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ORIGINAL ARTICLE
Year : 2021  |  Volume : 70  |  Issue : 1  |  Page : 25-29

Study of histological changes of placenta in pregnancy-induced hypertension in poorvanchal region of Uttar Pradesh, India


1 Department of Anatomy, Santosh Deemed to be University, Ghaziabad, Uttar Pradesh, India
2 Department Pathology, Government Medical College and Superfacility Hospital, Azamgarh, Uttar Pradesh, India
3 Department of Paedodontics and Preventive Dentistry, Santosh Dental College, Ghaziabad, Uttar Pradesh, India

Date of Submission20-Dec-2020
Date of Acceptance05-Mar-2021
Date of Web Publication07-Apr-2021

Correspondence Address:
Mr. Kumud Ranjan
Department of Anatomy, Government Medical College and Superfacility Hospital, Azamgarh - 276 128, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jasi.jasi_271_20

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  Abstract 


Introduction: The placenta is a fetomaternal organ. It is a connection of the fetus with the uterine wall of mother. Through the placenta, exchange of gases and nutrient supply takes place. Through the placenta, fetal blood tissue comes in direct contact with the maternal blood without any rejection. It is a special transient organ of pregnancy. In our study, we carried out the microscopic examination of the placenta in pregnancy-induced hypertension, i.e., syncytial knot, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, and calcified villous spot. Material and Methods: One hundred and fifty-two placentas of full-term pregnancy were collected from the labor room/operation theater of the Gynecology and Obstetrics Department of the Government Medical College and Superfacility Hospital Azamgarh. Out of one hundred and fifty-two placentas, 76 cases were controls from mothers with no known history of preexisting hypertension and 76 were collected from mothers with pregnancy-induced hypertension. Placentas were kept in 10% formalin for 24 h for fixation. After 24 h, tissues of placentas were passed through a series of the procedures from dehydration and clearing to wax impregnation before being sectioned from automated microtome. Time took for processing was 24 h. Five microns thick tissues sections were cut. Prepared slides were mounted in DPX and covered with the cover slip. Through binocular light, microscope slides were examined at ×10, ×40, and ×100 magnifications. Results: Histology in our study revealed that syncytial knots were present in placentas of all 100% of hypertensive and only 32.89% of normotensive mothers. Cytotrophoblastic proliferation was seen in 98.68% and 19.73% placentas of hypertensive and normotensive mothers, respectively. Fibrinoid necrosis of placenta was found in 88.15% of hypertensive and only 28.94% of normotensive mothers. The 100% placentas of the hypertensive mothers had endothelial proliferation as compared to controls. Calcified villous spots were seen in 84.21% and 31.57% of placentas of hypertensive and normotensive mothers, respectively. Discussion and Conclusion: Pregnancy-induced hypertension adversely affects the health of the fetus through its harmful effects on the placentas. Syncytial knots, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, and the calcified villous spots were present more in the placentas of hypertensive mothers in our study in comparison to the study of other authors. In our research, we found that endothelial proliferations were present in all placentas. If proper treatment is given to the mother in the early stage of pregnancy, it may prevent the death of a fetus. Hence, this study helps the clinician for early diagnosis and treatment of pregnancy-induced hypertension.

Keywords: Calcified villous spot, hypertensive placenta, normotensive placenta, placental fibrinoid necrosis


How to cite this article:
Singh V, Ranjan K, Tewarson S L, Singh R, Yadav Y. Study of histological changes of placenta in pregnancy-induced hypertension in poorvanchal region of Uttar Pradesh, India. J Anat Soc India 2021;70:25-9

How to cite this URL:
Singh V, Ranjan K, Tewarson S L, Singh R, Yadav Y. Study of histological changes of placenta in pregnancy-induced hypertension in poorvanchal region of Uttar Pradesh, India. J Anat Soc India [serial online] 2021 [cited 2021 Jun 14];70:25-9. Available from: https://www.jasi.org.in/text.asp?2021/70/1/25/313162




  Introduction Top


The placenta is a fetomaternal organ. It is a connection of the fetus with the uterine wall of mother.[1] Through the placenta, exchange of gases and nutrient supply and removal of waste takes place. Through the placenta, fetal blood comes in direct contact with the maternal blood without any rejection. It is a special transient organ of pregnancy.[2] The placenta provides an interface for nutrients and oxygen between fetal and maternal circulation for growth and development of the fetus.[3] Hemochorial type of placenta is present in the humans. In this type of placenta, exchange occurs between maternal and fetal blood while maintaining anatomical separation between the circulatory system of fetus and mother. Hypertension is a common complication of pregnancy; significantly, it contributes to perinatal and maternal morbidity and mortality.[4] Pregnancy-induced hypertension is a pregnancy-specific syndrome.[5] In this study, we designed to search the histopathological changes in the placenta due to pregnancy-induced hypertension. Complications of hypertension are reflected in the placenta macroscopically and microscopically.[6] In pregnancy-induced hypertensions due to maternal vasospasm, decreased blood flow occurs in the placenta. Constriction occurs in the fetal arteries these changes seen in the placenta. Pregnancy-induced hypertension affects all organ systems. Maternal vasospasm leads to fetal hypoxia, and it leads to fetal distress and ultimately, fetal death.[7]

The fetus depends on placenta for growth and development.[8] Pathological changes occur in the placenta in pregnancy-induced hypertension, such as infarction, calcification, diffuse placental thrombosis, inflammatory placental vasculopathy, and abnormal trophoblastic proliferation. Reduced blood flow occurs in the placenta due to pathological changes, which lead to uteroplacental insufficiency. 2%–8% maternal death occurs due to hypertension.[9] Cytotrophoblastic cellular proliferation, syncytial knots, and fibrin plaques are present more in the pregnancy-induced hypertensive then in normotensive placentas. In this study, we carried out an analysis of microscopic changes of placenta in pregnancy-induced hypertension; especially syncytial knots, cytotrophoblastic cellular proliferation, fibrinoid necrosis, endothelial proliferation, and calcified villous spots both in placentas of normotensive and hypertensive mothers.


  Material and Methods Top


The one hundred and fifty-two placentas of full-term pregnancy were collected from labor room/operation theater of Gynaecology and Obstetrics, Department of Government Medical College and Superfacility hospital Azamgarh, Uttar Pradesh of Poorvanchal Region India. Out of 152 placentas, 76 were from mothers with no known history of preexisting hypertension as controls and 76 were collected from mothers with hypertension. Subjects included in our research were aged between 20 and 44 years and were from all socioeconomic groups. There were no differences according to race culture or environmental conditions. All placentas were obtained either from a vaginal route or during cesarean section. The collected placentas were weighed on weighing machine graduated in grams after washing in running tap water and dried with blotting paper. We took morphometric examination of placentas. After 24 h for fixation, tissue pieces were passed through a series of procedures, i.e., from dehydration and clearing to wax impregnation before being sectioned by an automated microtome. Time taken for processing was 24 h. The tissues were sectioned at 5 μ by automated microtome. APES-coated glass slides used for sectioned tissues. Before staining slides were placed on a hot metallic plate at 60° for 30 min. Hematoxylin and eosin staining for slide were done. All slides prepare they passed through xylene −1 for 10 min and xylene −2 for next 10 min. Then kept in 100%, 95%, 80%, 70%, alcohol for 5 min each to dehydrate the sections. For staining, slides were placed into the Harris Hematoxylin solution for 5–10 min after that rehydrated with water. Again, tissues were washed with tap water then placed into 1% eosin for approximately 1–2 min. Finally, tissues were dehydrated by passing through increasing concentrations of alcohol and cleared in the solution of xylene for 5 min. The slides were allowed to dry before being mounted in DPX and covered with a cover slip. The prepared slides were examined under light microscope ×10, ×40, and ×100.


  Results Top


The histological examination showed that syncytial knot was present in all (100%) placentas of hypertensive mothers. Whereas it was seen only in 32.89% placentas of normotensive (controls) mothers. Thus, 67.10% placentas of normotensive mothers did not have any syncytial knot [Table 1] and [Figure 1], [Figure 2]a and [Figure 2]b. The 98.68% placentas of hypertensive mothers had cytotrophoblastic cell proliferation, but it was present in 19.73% of placentas of normotensive (control) mothers. It means 80.26% placentas of a normotensive mothers and 1.31% placentas of a hypertensive mothers were free of cytotrophoblastic cell proliferation [Table 1] and [Figure 3], [Figure 4]a and [Figure 4]b. Further, 88.15% of placentas of hypertensive mothers had fibrinoid necrosis. On the other hand, only 28.94% of placentas of normotensive (control) mothers had fibrinoid necrosis. It means that 71.05% placentas of the normotensive (control) mothers had no fibrinoid necrosis but 11.84% placentas of the hypertensive mothers had it [Table 1] and [Figure 5], [Figure 6]a and [Figure 6]b. Placentas of all (100%) hypertensive mothers had endothelial proliferation in comparison to placentas of normotensive mothers in histological examination [Table 1] and [Figure 7], [Figure 8]a and [Figure 8]b. It was seen that 84.21% of placentas of hypertensive mothers had calcified villous spots, whereas only 31.57% placentas of normotensive mothers had it. The 68.42% of normotensive mother's placentas had no calcified villous spots in 15.78% of hypertensive mother's placentas had no calcified villous spots [Table 1] and [Figure 9], [Figure 10]a and [Figure 10]b.
Table 1: A comparison of histological changes in normotensive and hypertensive (pregnancy.induced hypertension) placenta

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Figure 1: In histological review, there was syncytial knot in 100% placentas of hypertensive mothers. However, there was also a syncytial knot in 32.89% placentas of normotensive (control) mothers and no syncytial knot in 67.10% of placentas of normotensive (control) mothers

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Figure 2: (a) Histological slide of hypertensive placenta – arrows shows syncytial knot (×100). (b) Histological slide of normotensive placenta - Arrow shows syncytial knot (×40)

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Figure 3: In histological review, 98.68% of placentas of hypertensive mothers hadcytotrophoblastic cell proliferation, but there was also cytotrophoblastic cell proliferation in 19.73% of placentas of normotensive (control) mothers. It means that 80.26% placentas of a normotensive mother and 1.31% placentas of a hypertensive mother do not hadcytotrophoblastic cell proliferation

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Figure 4: (a) Histological slide of hypertensive placenta - Arrow shows cytotrophoblastic cellular proliferation (×40). (b) Histological slide of normotensive placenta - Arrow shows cytotrophoblast (×40)

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Figure 5: In histological examination, 88.15% of placentas of hypertensive mothers had fibrinoid necrosis, but in 28.94% of placentas of normotensive (control) mothers also had fibrinoid necrosis. It means that 71.05% placentas of the normotensive (control) mothers had no fibrinoid necrosis, but 11.84 placentas of the hypertensive mothers had no fibrinoid necrosis

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Figure 6: (a) Histological slide of hypertensive placenta-Arrow shows fibrinoid necrosis (×40). (b) Histological slide of normotensive placenta Arrow shows fibrinoid necrosis (×10)

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Figure 7: The 100% of placentas of hypertensive mothers had endothelial proliferation in comparison to control (normotensive) in histological examination

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Figure 8: (a) Histological slide of hypertensive placenta arrow shows endothelial proliferation (×40). (b) Histological slide of normotensive placenta-Arrow shows endothelium (×40)

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Figure 9: In the histological review, 84.21% of placentas of normotensive mothers had calcified villous spot but also calcified villous spot in 31.57% placenta of normotensive mothers. The 68.42% of normotensive mother's placentas had not calcified villous spot and 15.78% of hypertensive mother's placentas had not calcified villous spot

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Figure 10: (a) Histological slide of hypertensive placenta – arrow shows calcified villous spot (×40). (b) Histological slide of normotensive placenta – Arrow shows calcified villous spot

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  Discussion Top


5% to 8% of all maternal deaths are due to hypertension. Prevalence rate of pregnancy-induced hypertension is 5%–10%. Significant histological changes can be seen in placentas of hypertensive mothers with incidence much higher than the normotensive placentas. In histological review, syncytial knots were seen in all (100%) placentas of hypertensive mothers and in 32.89% placentas of normotensive mothers and no syncytial knots in 67.10% of placentas of normotensive mothers [Table 1] and [Figure 1], [Figure 2]a and [Figure 2]b. According to Genset,[10] there was extreme syncytial knots formation and stromal fibrosis in hypertensive mother's placenta. The syncytial knots and stromal fibrosis are responsible for reducing placental fetal perfusion. The major cause of increased syncytial knots formation was due to disturbance in the hormonal factors that leads to alteration in placental morphology and the effect of this shift in pregnancy-induced hypertension occurs in the mothers and low birth weight fetus is delivered. In extreme pregnancy-induced hypertension, the syncytial knots occur substantially more, i.e., the syncytial knots increase with the severity of hypertension during pregnancy.[11] Similar results were also reported by Majumdar et al.[12] and Rath et al.[13] 98.68% of placentas of hypertensive mothers had cytotrophoblastic cells proliferation, but only 19.73% of placentas of normotensive (control) mothers had it. It means 80.26% placentas of the normotensive mothers and 1.31% placentas of the hypertensive mothers had no cytotrophoblastic cell proliferation [Table 1] and [Figure 3], [Figure 4]a and [Figure 4]b. Cytotrophoblastic cellular proliferation was present more in hypertensive pregnancies.[14] Decreased blood flow occurs to the placenta due to cytotrophoblastic proliferation, resulting in a decreased blood supply to the fetus and subsequently leading to low birth weight of the fetus. Cytotrophoblastic proliferation of cells occurs more in the hypertensive mother's placenta as compared to controls. These placental alterations are directly proportional to illness and incidence of fetal outcome. Das et al.[15] reported similar findings, 88.15% of placentas of hypertensive mothers had fibrinoid necrosis but only 28.94% of placentas of normotensive mothers fibrinoid necrosis as well. It means that 71.05% placentas of normotensive mothers do not have fibrinoid necrosis but only 11.84% of hypertensive mothers were free of fibrinoid necrosis [Table 1] and [Figure 5], [Figure 6]a and [Figure 6]b. Fibrinoid necrosis occurs more in placentas of hypertensive mothers.[15] Endothelial proliferation was seen in all 100% in comparison to controls (normotensive) in histological review [Table 1] and [Figure 7], [Figure 8]a and [Figure 8]b. In other studies, more endothelial proliferation was seen in the hypertensive placentas than in the normotensive placentas. According to Damania et al.,[16] less perfusion occurs in the placenta due to endothelial proliferation, resulting in fetal hypoxia, and eventually fetal death. According to Di Salvo et al.,[17] tissue perfusion decreases due to endothelial proliferation, and ischemia occurs. Similar observations were also found by Pretorius et al.[18] In the histological review, 84.21% of placentas of pregnancy-induced hypertensive mothers had calcified villous spots, but only 31.57% placenta of normotensive mothers. The 68.42% of placentas of a normotensive mother had no villous spots calcified and 15.78% of placentas of a pregnancy-induced hypertensive mother had no villous spots [Table 1] and [Figure 9], [Figure 10]a and [Figure 10]b. Findings of Kofinas et al.[19] were in accordance with the findings of the present study. Qureshi et al.[20] also reported higher incidence of calcification in hypertensive than in normotensive placentas. According to Salmani et al.,[21] underperfussion of tissues occurs in severe pregnancy-induced hypertension. According to the Nahar et al.,[22] syncytial knot, fibrinoid necrosis, and calcified villous spots are more in hypertensive placentas. This was similar to our findings. Gibbins et al.[23] found excessive syncytial knots was present in hypertensive pregnancies. Rajyalakshmi et al.[24] found more syncytial knots, fibrinoid necrosis, and cytotrophoblastic cellular proliferation in hypertensive placentas. Biswa et al.[25] found cytotrophoblastic cells proliferation more in hypertensive placentas. Gore et al.[26] found more syncytial knots, fibrinoid necrosis, calcified villous spots, and cytotrophoblastic cellular proliferation in comparison to control and this was similar to our findings.


  Conclusion Top


Pregnancy-induced hypertension has an adverse effect on the health of fetus through its harmful effects on the placentas. In our study, syncytial knots, cytotrophoblastic cells proliferation, fibrinoid necrosis, endothelial proliferations, and calcified villous spots, these lesions are more present in the hypertensive mother's placentas in comparison to observations of other authors. In severe pregnancy-induced hypertension, underperfusion of tissues occurs. Proper treatment given to the mothers in early stage of pregnancy prevents complications. Thus, our study helps the clinician for early diagnosis and treatment to lower the mortality rates of mothers and fetuses.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Singh V. Textbook of Clinical Embryology. 2nd ed. New Delhi: Elsevier Relx India Pvt. Ltd.; 2017.  Back to cited text no. 1
    
2.
Sadler TW. Langman's Medical Embryology. 14th ed. New Delhi: Wolters Kluwer (India) Pvt. Ltd.; 2018.  Back to cited text no. 2
    
3.
Singh I. Human Embryology. 11th ed. New Delhi: Jaypee Brother Medical Publishers Pvt. Ltd.; 2014.  Back to cited text no. 3
    
4.
Dutta DC. Textbook of Obstetrics. 9th ed. New Delhi: Jaypee Brothers Medical Publishers Pvt. Ltd.; 2018.  Back to cited text no. 4
    
5.
Ahmad M. Study of placental changes in pregnancy induced hypertension. Int J Repord Contracepts Obstet Gynaecol 2013;2:524-7.  Back to cited text no. 5
    
6.
Landesmon R, Douglas RG, Holze E, The bulbar conjuctival vascular bed in toxmemias of pregnancies. Am J Obstet Gynaecol 1954;68:170-2.  Back to cited text no. 6
    
7.
Boyd PA, Scott A. Quantitative structural studies on human placentas associated with preeclampsia, essential hypertension and intrauterine growth retardation. Br J Obstet Gynecol 1985;92:714-21.  Back to cited text no. 7
    
8.
Brown MA. Pregnancy-induced hypertension: Pathogenesis and management. Aust N Z J Med 1991;21:257-60, 262, 264-73.  Back to cited text no. 8
    
9.
Roberts JM, Pearson G, Culter J. Summary of the NHLBI working group on research on hypertension during pregnancy. Hypertension 2003;41:437-45.  Back to cited text no. 9
    
10.
Genest DR. Estimating the time of death in stillborn fetuses: II. Histologic evaluation of the placenta; a study of 71 stillborns. Obstet Gynecol 1992;80:585-92.  Back to cited text no. 10
    
11.
Kurdukar MD, Deshpande NM, Shete SS, Zawar MP. Placenta in PIH. Indian J Pathol Microbiol 2007;50:493-7.  Back to cited text no. 11
[PUBMED]    
12.
Majumdar S, Dasgupta H, Bhattacharya K. A study of placenta in normal and hypertensive pregnancy. J Anat Soc India 2005;54:1-9.  Back to cited text no. 12
    
13.
Rath G, Garg K, Sood M. Insertion of umbilical cord to the placenta in hypertensive mothers. J Anat Soc India 2000;49:149-54.  Back to cited text no. 13
    
14.
Udainia A, Bhagwat SS, Mehta CD. Relation between placental surface area, infarction and fetal distress in pregnancy induced hypertension with its clinical relevance. J Anat Soc India 2004;53:27-30.  Back to cited text no. 14
    
15.
Das B, Dutta S, Chakraborthy P, Nath P. Placental morphology in hypertensive disorders of pregnancy and its correlation with fetal outcome. J Obstet Gynaecol India 1996;46:40-6.  Back to cited text no. 15
    
16.
Damania KR, Salvi VS, Ratnaparki SK. The placenta in hypertensive disorder in pregnancy. J Obstet Gynaecol India 1989;39:28-31.  Back to cited text no. 16
    
17.
Di Salvo DN, Benson CB, Laing FC, Brown DL, Frates MC, Doubilet PM. Sonographic evaluation of the placental cord insertion site. AJR Am J Roentgenol 1998;170:1295-8.  Back to cited text no. 17
    
18.
Pretorius DH, Chau C, Poeltler DM, Mendoza A, Catanzarite VA, Hollenbach KA. Placental cord insertion visualization with prenatal ultrasonography. J Ultrasound Med 1996;15:585-93.  Back to cited text no. 18
    
19.
Kofinas AD, Penry M, Swain M, Hatjis CG. Effect of placental laterality on uterine artery resistance and development of preeclampsia and intrauterine growth retardation. Am J Obstet Gynecol 1989;161:1536-9.  Back to cited text no. 19
    
20.
Qureshi F, Jacques SM, Reyes MP. Placental histopathology in syphilis. Hum Pathol 1993;24:779-84.  Back to cited text no. 20
    
21.
Salmani D, Purushothaman S, Somashekara SC, Gnanagurudasan E, Sumangaladevi K, Harikishan R, et al. Study of structural changes in placenta in pregnancy-induced hypertension. J Nat Sci Biol Med 2014;5:352-5.  Back to cited text no. 21
    
22.
Nahar L, Nahar K, Hossain MI, Yasmin H, Annur BM. Placental changes in pregnancy induced hypertension and its impacts on fetal outcome. Mymensingh Med J 2015;24:9-17.  Back to cited text no. 22
    
23.
Gibbins KJ, Silver RM, Pinar H, Reddy UM, Parker CB, Thorsten V, et al. Stillbirth, hypertensive disorders of pregnancy, and placental pathology. Placenta 2016;43:61-8.  Back to cited text no. 23
    
24.
Rajyalakshmi S, Vani BS, Jijiya Bai P. Placental pathology in different degrees of pregnancy induced hypertension. Trop J Pathol Microbiol 2019;5:988-96.  Back to cited text no. 24
    
25.
Biswa M, Gyanaranjan N, Das SR. Histopathological study of placenta in pregnancy with hypertension in Western Odisha. IOSR J Dent Med Sci 2017;16:100-4.  Back to cited text no. 25
    
26.
Gore CR, Pandey A, Shetty A, et al. A study on histopathological changes in placenta in pre-eclampsia/eclampsia: A case-control study in tertiary care center, Western India. Indian Journal of Pathology and Oncology 2018:5:385-90.  Back to cited text no. 26
    


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