Mohamed Abdel Monem DKHIL, Reda Awadallah SALEH

Structural Changes of Placenta in Preeclamptic Patients: Light and Electron Microscopic Study

Background: Preeclampsia is a disorder that occurs only during pregnancy and the postpartum period and affects both the mother and the unborn baby. It is a rapidly progressive condition characterized by high blood pressure and the presence of protein in the urine. The study was designed to investigate the histological and ultrastructural changes in placentas from pregnancies complicated by preeclampsia. Methods: Paraffin sections from placenta biopsies were prepared for light microscopic examination. For ultrastructural examination, biopsies were prepared and examined by digital scanning electron microscope. Results: Light microscopic examinations showed that the nuclei of syncytiotrophoblast layer were aggregated into clusters in numerous sprouts and in long anastomosing strands. Villous connective tissue core was progressively condensed while the fetal placental capillaries regressed up to complete disappearance. Endothelial degenerative and atheromatous changes were seen in placental stem vessels, also basal decidual arterioles showed endothelial degeneration, progressive fibrosis, and obliteration. By SEM, villous tissues from the preeclamptic cases demonstrated elongated villi with wrinkled surfaces and covered with fibrin-like plaques. Capillary loops in preeclamptic cases were sparse in number and significantly longer compared to the control cases. They exhibited fewer branches and majority of the loops were uncoiled. Conclusions: In placentas complicated by preeclampsia, ischemic damage of placental tissue with maldeveloped terminal villi occurs. These findings are consistent with an increase in fetoplacental vascular impedance where absent end-diastolic flow velocity was demonstrated in umbilical artery before delivery. These findings account for impaired gas and nutrient transfer in this disorder.

Anahtar Kelimeler:

Histology, placenta, preeclamptic patients

Structural Changes of Placenta in Preeclamptic Patients: Light and Electron Microscopic Study

Keywords:

Histology, placenta, preeclamptic patients,

PDF

___

Kaufmann P, Burton G. Anatomy and genesis of the placenta. In: Knobil E., Neill JD, editors. The physiology of reproduction. New York: Raven Press; 1994; 441-483.
Eik-Nes S, Brubakk AO, Ulstein M. Measurement of human fetal blood flow. BMJ 1980; 1: 283-284.
Allaire AD, Ballenger KA, Wells S R, McMahon MJ, Lessey BA. Placental apoptosis in preeclampsia. Obstet Gynecol 2000; 96: 271-276.
Ishihara N, Matsuo H, Murakoshi H, Laoag-Fernandez JB, Samoto T, Maruo T. Increased apoptosis in the syncytiotrophoblast in human term placentas complicated by either preeclampsia or intrauterine growth retardation. Am J Obstet Gynecol 2002; 186: 158-166.
Levy R, Smith SD, Chandler K, Sadovsky Y, Nelson DM. Apoptosis in human cultured trophoblasts is enhanced by hypoxia and diminished by epidermal growth factor. Am J Physiol Cell Physiol. 2000; 278: 982-988.
Hu R, Zhou S, Li X. Altered Bcl-2 and Bax expression is associated with cultured first trimester human cytotrophoblasts apoptosis induced by hypoxia. Life Sci 2006; 79: 351-355.
Benirschke K, Kaufmann P. Pathology of the human placenta.2nd ed. New York: Springer Verlag; 1990.
Moldenhauer JS, Stanek J, Warshak C, Khoury J, Sibai B. The frequency and severity of placental findings in women with preeclampsia are gestational age dependent. Am J Obstet Gynecol 2003; 189: 1173-1177.
Stallmach T, Hebisch G, Orban P, Lu X. Aberrant positioning of trophoblast and lymphocytes in the feto-maternal interface with pre-eclampsia. Virchows Arch 1999; 434: 207-211.
King A, Burrows TD, Hiby SE, Bowen JM, Joseph S, Verma S et al. Surface expression of HLA-C antigen by human extravillous trophoblast. Placenta 2000; 21: 376-87.
Dey S K, Lim H, Das SK, Reese J, Paria BC, Daikoku T et al. Molecular cues to implantation. Endocr Rev 2004; 25: 341-373.
Nikitenko LL, Blucher N, Fox SB, Bicknell R, Smith DM, Rees MC. Adrenomedullin and CGRP interact with endogenous calcitonin- receptor-like receptor in endothelial cells and induce its desensitisation by different mechanisms. J Cell Sci 2006; 119: 910-922.