study Design and Setting This prospective observational study was conducted in the Department of Obstetrics and Gynaecology at a tertiary care teaching hospital in southern India over an 18-month period from January 2025 to November 2025. The study protocol received approval from the Institutional Ethics Committee, and written informed consent was obtained from all participants prior to enrollment. Study Population and Sampling Pregnant women diagnosed with preeclampsia after 20 weeks of gestation presenting to the antenatal clinic or admitted to the obstetric ward were systematically screened for eligibility. Consecutive sampling was employed to recruit participants meeting inclusion criteria until the desired sample size was achieved. Inclusion Criteria Women were eligible for inclusion if they met all following criteria: (1) singleton pregnancy with gestational age ≥20 weeks confirmed by first-trimester ultrasound or reliable last menstrual period; (2) systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90 mmHg measured on two occasions at least 4 hours apart; (3) proteinuria ≥300 mg in 24-hour urine collection or protein/creatinine ratio ≥0.3 or dipstick proteinuria ≥2+ (when quantitative methods unavailable), or in the absence of proteinuria, new-onset hypertension with evidence of maternal end-organ dysfunction. Exclusion Criteria Exclusion criteria comprised: (1) chronic hypertension diagnosed before pregnancy or before 20 weeks gestation; (2) pre-existing renal disease including chronic kidney disease or glomerulonephritis; (3) diabetes mellitus (pre-gestational or gestational); (4) autoimmune disorders including systemic lupus erythematosus or antiphospholipid syndrome; (5) multiple pregnancy; (6) known liver disease or chronic hepatitis; (7) hyperuricemia secondary to gout or medication; (8) hemolytic disorders; (9) refusal to provide consent. Sample Size Calculation Sample size was calculated for comparison of two independent means using the formula: n = 2(Zα + Zβ)²σ²/d², where Zα represents the Z-value for type I error (1.96 for 95% confidence), Zβ represents the Z-value for type II error (0.84 for 80% power), σ represents pooled standard deviation, and d represents expected mean difference. Based on pilot data and previous literature suggesting mean serum uric acid levels of 7.2±2.0 mg/dL in severe preeclampsia versus 5.5±1.8 mg/dL in mild preeclampsia, with expected mean difference of 1.7 mg/dL, the calculated minimum sample size was 44 participants per group. Accounting for potential 10% attrition, a total of 100 participants (50 per group) were targeted for enrollment. Classification of Disease Severity Participants were classified into two groups based on severity criteria adapted from the American College of Obstetricians and Gynecologists guidelines. Severe preeclampsia was diagnosed in the presence of any of the following features: systolic blood pressure ≥160 mmHg or diastolic blood pressure ≥110 mmHg on two occasions at least 4 hours apart; thrombocytopenia (platelet count <100,000/μL); elevated liver enzymes (at least twice upper normal limit) or severe persistent right upper quadrant or epigastric pain; serum creatinine >1.1 mg/dL or doubling of serum creatinine; pulmonary edema; new-onset headache unresponsive to medication; or visual disturbances. Women not meeting these criteria were classified as mild preeclampsia. Clinical Evaluation and Laboratory Investigations All participants underwent comprehensive clinical evaluation at enrollment, including detailed history, physical examination, and blood pressure measurement using standardized technique with appropriately sized cuff after 5 minutes rest in sitting position. Following overnight fasting, 5 mL venous blood samples were collected in plain and EDTA vacutainers for biochemical and hematological investigations. Serum uric acid was measured using enzymatic colorimetric method (uricase-peroxidase method) with autoanalyzer, with normal reference range of 2.5-6.0 mg/dL. Serum lactate dehydrogenase was measured using kinetic UV method based on NADH consumption, with normal reference range of 140-280 IU/L. Additional investigations included complete blood count, liver function tests (serum bilirubin, aspartate aminotransferase, alanine aminotransferase, total protein, albumin), renal function tests (serum creatinine, blood urea nitrogen), and 24-hour urinary protein estimation. Coagulation profile was performed when indicated. Maternal and Fetal Monitoring All participants received standard care according to institutional protocol. Women with severe preeclampsia were hospitalized for close monitoring and received antihypertensive therapy (methyldopa, nifedipine, or labetalol) to maintain blood pressure <150/100 mmHg. Magnesium sulfate prophylaxis was administered according to established protocols for seizure prevention in severe cases. Corticosteroids for fetal lung maturation were administered when delivery was anticipated before 34 weeks. Fetal surveillance included serial ultrasound for fetal growth assessment, amniotic fluid volume evaluation, and Doppler velocimetry when indicated. Non-stress testing was performed biweekly for mild and daily for severe preeclampsia. Delivery timing was individualized based on disease severity, gestational age, and maternal-fetal condition, with planned delivery at 37 weeks for mild and 34 weeks for severe preeclampsia in stable cases. Outcome Measures Primary outcome measures included maternal complications (eclampsia, HELLP syndrome, acute kidney injury, pulmonary edema, placental abruption, disseminated intravascular coagulation, cerebrovascular accident) and perinatal outcomes (preterm delivery <37 weeks, cesarean delivery for maternal or fetal indications, birth weight, 5-minute Apgar score <7, neonatal intensive care unit admission, perinatal death). Secondary outcomes included need for intensive care unit admission and duration of hospitalization. Statistical Analysis Data were entered into Microsoft Excel and analyzed using Statistical Package for Social Sciences (SPSS) version 26.0. Normality of continuous variables was assessed using Kolmogorov-Smirnov test. Continuous variables were expressed as mean ± standard deviation and compared between groups using independent samples Student's t-test. Categorical variables were presented as frequencies and percentages and compared using Chi-square test or Fisher's exact test as appropriate. Pearson correlation coefficient was calculated to assess linear relationship between uric acid, LDH, and other continuous variables. Receiver operating characteristic (ROC) curve analysis was performed to determine optimal threshold values of uric acid and LDH for predicting severe preeclampsia and adverse outcomes. Area under curve (AUC) with 95% confidence intervals was calculated, with AUC >0.7 considered acceptable discrimination. Sensitivity, specificity, positive predictive value, and negative predictive value were calculated for selected cut-off values. A two-tailed p-value <0.05 was considered statistically significant for all analyses.

Study Participants and Baseline Characteristics During the 18-month study period, 124 pregnant women with preeclampsia were screened for eligibility. Twenty-four women were excluded (12 with chronic hypertension, 5 with pre-existing renal disease, 4 with diabetes mellitus, 2 with multiple pregnancy, 1 declined participation), resulting in final enrollment of 100 participants who completed follow-up until delivery. Based on severity criteria, 60 women (60%) were classified as mild preeclampsia and 40 women (40%) as severe preeclampsia. Table 1 presents baseline maternal demographic and clinical characteristics. The mean maternal age was comparable between groups (26.8±3.7 years in mild versus 27.4±4.1 years in severe preeclampsia, p=0.449). Mean gestational age at diagnosis was significantly earlier in the severe preeclampsia group (32.4±3.2 weeks versus 34.8±2.6 weeks, p<0.001). Nulliparity was more prevalent in the severe group (67.5% versus 48.3%), though this difference did not achieve statistical significance (p=0.056). Mean body mass index and history of preeclampsia in previous pregnancy showed no significant differences between groups. Table 1: Baseline Maternal Demographic and Clinical Characteristics Parameter Mild Preeclampsia (n=60) Severe Preeclampsia (n=40) p-value Maternal age (years) 26.8 ± 3.7 27.4 ± 4.1 0.449 Gestational age at diagnosis (weeks) 34.8 ± 2.6 32.4 ± 3.2 <0.001 Nulliparity, n (%) 29 (48.3) 27 (67.5) 0.056 Body mass index (kg/m²) 25.4 ± 3.2 26.1 ± 3.6 0.322 Previous preeclampsia, n (%) 6 (10.0) 5 (12.5) 0.689 Systolic blood pressure (mmHg) 148.6 ± 6.4 168.4 ± 12.3 <0.001 Diastolic blood pressure (mmHg) 96.2 ± 4.8 112.6 ± 8.4 <0.001 24-hour urinary protein (g) 1.2 ± 0.6 3.8 ± 2.1 <0.001 Biochemical Parameters Table 2 demonstrates comprehensive comparison of biochemical parameters between mild and severe preeclampsia groups. Mean serum uric acid levels were significantly elevated in women with severe preeclampsia compared to mild disease (7.3±1.2 mg/dL versus 5.0±0.9 mg/dL, p<0.001). The proportion of women with uric acid levels exceeding 6.5 mg/dL was substantially higher in the severe group (75.0% versus 13.3%, p<0.001). Similarly, mean serum LDH levels demonstrated marked elevation in severe preeclampsia (694.6±156.3 IU/L versus 416.8±88.4 IU/L, p<0.001). LDH levels exceeding 600 IU/L were observed in 62.5% of severe cases compared to only 6.7% of mild cases (p<0.001). Liver aminotransferases showed significant elevation in severe disease, with mean AST of 186.4±124.6 IU/L versus 52.3±28.4 IU/L (p<0.001) and mean ALT of 168.2±106.8 IU/L versus 48.6±24.2 IU/L (p<0.001). Platelet counts were significantly lower in severe preeclampsia (162.4±54.3 × 10³/μL versus 224.6±48.2 × 10³/μL, p<0.001), and serum creatinine was elevated (1.2±0.4 mg/dL versus 0.8±0.2 mg/dL, p<0.001). Table 2: Comparison of Biochemical Parameters Between Groups Parameter Mild Preeclampsia (n=60) Severe Preeclampsia (n=40) p-value Serum uric acid (mg/dL) 5.0 ± 0.9 7.3 ± 1.2 <0.001 Uric acid >6.5 mg/dL, n (%) 8 (13.3) 30 (75.0) <0.001 Lactate dehydrogenase (IU/L) 416.8 ± 88.4 694.6 ± 156.3 <0.001 LDH >600 IU/L, n (%) 4 (6.7) 25 (62.5) <0.001 Aspartate aminotransferase (IU/L) 52.3 ± 28.4 186.4 ± 124.6 <0.001 Alanine aminotransferase (IU/L) 48.6 ± 24.2 168.2 ± 106.8 <0.001 Platelet count (×10³/μL) 224.6 ± 48.2 162.4 ± 54.3 <0.001 Serum creatinine (mg/dL) 0.8 ± 0.2 1.2 ± 0.4 <0.001 Total bilirubin (mg/dL) 0.7 ± 0.3 1.4 ± 0.8 <0.001 Correlation analysis revealed significant positive correlation between serum uric acid and LDH levels (r=0.742, p<0.001). Both biomarkers demonstrated significant positive correlations with systolic blood pressure, diastolic blood pressure, proteinuria, liver enzymes, and serum creatinine, while showing negative correlation with platelet count and gestational age at delivery. Maternal and Perinatal Outcomes Table 3 presents comprehensive maternal and perinatal outcomes stratified by disease severity. Maternal complications were significantly more frequent in the severe preeclampsia group. Eclampsia occurred in 6 women (15.0%) with severe disease compared to none in the mild group (p=0.002). HELLP syndrome developed in 8 women (20.0%) with severe preeclampsia versus 1 woman (1.7%) with mild disease (p=0.001). Placental abruption complicated 5 severe cases (12.5%) and no mild cases (p=0.007). Acute kidney injury requiring dialysis occurred in 2 severe cases (5.0%). Overall, any maternal complication occurred in 32.5% of severe versus 5.0% of mild preeclampsia (p<0.001). Table 3: Maternal and Perinatal Outcomes According to Disease Severity Outcome Mild Preeclampsia (n=60) Severe Preeclampsia (n=40) p-value Maternal Outcomes Eclampsia, n (%) 0 (0.0) 6 (15.0) 0.002 HELLP syndrome, n (%) 1 (1.7) 8 (20.0) 0.001 Placental abruption, n (%) 0 (0.0) 5 (12.5) 0.007 Acute kidney injury, n (%) 0 (0.0) 2 (5.0) 0.088 Pulmonary edema, n (%) 0 (0.0) 3 (7.5) 0.038 Any maternal complication, n (%) 3 (5.0) 13 (32.5) <0.001 ICU admission, n (%) 2 (3.3) 9 (22.5) 0.002 Perinatal Outcomes Gestational age at delivery (weeks) 37.4 ± 1.6 34.8 ± 2.8 <0.001 Preterm delivery <37 weeks, n (%) 11 (18.3) 24 (60.0) <0.001 Preterm delivery <34 weeks, n (%) 2 (3.3) 12 (30.0) <0.001 Cesarean delivery, n (%) 28 (46.7) 32 (80.0) 0.001 Birth weight (grams) 2724 ± 384 2186 ± 562 <0.001 Low birth weight <2500 g, n (%) 14 (23.3) 24 (60.0) <0.001 5-minute Apgar <7, n (%) 3 (5.0) 9 (22.5) 0.007 NICU admission, n (%) 10 (16.7) 21 (52.5) <0.001 Perinatal death, n (%) 0 (0.0) 2 (5.0) 0.088 Perinatal outcomes were similarly adversely affected in severe preeclampsia. Mean gestational age at delivery was significantly earlier (34.8±2.8 weeks versus 37.4±1.6 weeks, p<0.001). Preterm delivery before 37 weeks occurred in 60.0% of severe cases compared to 18.3% of mild cases (p<0.001), with early preterm delivery (<34 weeks) occurring in 30.0% versus 3.3% (p<0.001). Cesarean delivery was performed in 80.0% of severe versus 46.7% of mild cases (p=0.001), primarily for maternal or fetal indications. Mean birth weight was significantly lower in the severe group (2186±562 g versus 2724±384 g, p<0.001), with low birth weight (<2500 g) affecting 60.0% versus 23.3% of infants (p<0.001). Five-minute Apgar scores <7 were observed more frequently in severe disease (22.5% versus 5.0%, p=0.007). NICU admission was required for 52.5% of infants born to mothers with severe preeclampsia compared to 16.7% in mild disease (p<0.001). Two perinatal deaths (one stillbirth, one early neonatal death) occurred in the severe group. When stratified by biomarker levels, women with serum uric acid >6.5 mg/dL experienced maternal complications in 31.6% versus 4.8% with levels ≤6.5 mg/dL (p<0.001). Similarly, LDH >600 IU/L was associated with 37.9% maternal complication rate versus 6.8% when LDH ≤600 IU/L (p<0.001). Preterm delivery occurred in 56.4% with elevated uric acid versus 18.3% with normal levels (p<0.001), and in 58.6% with elevated LDH versus 17.9% with normal LDH (p<0.001). ROC curve analysis demonstrated that serum uric acid at cut-off value of 6.5 mg/dL predicted severe preeclampsia with sensitivity 75.0%, specificity 86.7%, positive predictive value 78.9%, and negative predictive value 83.9% (AUC 0.862, 95% CI 0.791-0.933). LDH at cut-off of 600 IU/L yielded sensitivity 62.5%, specificity 93.3%, positive predictive value 86.2%, and negative predictive value 79.4% (AUC 0.854, 95% CI 0.780-0.928). Combined elevation of both markers predicted severe disease with specificity 96.7% and positive predictive value 92.3%.

This prospective observational study demonstrates that serum uric acid and lactate dehydrogenase levels are significantly elevated in severe preeclampsia and show strong associations with adverse maternal and perinatal outcomes. Both biomarkers exhibited good discriminatory ability for disease severity and complication prediction, supporting their potential utility for risk stratification in clinical practice. Our finding of significantly elevated mean uric acid levels in severe versus mild preeclampsia (7.3±1.2 versus 5.0±0.9 mg/dL) aligns with extensive previous literature. A large multicenter study by Thangaratinam et al. involving over 3,000 women demonstrated progressive increase in uric acid levels with disease severity, with values exceeding 6.0 mg/dL associated with increased adverse outcomes [11]. The pathophysiological basis for hyperuricemia in preeclampsia is multifactorial, involving decreased renal clearance due to reduced glomerular filtration and increased tubular reabsorption, along with enhanced tissue breakdown and oxidative stress [12]. More importantly, uric acid appears to play an active pathogenic role rather than serving merely as a disease marker. Experimental studies have demonstrated that uric acid induces endothelial dysfunction through multiple mechanisms including reduction of nitric oxide bioavailability, activation of the renin-angiotensin system, stimulation of inflammatory pathways, and promotion of oxidative stress [13]. These effects directly contribute to the hypertension and end-organ dysfunction characteristic of preeclampsia. Furthermore, elevated maternal uric acid may adversely affect placental function and fetal development, potentially explaining associations with intrauterine growth restriction and adverse perinatal outcomes observed in our study. The significantly elevated LDH levels in severe preeclampsia (694.6±156.3 IU/L versus 416.8±88.4 IU/L in mild disease) reflect widespread cellular injury and tissue damage affecting multiple organ systems. LDH is a cytoplasmic enzyme released from damaged cells, with elevation in preeclampsia resulting from hepatocellular injury, endothelial damage, hemolysis, and placental dysfunction [14]. Importantly, LDH serves as one of the diagnostic criteria for HELLP syndrome, a severe variant of preeclampsia associated with substantial maternal and perinatal morbidity [15]. In our cohort, 8 women (20%) with severe preeclampsia developed HELLP syndrome, all demonstrating markedly elevated LDH levels. Previous studies have yielded variable results regarding optimal LDH cut-off values for predicting adverse outcomes. Qublan et al. identified LDH >800 IU/L as predictor of maternal complications [16], while Jaiswar et al. reported significant associations at lower thresholds of >600 IU/L [17]. Our ROC curve analysis identified 600 IU/L as the optimal cut-off, yielding good specificity (93.3%) and positive predictive value (86.2%) for severe disease. This threshold may represent a practical value for clinical decision-making, though validation in larger diverse populations is warranted. The strong correlation between uric acid and LDH levels (r=0.742) observed in our study suggests common underlying pathophysiological mechanisms, particularly endothelial dysfunction and oxidative stress. Combined elevation of both markers demonstrated very high specificity (96.7%) for severe disease, indicating that women with elevation of both biomarkers represent a particularly high-risk subgroup warranting intensive monitoring and potentially earlier delivery. Our findings regarding maternal complications align with established literature demonstrating increased risks of eclampsia, HELLP syndrome, and placental abruption in severe preeclampsia [18]. The 15% eclampsia rate in our severe preeclampsia group, despite magnesium sulfate prophylaxis, highlights the unpredictable nature of this complication and the importance of close monitoring. The association between elevated biomarkers and these complications suggests potential utility for guiding prophylactic interventions and delivery timing. The perinatal outcomes observed in our study, particularly the 60% preterm delivery rate and 52.5% NICU admission rate in severe preeclampsia, underscore the substantial neonatal burden of this condition. Earlier gestational age at disease onset and delivery in severe cases contributes significantly to prematurity-related morbidity. The two perinatal deaths in our severe group, while representing relatively favorable outcomes compared to some resource-limited settings, emphasize the ongoing need for improved prediction and prevention strategies. The clinical utility of serum uric acid and LDH measurements lies in their widespread availability, low cost, rapid turnaround time, and integration into routine laboratory panels. Unlike specialized biomarkers such as angiogenic factors that require sophisticated facilities and substantial expense, these tests can be performed in virtually any clinical setting, making them particularly valuable for resource-limited environments where preeclampsia burden is highest. Their ability to predict disease severity and adverse outcomes can inform decisions regarding hospitalization, surveillance intensity, corticosteroid administration, and delivery timing. Several strengths enhance the validity of our findings. The prospective design with systematic data collection minimized recall and selection bias. Use of standardized diagnostic criteria and laboratory methods ensured consistency. Comprehensive assessment of both maternal and perinatal outcomes provided holistic evaluation of predictive utility. Statistical analysis including ROC curves allowed determination of optimal threshold values with clinical applicability. However, several limitations warrant acknowledgment. The single-center design may limit generalizability to populations with different demographics, disease prevalence, or healthcare systems. The modest sample size, while adequate for primary objectives, may have limited power for detecting associations with less common outcomes such as maternal mortality. Absence of serial biomarker measurements prevented assessment of temporal trends and response to treatment. Lack of comparison with other proposed biomarkers such as angiogenic factors precluded comprehensive evaluation of relative predictive performance. Finally, the observational design cannot establish causality or guide specific interventions, which would require randomized controlled trials.

This prospective observational study demonstrates that serum uric acid and lactate dehydrogenase represent valuable, accessible, and cost-effective biochemical markers for predicting disease severity and adverse outcomes in preeclampsia. Women with severe preeclampsia exhibit significantly elevated levels of both biomarkers, which show strong associations with maternal complications including eclampsia, HELLP syndrome, and placental abruption, as well as adverse perinatal outcomes including preterm delivery, low birth weight, and neonatal intensive care unit admission. Threshold values of serum uric acid >6.5 mg/dL and LDH >600 IU/L demonstrate good discriminatory ability for identifying high-risk women who may benefit from intensified surveillance and earlier intervention. The widespread availability and low cost of these tests make them particularly suitable for implementation in resource-limited settings where the burden of preeclampsia-related morbidity and mortality is highest. Integration of these biomarkers into routine clinical evaluation of women with preeclampsia can facilitate early risk stratification, guide intensive monitoring strategies, inform decisions regarding hospitalization and delivery timing, and ultimately contribute to improved maternal and perinatal outcomes. Healthcare providers should consider incorporating serum uric acid and LDH measurements into standard assessment protocols for preeclampsia management, particularly in settings where more sophisticated biomarkers are unavailable or cost-prohibitive.

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