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Table of Contents
ORIGINAL ARTICLE
Year : 2020  |  Volume : 69  |  Issue : 3  |  Page : 166-170

A study of microscopic changes in the placenta in gestational diabetes mellitus


1 Department of Anatomy Santosh Deemed to be University, Ghaziabad NCR, Delhi, India
2 Department of Pathology, GMC, Azamgarh, Uttar Pradesh, India

Date of Submission13-Jul-2020
Date of Acceptance02-Sep-2020
Date of Web Publication30-Sep-2020

Correspondence Address:
Mr. Kumud Ranjan
Department of Anatomy, Santosh Deemed to be University, Ghaziabad, NCR, Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JASI.JASI_133_20

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  Abstract 


Introduction: Gestational diabetes mellitus is a complication connected with pregnancy defined as any degree of glucose intolerance that appears during pregnancy with normal values before and usually after the pregnancy. We investigated histological changes of the gestational diabetic placenta and non-diabetic placenta. Research work accomplished in the department of Anatomy, government medical college and superfacility hospital Azamgarh. Placenta collected from the labour room/operation theatre of the department of Obstetrics and Gynecology, government medical college and superficiality hospital, Azamgarh. Material and Methods: Sixty-two freshly delivered placentas were collected – 31 placentas from diabetic mother and 31 placentas from non-diabetic mother (control group). All parturient were aged between 20 to 44 years. This placenta measured on a weighing machine graduated in grams. An approximately 5mm piece of the diabetic placenta was taken and processed for histological examination. Results: Microscopic examination explained dilated blood vessels, subtrophoblastic basement membrane thickness and chorangiosis present in all gestational diabetic placenta. Vessels thrombosis present in 83.87 per cent of the gestational diabetic placenta. Nucleated RBCs. were present in 93.54 per cent of the gestational diabetic placenta. Discussion and Conclusion: Gestational diabetes mellitus induces significant changes in the placenta, both gross and histologic. Effective glycemic regulation is better options for reducing anomalies that cause gestational diabetes. We find dilated blood vessels and necrosis in 100 percent of gestational diabetic placenta and 9.60 percent of nondiabetic placenta. The thickness of the subtrophoblastic basement membrane was present in 100% of the gestational diabetic placenta and 16.12% of the non-diabetic placenta. Vessel thrombosis occurs in 83.87% of gestational diabetic placenta, and 12.90% of non-diabetic placenta. In 93.54 percent of gestational diabetic placenta and 32.25 percent of non-diabetic placenta, nucleated RBC occurs.

Keywords: Chorangiosis, gestational diabetes mellitus, microscopic, placenta


How to cite this article:
Singh V, Ranjan K, Tewarson S L. A study of microscopic changes in the placenta in gestational diabetes mellitus. J Anat Soc India 2020;69:166-70

How to cite this URL:
Singh V, Ranjan K, Tewarson S L. A study of microscopic changes in the placenta in gestational diabetes mellitus. J Anat Soc India [serial online] 2020 [cited 2020 Oct 19];69:166-70. Available from: https://www.jasi.org.in/text.asp?2020/69/3/166/296907




  Introduction Top


The placenta is a fetomaternal organ. It consists of two components: (a) fetal component and (b) maternal component. Fetal component develops from chorion frondosum and maternal component develops from decidua basalis. This is a complex organ of short life span. This is responsible for the transfer of nutrients and waste products between fetal and maternal circulations. The placenta must integrate signals from fetus and mother in an effort to match fetal demand with maternal nutrient.[1],[2] It actually plays an important role in fetal growth and development. Maternal disease that results in abnormal growth and development of the placenta during early pregnancy and mid-pregnancy is directly associated with decreased fetal growth and development in the late pregnancy.[3] Gestational diabetes mellitus (GDM) is a complication connected with pregnancy defined as any degree of glucose intolerance that appears during pregnancy with normal values before and usually after the pregnancy. Diabetes mellitus in pregnancy is known as GDM because woman is nondiabetic before pregnancy. Any degree of glucose intolerance commencement during pregnancy is known as GDM.[4],[5] GDM represents nearly 90% of all pregnancies complicated by diabetes mellitus.[6] It affects 2%–5% of all pregnancies.[7] GDM during pregnancy produces varieties of placental abnormalities such as distension of basal membrane of trophoblast proliferation of cells of the endothelium and decreased vascular surfaces of terminal villi. These changes depend upon the quality of glycemic control achieved during the critical period of the placental development.[1] An alteration of the placental function due to uncontrolled GDM results in disturbances of the growth and development of fetus macrosomia, congenital malformations, and intrauterine growth retardation.[8],[9]
Figure 1: Dilated blood vessel and necrosis present in 100% of the gestational diabetic placenta and 9.60% of the nondiabetic placenta

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Figure 2: Subtrophoblastic basement membrane thickness present in 100%of the gestational diabetic placenta & 16.12% of the nondiabetic placenta

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Figure 3: Vessels thrombosis present in 83.87% of the gestational diabetic placenta and 12.90% of the non-diabetic placenta

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Figure 4: Nucleated RBCs present in 93.54% of the gestational diabetic placenta and 32.25% of the non-diabetic placenta.

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Figure 5: Chorangiosis present in 100% of the gestational diabetic placenta and 3.22% of the non- diabetic placenta

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Figure 6: (a) Fetal surface of the gestational diabetic placenta. (b) Maternal surface of the gestational diabetic placenta

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  Material and Methods Top


Sixty-two freshly delivered placentas were collected – 31 placentas from the diabetic mother and 31 placentas from the nondiabetic mother (control group). All parturient were aged between 20 and 44 years. Research work was accomplished in the Department of Anatomy, Government Medical College and Superfacility Hospital, Azamgarh. Placenta was collected from the labor room/operation theater of the Department of Obstetrics and Gynaecology, Government Medical College and Superfaciality Hospital, Azamgarh. There were no differences according to race culture or environment. The placenta was obtained either from the vaginal route or cesarean section. After washed with the running tap water and dried with the blotting paper, the collected placenta was weighed from the weighing machine graduated in the grams. We took morphometric and macroscopic examination; after that, the placenta was kept in 10% formalin for 24 h for fixation. After 24 h, this fixed tissue of the placenta passes through a series of procedure from dehydration and clearing to wax impregnation before being sectioned from the microtome. Time took for processing was 24 h, and using microtome instrument, tissues were sectioned at 5 μm. APES-coated glass slide was used for sectioned tissues. The slide was placed on the hot metallic plate at 60° for 30 min before staining. After that, hematoxylin and eosin staining was done. Slides were prepared and they are passed through xylene-1 for 10 min and xylene-2 for the next 10 min. After that, slides were placed into 100%, 95%, 80%, and 70% alcohol for 5 min each to dehydrate the slides. Slides were placed into the Harris hematoxylin solution for 5–10 min and rehydrate with water thereafter. Again, tissues were washed with tap water and then placed into 1% eosin for approximately 1–2 min. Finally, tissues were dehydrated by passing through increasing concentration of alcohol and cleared in the solution of xylene for 5 min. Prepared slides were mounted in DPX and covered with the cover slip. Through binocular light microscope, slides were examined at ×10, ×40, and ×100.
Figure 7: (a) Fetal surface of the nondiabetic placenta. (b) Maternal surface of the nondiabetic placenta

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Figure 8: (a) The histological slide of the gestational diabetic placenta - Arrow showing dilated blood vessel and necrosis, ×100. (b) The histological slide of the nondiabetic placenta - Arrow showing blood vessels, ×40

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Figure 9: (a) The histological slide of the gestational diabetic placenta - Arrow showing subtrophoblastic basement membrane thickness, ×40. (b) The histological slide of the nondiabetic placenta - Arrow showing basement membrane of the trophoblast, ×40

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Figure 10: (a) The histological slide of the gestational diabetic placenta - Arrow showing vessel thrombosis, ×40. (b) The histological slide of the nondiabetic placenta - Arrow showing blood vessel without thrombosis, ×40

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Figure 11: (a) The histological slide of the gestational diabetic placenta - Arrow showing nucleated red blood cell, ×40. (b) The histological slide of the nondiabetic placenta - Arrow showing nonnucleated red blood cell, ×40

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Figure 12: (a) The histological slide of the gestational diabetic placenta - Arrow showing chorangiosis in the chorionic villi, ×40. (b) The histological slide of the nondiabetic placenta - Arrow showing fetal blood vessels in chorionic villi, ×40

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  Results Top


Dilated blood vessel and necrosis present in 100% of the gestational diabetic placenta and 9.60% of the nondiabetic placenta shows in [Table 1].
Table 1: Presents a comparison of the diabetic (gestational diabetes) and non-diabetic placenta histological changes

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Subtrophoblastic basement membrane thickness presents in 100% of the gestational diabetic placenta and 16.12% of the nondiabetic placenta.

Vessels thrombosis presents in 83.87% of the gestational diabetic placenta and 12.90% of the nondiabetic placenta shows in [Table 1].

Nucleated red blood cell (RBCs) present in 93.54% of the gestational diabetic placenta and 32.25% of the nondiabetic placenta shows in [Table 1].

Chorangiosis presents in 100% of the gestational diabetic placenta and 3.22% of the nondiabetic placenta shows in [Table 1].

Hence, in our study, chorangiosis subtrophoblastic basement membrane thickness and dilated blood vessels and necrosis present in 100% of the gestational diabetic placenta [Table 1].


  Discussion Top


GDM is a complication connected with pregnancy defined as any degree of glucose intolerance that appears during pregnancy with normal values before and usually after the pregnancy. Diabetes mellitus in pregnancy is known as GDM because woman is nondiabetic before pregnancy. Any degree of glucose intolerance commencement during pregnancy is known as GDM.[4],[5] The disturbance in the adaptation in the metabolism of carbohydrate during the pregnancy causes GDM. The poorly controlled gestational diabetic placenta shows villous edema and marked fibrin thrombi in the syncytiotrophoblast. Brudenell and Doddridge [10] suggested that villous edema is common in the diabetic placenta. Shen-Schwarz et al.[11] observed similar findings. The diabetes mellitus influences organ system such as cardiovascular excretory and central nervous system.[12] Diabetes mellitus during pregnancy affects both mother and fetuses.[13] When metabolic control is good, the mortality rate reduces in the normal population.[14] The macrosomia and large babies are common in GDM.[15] The villous immaturity are most common in the GDM.[16] We observed that the gestational diabetic placenta shows dilated blood vessel and necrosis in 100% of cases. However, the nondiabetic placenta shows dilated blood vessel and necrosis only in 9.60% of the placenta. According to the study of Jauniaux and Burton (2006),[17] GDM causes dilatation of blood vessels and necrosis of the blood vessels. Subtrophoblastic basement membrane thickness increases in the placenta due to GDM. We observed that 100% of the gestational diabetic placenta has subtrophoblastic basement membrane thickness and 16.12% of the nondiabetic placenta has subtrophoblastic basement membrane thickness [Table 1]. According to Hirota [18] and Okudaira et al.,[19] the poorly controlled GDM thickness of the basement membrane of syncytiotrophoblast increases. The basement membrane thickness in the gestational diabetic placenta is due to the deposition of mucopolysaccharide. We observed that thrombosis presents 83.87% of the gestational diabetic placenta and 12.90% of the nondiabetic placenta shows in [Table 1]. We observed that 93.54% of the gestational diabetic placenta has nucleated RBC and 32.25% of the nondiabetic placenta has nucleated RBC [Table 1]. According to Daskalakis et al.,[20] nucleated RBC presents more in the gestational diabetic placenta. We observed that chorangiosis presents in 100% of the gestational diabetic placenta and 3.22% of the nondiabetic placenta [Table 1]. Verma et al.[21] observed chorangiosis seen more in the gestational diabetic placenta as compared to the control. The GDM causes reduced flow of blood through the intervillous space. This reduced supply of the blood is due to vascular compromise.[2] The angiogenesis occurs due to uncontrolled GDM. 25% surfaces of the villi were taken up by the capillary bed in the gestational diabetic placenta and 50% surfaces of the villi were taken up by the capillary bed in the nondiabetic placenta. Maternal hyperglycemia may impact on the vascular permeability of the placenta. Hyperglycemia has shown to have a direct effect, acting as a proconstrictor,[22] procoagulator,[23] proinflammatory,[24] proangiogenic [25] and propermeability agent.[26] According to Lal et al.,[27] the gestational diabetic placenta showed degenerative changes (dilated blood vessels and necrosis), vessel thrombosis, subtrophoblastic basement membrane thickness, and presence of nucleated RBC. This observation supports our findings. According to Verma et al.,[28] finding of the histological examination such as fibrinoid necrosis, villous edema, villous fibrosis, and chorangiosis more often present in the gestational diabetic placenta compared with the control. This finding supports our findings. Hence, in our study, chorangiosis, subtrophoblastic basement membrane thickness, and dilated blood vessels and necrosis present in 100% of the gestational diabetic placenta [Table 1].


  Conclusion Top


Diabetes mellitus causes profound gross as well as histological changes in the placenta. The good glycemic control is better options for reducing diabetes-induced abnormalities. In our research work, we found dilated blood vessel and necrosis in 100% of the gestational diabetic placenta and 9.60% of the nondiabetic placenta [Table 1]. Subtrophoblastic basement membrane thickness present in 100% of the gestational diabetic placenta and 16.12% of the nondiabetic placenta [Table 1]. Vessels thrombosis presents in 83.87% of the gestational diabetic placenta and 12.90% of the nondiabetic placenta [Table 1]. Nucleated RBC presents in 93.54% of the gestational diabetic placenta and 32.25% of the nondiabetic placenta. Hence, in our study, chorangiosis, subtrophoblastic basement membrane thickness, and dilated blood vessels and necrosis present in 100% of the gestational diabetic placenta.

Ethical approval

The study was approved by the institutional ethics committee.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12]
 
 
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  [Table 1]



 

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