HISTOMORPHOLOGICAL AND MORPHOMETRICAL CHANGES OF PLACENTAL TERMINAL VILLI OF NORMOTENSIVE AND HYPERTENSIVE MOTHERS

L Madhu; S L Karthavya; B G Lepakshi

doi:10.22270/ijmspr.v1i3.8

Authors

L Madhu Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India
S L Karthavya Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India
B G Lepakshi Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

DOI:

https://doi.org/10.22270/ijmspr.v1i3.8

Keywords:

Histology, Hypertension, Morphometry, Placenta, Preeclampsia, Terminal villi

Abstract

Background & Objectives: Placental examination has clinical value in preeclampsia (PE) and IUGR. The luminal diameter of the uterine spiral arterioles in women with PE is narrowed leading to placental ischemia thus causing fetal hypoxia and pathological changes in placenta. The main objective of the present study is to compare morphological and histomorphometrical changes in placentas of preeclamptic and normotensive mothers. Methods: 50 placentas from both vaginal and LSCS delivery were collected at Dept. of OBG in a tertiary care center, half of them from normotensive pregnancies and the rest from preeclamptic mothers. An inclusion criterion for control was normal blood pressure and no proteinuria. Exclusion criteria for both control and study group was DM, obesity, severe anemia or any systemic disorders. Placental thickness, weight, diameter and surface area were recorded. Histopathological sections stained with H&E were observed for surface area and diameter of TV. Results: The mean placental weight in PE was 430 g. The placental diameter was decreased in PE (16 cm) compared to controls (19 cm). Neonatal weight followed the same trend. Histologically, the changes in the TV and blood vessels was significant; there was decrease in the diameter of villi in PE cases(0.01 μm) when compared to controls (0.05 μm). There was significant decrease in the diameter of blood vessels in PE (0.0049 μm) than in controls (0.01 mm). Conclusion: This study has revealed that there are significant changes in the placenta in cases of PE both morphologically and histologically. There is also a need for further studies to prove the molecular and genetic factors involved in preeclampsia.

Author Biographies

L Madhu , Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

S L Karthavya , Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

B G Lepakshi , Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

Department of Obstetrics and Gynecology, Shimoga Institute of Medical Sciences, Shimoga-577201, Karnataka, India

References

Abitbol M M (1982), “Simplified technique to produce toxemia in the rat: considerations on cause of toxemia”, Clin. Exp. Hypertens., Vol. B1, pp. 93-103 [PubMed:7184666]

ACOG (2002), “American College of Obstetricians and Gynecologists practice bulletin. Diagnosis and management of preeclampsia and eclampsia”, Int. J. Gynaecol. Obstet., Vol. 77, pp. 67-75 [PubMed: 12094777].

Basso O, Christensen K and Olsen J (2001), “Higher risk of preeclampsia after change of partner. An effect of longer interpregnancy intervals?”, Epidemiology, Vol. 12, pp. 624-629 [PubMed:11679788]

Bdolah Y, Karumanchi S A and Sachs B P (2005), “Recent advances in understanding of preeclampsia”, Croat Med J., Vol. 46, pp. 728-36.

Cartwright J E, Fraser R, Leslie K, Wallace A E, James J L (2010), “Remodeling at the maternal- fetal interface: relevance to human pregnancy disorders”, Reproduction, Vol. 140, pp. 803-13.

Duckitt K and Harrington D (2005), “Risk factors for preeclampsia at antenatal booking: Systematic review of controlled studies”, BMJ, Vol. 330, pp. 565. [PMCID:PMC554027] [PubMed:15743856]

Kaufmann P, Black S and Huppertz B (2003), “Endovascular trophoblast invasion: implications for the pathogenesis of intrauterine growth retardation and preeclampsia”, Biol. Reprod., Vol. 69, pp. 1-7 [PubMed: 12620937].

Hunka Piller N M and Fisher S J (2008), Chapter 12, “Placental remodeling of the uterine vasculature”, Methods Enzymol., Vol. 445, pp. 281-302 [PMCID: PMC2857511] [PubMed : 19022064]

Kanasaki K, Palmsten K, Sugimoto H, Ahmad S, Hamano Y, Xie L, Parry S, Augustin H G, Gattone V H, Folkman J et al. (2008), “Deficiency in catechol-O methyltransferase and 2-methoxyestradiol is associated with preeclampsia”, Nature, Vol. 453, pp. 1117-1121 [PubMed:18469803]

Khong T Y, De Wolf F, Robertson W B, Brosens eye (1986). “Inadequate maternal vascular response to placentations in pregnancies complicated by preeclampsia and by small-for-gestational age infants”, Br. J. Obstet. Gynaecol., Vol. 93, pp. 1049-105 [PubMed: 3790464]

Kupferminc M J, Peaceman A M, Wigton T R, Rehnberg K A, Socol M L (1994), “Tumor necrosis factor-alpha is elevated in plasma and amniotic fluid of patients with severe preeclampsia”, Am. J. Obstet. Gynaecol., Vol. 170, pp. 1752-1757; discussion 1757- 1759. [PubMed:8203436]

Levine R J, Maynard S E, Qian C, Lim K H, England L J, Yu K F, Schisterman E F, Thadhani R, Sachs B P, Epstein F H et al. (2004), “Circulating angiogenic factors and the risk of preeclampsia”, N. Engl. J. Med., Vol. 350, pp. 672-683 [PubMed: 14764923].

Makris A, Thornton C, Thompson J, Thomson S, Martin R, Ogle R, Waugh R, McKenzie P, Kirwan P, Hennessy A (2007), “Uteroplacental ischemia results in proteinuric hypertension and elevated sFLT 1”, Kidney Int., Vol. 71, pp. 977-984 [PubMed:17377512]

Makris A, Xu B, Yu B, Thornton C, Hennessy A (2006), “Placental deficiency of interleukin 10 (IL-10). In preeclampsia and its relationship to an IL10 promoter polymorphism”, Placenta, Vol. 27, pp. 445- 451 [PubMed: 16026832]

Mardi K and Sharma J (2003), “Histopathological evaluation of placentas in IUGR pregnancies”, Indian J Pathol Microbiol., Vol. 46, pp. 551- 4.

Myatt L (2002), “Role of placenta in preeclampsia”, Endocrine, Vol. 19, pp. 103- 11.

Roberts J M and Hubel C A (2009), “The two stage model of preeclampsia; variations on the theme”, Placenta, 30 Suppl. A, S32-S37 [PMCID: PMC2680383] [PubMed:19070896]

Sankar K D, Bhanu P S, Kiran S, Ramakrishna B A, Shanthi V (2012), “Vasculosyncytial membrane in relation to syncytial knots complicates the placenta in preeclampsia: a histomorphometrical study”, Anat Cell Biol., Vol. 45, pp. 86-91.

Sankar Devi K, Sharmila Bhanu P, Ramalingam K, Sujatha Kiran B A and Ramakrishna (2013), “Histomorphological and morphometrical changes of placental terminal villi of normotensive and preeclamptic mothers”, Anat Cell Biol., Vol. 46, pp. 285-290.

Tal R, Shaish A, Barshack I, Polak-Charcon S, Afek A, Volkov A, Feldman B, Avivi C, Harats D (2010), “Effects of hypoxia indivisible factor 1alpha overexpression in pregnant mice: possible implications for preeclampsia and intrauterine growth restriction”, Am. J. Pathol., Vol. 177, pp. 2950-2962. [PMCID:PMC2993274] [PubMed:20952590]

Vogel P (2005), “The current molecular phylogeny of eutherian mammals challenges previous interpretations of placental evolutions”, Placenta, Vol. 26, pp. 591-6.