Objectives: To evaluate histological changes of placental villi and blood vessels in pregnancy complicated by pre-eclampsia (PE) and their relation to clinical data.
Patients & Methods: The study included 100 pregnant women developing PE at any time throughout pregnancy (PE group) and another 100 pregnant free of PE (Control group). Collected data included age, gestational age (GA), manifestations and severity of PE, neonatal birth weight (BW) and placental weight (PW). Placental tissue was obtained for light and electron microscopic examination
Results: BW and PW showed negative significant correlation with maternal BMI, presence and severity of PE. GA and development of PE were significant predictors for low PW which is significant predictor for low BW. Placentas of PE group showed aggregation of syncytiotrophoblast cells, hyaline degeneration of connective tissue core and endothelial lining of stem blood vessel (SBV) and villous core is devoid of fetal blood vessel. Diffuse fibrous tissue formation, hypertrophic musculosa of SBV up to endarteritis obliterans (EAO) and placental tissue bridges crossing intervillous spaces and villous arborization formed only of connective tissue with no cellular elements. Electron microscopy confirmed these findings and showed attenuated blood vessels and excessive villous arborization covered with fibrin like material.
Conclusion: Development of placental EAO with diminution of placental growth and proper invasion may underlie development of PE. Reduced PW is a reflection of this histological affection and was negatively correlated with severity of PE. Early PE is associated with more severe clinical manifestation and aggressive histological changes.
Keywords: Pre-eclampsia, Placental weight, Histological placental changes, Neonatal birth weight
Introduction
The placenta is a transient organ that forms during pregnancy to support the growth and development of the fetus. During human placental development, trophoblast cells differentiate through two major pathways. In the villous pathway, cytotrophoblast cells fuse to form multinucleated syncytiotrophoblast. In the extravillous pathway, cytotrophoblast cells acquire an invasive phenotype and differentiate into either interstitial extravillous trophoblasts, which invade the decidua and a portion of the myometrium, or endovascular extravillous trophoblasts, which remodel the maternal vasculature. These differentiation events are tightly controlled by the interplay of oxygen tension, transcription factors, hormones, growth factors, and other signaling molecules. More recently, microRNAs have been implicated in this regulatory process (1, 2, 3).
The human placenta is a hemochorial placenta, which means that maternal blood is in direct contact with fetal trophoblast. The syncytiotrophoblast invades maternal venous sinuses relatively early and invades the spiral arterioles on the 17th or 18th day after conception. The lacunae, or lakes formed by maternal tissue fluid and blood, form the intervillous space; throughout the rest of pregnancy maternal blood circulates freely within the intervillous space. The placenta is divided into cotyledons, each supplied by a major branch of the umbilical artery and drained by a major tributary to the umbilical vein. These vessels enter stem villi, which branch and rebranch like a tree to form microscopic terminal villi suspended within the intervillous space. Each cotyledon has several anchoring villi which extend into the decidua basalis and are anchored to it by syncytial cells and fibrin (4, 5, 6).
Pre-eclampsia (PE) occurs in at least 5–8% of all pregnancies, and is defined as new onset hypertension with proteinuria during pregnancy and typically, occurs after 20 weeks gestation. PE and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death, responsible for 76,000 maternal and 500,000 infant deaths each year. PE is a severe multisystem disorder, but its prevention, early diagnosis, and treatment are insufficient, since etiology and pathogenesis of the disease are still not totally understood (7, 8, 9).
The current prospective comparative clinico-anatomical study aimed to evaluate histological changes of placental villi and their blood vessels in pregnancy complicated by pre-eclampsia and their relation to clinical data and pregnancy outcome.
Materials & Methods
Patients
The present study was conducted at Department of Obstetrics & Gynecology, Benha University Hospital and Department of Anatomy, Faculty of Medicine, Benha University since Sep 2012 till Jan 2014. After approval of the study protocol by the Local Ethical Committee and obtaining written fully informed patients' consents, all pregnant women attending to antenatal care unit were enrolled in the study to select 100 pregnant women developing PE at any time throughout their course of pregnancy (PE group) and another 100 pregnant women completed their pregnancy free of PE manifestations as Control group. Exclusion criteria included previous history of pregnancy-related hypertension, multiple gestation and preexisting medical conditions such as diabetes, chronic hypertension, and renal diseases.
Pre-eclampsia was diagnosed by the presence of gestational hypertension beginning after the 12th week of pregnancy with an absolute systolic blood pressure ≥140 mmHg and/or diastolic blood pressure of ≥90 mmHg on at least two occasions, 4 hours apart, and proteinuria (one dipstick measurement ≥2+ on a voided random urine sample) (10). Ultrasonographic examination was conducted to confirm the gestational age, determine placental volume and to exclude the presence of fetal congenital abnormalities and intrauterine growth restriction.
Antepartum data collection included the following data:
1. Age: patients were categorized into Group 1 included patients aged 39 years (11).
2. Gravidity and parity of enrolled pregnant women were determined.
3. Gestational age (GA): patients were categorized into Group 1 included patients with GA40 weeks (12).
4. Blood pressure measurements and grading according to the international classification of hypertension into: Normotensive (Degree 0) with systolic arterial pressure (SAP) 150-160 mmHg and DAP of >100-109 mmHg and Severe hypertensive (Degree 3) with SAP >160 mmHg and DAP ≥110 mmHg (13).
5. Proteinurea: level of proteinurea was arbitrarily determined using dipstick test and patients were categorized into according to extent of protein in urine as Normal: free from albuminurea (score = 0); Mild albuminurea (+; score = 1), Moderate albuminurea (++; score = 2) and Severe albuminurea (+++; scored =3) (14).
6. Edema was evaluated clinically as present (score=1) or absent (score=0) (14).
7. Severe PE was defined depending on the presence of at rest SAP of ≥160 mmHg or DAP of ≥110 mmHg on two occasions and proteinuria of ≥3+ by dipstick method. Other clinical manifestations such as oliguria, cerebral or visual disturbances, pulmonary edema or cyanosis, epigastric or hypocondrial pain indicating hepatic rupture, impaired liver function of unclear pathology or intrauterine growth restriction (IUGR) indicate severe PE (15).
Postpartum data collection included the following data:
1. Neonatal birth weight (BW): low BW was defined as neonatal body weight of |
