Zeynep Gedik ÖZKÖSE, Burak ÖZKÖSE, Alev Atış AYDIN, Nermin GÜNDÜZ
Anatolian Journal of Obstetrics and Gynecology Research - 2026;3(2):149-156
Purpose: To compare histopathological findings associated with reduced uteroplacental perfusion between [early-onset preeclampsia (EOPE), <34 weeks] and [late-onset preeclampsia (LOPE), >=34 weeks] placentas, and to evaluate whether placental morphology may contribute to understanding differences between these subtypes. Methods: This prospective observational cohort study was performed with the participation of women diagnosed with preeclampsia according to 2013 American College of Obstetricians and Gynecologists criteria who were divided into EOPE and LOPE subgroups. Placenta samples were collected after delivery, fixed in formalin, and evaluated after hematoxylin-eosin staining. Histopathological findings were assessed according to Amsterdam Placental Workshop Group Consensus criteria and reviewed by a blinded perinatal histopathologist. Comparisons between groups were performed using Student's t-test, Mann-Whitney U test, chi-square test, Fisher's exact test, and binary logistic regression where appropriate. A p value <0.05 was considered statistically significant. Results: A total of 75 women were recruited, 33 (44%) with EOPE and 42 (56%) with LOPE. Villous infarction and cytotrophoblast cell proliferation were significantly more prevalent in the EOPE group (p=0.026 vs. p=0.043). Fibrinoid necrosis showed a non-significant tendency toward higher prevalence in EOPE. Syncytiotrophoblastic knotting was present in over 93% of cases in both groups (p=0.852). Perivillous fibrin deposits were present in all cases. Hemolysis, elevated liver enzymes, low platelets syndrome was observed only in the EOPE group (24.24% vs. 0%; p=0.001). Intrauterine growth restriction was significantly more common in EOPE (odds ratio 4.70) (48.48% vs. 16.67%; p=0.003). Mean birth weight, placental weight and Apgar scores at 1 minute and 5 minutes were all significantly lower in the EOPE group. Conclusion: Placental defects revealing reduced uteroplacental perfusion included villous infarction and cytotrophoblastic proliferation which were significantly more prevalent in EOPE. Syncytiotrophoblastic knotting and perivillous fibrin deposition were highly prevalent in both groups, suggesting shared ischemic mechanisms. These findings support the hypothesis that EOPE and LOPE may differ in the degree and pattern of placental involvement while sharing several underlying pathophysiological mechanisms. Further studies are needed before routine implementation can be recommended in all preeclamptic pregnancies.
