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2023, Volume 39, Number 1, Page(s) 001-008
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DOI: 10.5146/tjpath.2021.01563 |
Proportionality of Clinical Outcome and Placental Changes to the Increasing Severity of Maternal Hypertension- An Observational Study |
Priyadharshini BARGUNAM, Parvathi JIGALUR, Purushotham REDDY |
Department of Pathology, Karnataka Institute of Medical Sciences, KARNATAKA, INDIA |
Keywords: Placental Infarct, Maternal Hypertension, Preeclampsia, Eclampsia, IUGR, Fetal death, Increased Syncytial knots, Hypermature Villi |
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Objective: Preeclampsia and eclampsia remain the major causes of maternal and perinatal mortality and morbidity worldwide, causing 12–15%
of direct maternal deaths. Although preeclampsia and related hypertensive disorders of pregnancy continue to affect 8% of all pregnancies,
the incidence of preeclampsia has increased 40% in recent years. This study was carried out to analyse the different placental lesions and fetal
outcome in different grades of maternal hypertension and to see if there is a linear relationship of the same.
Material and Method: A total of 539 placenta specimens received at the department of Pathology from October 2017 to March 2019 were
collected after obtaining informed consent. Of the 539 placentas, 87 hypertensive cases were graded and grouped according to the severity as
gestational hypertension, mild preeclampsia, severe preeclampsia, eclampsia, and chronic hypertension and compared with 88 normotensive
cases. The gross and microscopic findings were tabulated and analysed using the Statistical Package for the Social Sciences (SPSS) software.
Results: Incidence of fetal death and growth restriction increased with increasing grade of maternal hypertension (p= 0.001). Abnormal shape
of placenta (p= 0.034) and abnormal umbilical cord insertion (p= 0.028) were seen significantly more in the hypertensive group than in the
normotensive group. Infarct and abnormal vasculo-syncytial membrane (p< 0.05) and abnormal villous maturation (p= 0. 039) were significantly
increased in the hypertensive group than the normotensive group.
Conclusion: The incidence of adverse fetal outcome and placental changes suggestive of feto-maternal malperfusions shows a proportional trend
with the increasing grade of maternal hypertension. |
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Preeclampsia and eclampsia remain the major causes of
maternal and perinatal mortality and morbidity worldwide,
causing 12–15% of direct maternal deaths 1,2. Although
preeclampsia and related hypertensive disorders of
pregnancy continue to affect 8% of all pregnancies, the
incidence of preeclampsia has seen a 40% increase in recent
years 3. Placental maternal and fetal vascular malperfusion
lesions are independently associated with increased risk
for preeclampsia recurrence 4. Hence, unlike placental
examination in other cases wherein it’s just an autopsy
post exposure, detailed examination of the placenta
and documentation of the placental lesions in maternal
hypertension can provide valuable data that can prevent
and predict the same in future pregnancies. This study was
carried out to analyse the various placental lesions and fetal
outcome in different grades of maternal hypertension and
to see if there is a linear relationship of the same. |
Top
Abstract
Introduction
Methods
Results
Disscussion
Conclusion
References
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All placenta specimens received at the department of
Pathology from October 2017 to March 2019 were collected
after obtaining informed consent. All the cases with
maternal hypertension, irrespective of the gestational age
and fetal outcome were included in this study. Unbooked
cases and cases without clinical history and imaging
findings were excluded. Out of the 539 cases included in
this study, 87 cases had a maternal history of hypertension.
These placentas were compared with 88 other normotensive
placentas grossly and microscopically and the results were
analysed for statistical significance. The 87 hypertensive
cases were graded and grouped according to the severity
as gestational hypertension, mild preeclampsia, severe
preeclampsia, eclampsia, and chronic hypertension.
The collected placenta specimens were preserved in 10%
formalin immediately after delivery. Intact specimen were
subjected to thorough gross examination for the measurement of weight, diameter and thickness and cut open by
loafing it according to Amsterdam guidelines 5. After
adequate fixation over a period of 24-48 hours, representative
bits were taken for microscopic examination, processed
and stained with haematoxylin and eosin, and studied. Special
stains were used whenever required.
Parenchyma were examined for villitis, calcification, fibrin
deposition (grading used), acute or chronic infarct, abnormal
maturation, villous edema, fetal vessel thrombosis,
endarteritis of stem villi, crowding and the status of the
vasculo-syncytial membrane. Syncytial knots were counted
in 100 tertiary villi and compared with the standards.
Umbilical cords were examined for signs of infection and
umbilical artery thrombosis. Membranes were examined
for signs of infection and amniotic fluid irritation. The
results were statistically analysed using Statistical Package
for the Social Sciences (SPSS) version 21. |
Top
Abstract
Introduction
Methods
Results
Disscussion
Conclusion
References
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Effects on Fetal Outcome
There was a trend observed in the study, and showed
increased adverse fetal outcome such as fetal death and
growth restriction with increasing grade of maternal
hypertension, which was found to be statistically significant (p= 0.001, wherein p stands for probability value) as shown
in Figure 1, 2, and Table I.
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Figure 1: Increased percentage of fetal death with increasing
grade of maternal hypertension. |
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Figure 2: Trend of growth restriction with increasing grade of
hypertension. |
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Table I: Effects of maternal hypertension on placentae and fetal outcome. |
Twelve (33.3%) cases of gestational hypertension, 6 (50%)
cases of the mild preeclampsia group, 17 (73.9%) cases
of severe preeclampsia, 7 (87.5%) cases of the eclampsia
group, and 7 (87.5%) cases of chronic hypertension resulted
in preterm delivery of the fetuses, further adding to the fetal
complication (p= 0.0001).
Gross Placental Changes
Abnormal shape of the placenta was seen more commonly
in the hypertensive group than in the normotensive
group, which was found to be statistically significant (p=
0.034). Abnormal shape was seen the most in gestational
hypertension in 6 (37.5%) cases followed by severe
preeclampsia in 5 (31.3%) cases. Abnormal umbilical cord
insertion was significantly increased in the hypertensive
group compared to the normotensive group (p= 0.028).
Figure 3-6 show various gross changes in the placentas of
the hypertensive group.
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Figure 3: Showing placenta of 37-week-old intrauterine dead
(IUD) fetus, with maternal history of severe preeclampsia, showing
large areas of chronic infarct and an area of acute parenchymal
thrombus, probably because of abruption. The umbilical cord was
marginally inserted and microscopy revealed the thrombus with
increased syncytial knots and chorioamnionitis. |
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Figure 4: Showing placenta of 39-week IUD fetus with maternal
history of gestational hypertension, showing multiple infarcts. |
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Figure 5: Showing placenta of a 29-week IUD fetus, with maternal
history of eclampsia and Hemolysis, Elevated Liver enzymes,
and Low Platelet count (HELLP) Syndrome, showing various
stages of infarct- Acute and Remote. The fetus showed features
of gross intra-uterine growth restriction. The umbilical cord was
hypocoiled. Microscopy revealed infarct, increased syncytial
knots and poor vasculo-syncytial membrane. |
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Figure 6: Showing cut section of placenta and en bloc 32-
week dead fetus, with maternal history of eclampsia and severe
anaemia. Placenta shows a parenchymal thrombus progressing
to chronic infarct. Microscopy confirmed the gross placental
changes. The en bloc fetus shows an absent left lung, cardiomegaly,
splenomegaly, and hypoplastic liver. The cause of death here is
multiple congenital anomalies and not the placental changes due
to hypertension. |
Microscopic Changes
Infarct and abnormal vasculo-syncytial membrane were
seen increasing significantly with increasing grade of hypertension (p< 0.05), as shown in Figure 7, 8, and Table
I. Abnormal villous maturation was increased in the
hypertensive group than the normotensive group (p= 0.
039). Figures 9A-D and 10A-F show various microscopic
changes in the placentas of the hypertensive group.
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Figure 8: Syncytial knots and vasculo-syncytial membrane status
in increasing grades of maternal hypertension. |
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Figure 9: Showing microscopic images of a case of antepartum eclampsia, A) Obliterated and spasmodic blood vessels in a stem villus
(100x magnification), B) Acute atherosis of blood vessels with infiltration by foamy cells (300x), C) Congested blood vessels and
haemorrhage with increased syncytial knots (400x), D) Crowded and congested villi with increased syncytial knots (10x). |
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Figure 10: Showing microscopic images of a case of severe preeclampsia diagnosed at 26 week of gestation. A) Crowded villi with
increased syncytial knots and perivillous fibrin (40x), B) Increased syncytial knots (400x), C) Area of infarct showing ghost villi as
compared with the surrounding normal villi (10x), D) Ghost villi (100x), E) Obliterated vessels (40x), F) Acute atherosis with infiltration
by foamy cells (400x). |
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Top
Abstract
Introduction
Methods
Results
Disscussion
Conclusion
References
|
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In this study, 87 placentas with a maternal history of
hypertension were compared with 88 other normotensive placentas grossly and microscopically and the results
were analysed. The 87 hypertensive cases were graded
and grouped according to the severity as gestational
hypertension, mild preeclampsia, severe preeclampsia, and
eclampsia according to American College of Obstetricians
and Gynecologists (ACOG) Guidelines and compared with
chronic hypertensive and normotensive cases.
Hypertension was classified and graded as follows as per
the ACOG guidelines: 6
• Gestational Hypertension: Blood pressure >140/90 mm
Hg (millimetres of mercury) presenting after 20 weeks
of pregnancy without significant proteinuria.
• Preeclampsia: Blood pressure >140/90 mmHg presenting
after 20 weeks of pregnancy with significant proteinuria
(>30 mg/ml (milligrams/millilitre), or >300
mg/day or at least 1g/L (grams/litre) [2+] on dipstick
testing).
• Severe Preeclampsia: Blood pressure >160/110 mm
Hg presenting after 20 weeks of pregnancy with
significant proteinuria (>30 mg/ml, or >300 mg/day or
at least 1g/L [2+] on dipstick testing) with symptomatic
manifestation.
• Eclampsia: Eclampsia was defined as the presence
of new-onset grand mal seizures in a woman with
preeclampsia. Eclampsia can occur before, during or
after labour.
Chronic hypertension is high blood pressure that either
precedes pregnancy, or is diagnosed within the first 20
weeks of pregnancy, or does not resolve by the 12-week
postpartum check-up. Two categories of severity are recognized: mild (up to 179 mmHg systolic and 109 mmHg) and
severe (≥180 systolic or 110 diastolic). Chronic hypertension
complicates about 5% of all pregnancies, and prevalence
rates are increasing due to delayed childbearing 7.
Although the exact pathogenesis is unknown, inadequate
trophoblast invasion leading to incomplete remodelling
of the uterine spiral arteries is considered to be a primary
cause of placental ischemia 8. Thus the poorly perfused
and hypoxic placenta is thought to synthesize and release
increased amounts of vasoactive factors such as soluble
fms-like tyrosine kinase-1 (sFlt-1), cytokines, and possibly
the angiotensin II (ANG II) type 1 receptor autoantibodies
(AT1-AA) and these are thought to induce widespread
activation/dysfunction of the maternal endothelium in the
vessels of the kidney and other organs that ultimately results
in hypertension 8,9,10. It is postulated that the ischemic
placenta contributes to endothelial cell dysfunction in
the maternal vasculature by inducing an alteration in the
balance of circulating levels of angiogenic/antiangiogenic
factors such as vascular endothelial growth factor (VEGF),
placental growth factor (PlGF), and sFlt-1 11,12, though
sFlt-1 levels play a key role in initiating the symptoms of
preeclampsia 11,13.
Classic pathologic findings in the placenta associated with
hypertensive disease during pregnancy include lesions of
uteroplacental malperfusion such as decidual vasculopathy,
placental infarctions, ischemic changes (such as increased
syncytial knots, villous agglutination, accelerated villous
maturation, and villous hypovascularity), increased
perivillous fibrin, and chronic deciduitis 14,15,16.
A recent meta-analysis done to calculate the recurrence rate
of hypertensive disorder of pregnancy concluded that the
recurrence rate in the subsequent pregnancy was 20.7% and
the recurrence rate was 13.8% specifically for preeclampsia
17, reiterating the need for placental examination in all
cases of maternal hypertension.
There was a trend observed in this study, and showed
increased adverse fetal outcome such as fetal death and
growth restriction with increasing grade of maternal
hypertension. This is in comparison with the study done
by Navbir. 18.
The placental weight is a surrogate for placental function
19, and the feto-placental weight ratio has been suggested
as a possible indicator of adequacy of placental reserve
capacity in fetal growth restriction (FGR) 20. Kher and
Zawar and several other studies elsewhere 21,22 have
reported a significant reduction in the feto-placental weight
ratio. Fox and Sebire 23 explained that this decreased
feto-placental weight ratio is because of a compensatory
hypertrophy of the placenta under the influence of the
unfavourable maternal environment. In our study, the
feto-placental weight ratio was not calculated because
we couldn’t weigh placentas without fixation errors. The
Amsterdam Consensus Placental Sampling guidelines
state that the placenta should be weighed after trimming
the extra placental membranes and umbilical cord, and
notation of whether the placenta was fresh or fixed when
measured and should be compared with contemporary
placental weight standards derived from the respective local
or similar population 5. Fixation of the placenta will affect
its weight, with an increase of 3% to 6% 24. Few samples
were received from remote parts of Karnataka, which had
been preserved in formalin for days before they reached
our department. That caused considerable variation in the
weight, causing lack of uniformity, which is a drawback of
this study.
Preterm delivery is a leading cause of perinatal morbidity
and mortality and a major cost burden to the health care
system. In our study, 12 (33.3%) cases of gestational
hypertension, 6 (50%) cases of mild preeclampsia group,
17 (73.9%) cases of severe preeclampsia, 7 (87.5%) cases of eclampsia group, and 7 (87.5%) cases of chronic
hypertension resulted in preterm delivery of the fetuses,
further adding to the fetal complication (p= 0.0001).
Abnormal shape of placenta was seen more in the
hypertensive group than in the normotensive group,
which was found to be statistically significant (p= 0.034).
Abnormal shape was seen most in gestational hypertension
in 6 (37.5%) cases followed by severe preeclampsia in 5
(31.3%) cases. Abnormal umbilical cord insertion was
significantly increased in the hypertensive group than in
the normotensive group (p= 0.028).
Infarct and abnormal vasculo-syncytial membrane were
seen to increase significantly with increasing grade of
hypertension (p< 0.05), as shown in Figure 7, 8 and Table
I. Ezeigwe et al. concluded that in preeclampsia/ eclampsia
the degree of placental involvement by infarction was
inversely proportional to fetal birth weight 25.
In our study, abnormal villous maturation was seen to
increase more in the hypertensive group than in the
normotensive group (p= 0. 039). Ruiz-Quiñonez et al
26 concluded that the Placenta Maturity Index {PMI=
number of vasculo-syncytial membranes (VSM) in 1
mm2 divided by VSM thickness (mm)} was increased in
preeclampsia, but not in gestational hypertension. Placental
hypermaturity was also associated with the diagnosis of
Small for Gestational Age (SGA) in newborns.
A retrospective case–control study conducted by Devisme
et al. 27 found that infarcts (65.9% versus 13.2%; p< 0.001)
and placental abruption (p< 0.001) were most frequent
among women with preeclampsia. Increased syncytial
knots (90% versus 9%; p< 0.001), infarcts, basal decidual
vasculopathy (51% vs. 8%; p< 0.001), hypermature villi
(72% vs. 16%; p< 0.001) were significantly associated with
pre-eclampsia, which is comparable with our study.
A meta- analysis done by Falco et al. 28 concluded that
both placental villous and vascular histopathological lesions
is higher, by a factor of four to seven-fold, in preeclampsia
compared to normal pregnancies, though the lesions are
not specific for preeclampsia. Gibbins et al. 29 performed
a population-based cohort study of all stillbirths and a
sample of live births from 2006 to 2008 in five catchment
areas and compared placental pathology between stillbirths
and those with and without Preeclampsia/Gestational
Hypertension (PE/ GH) and found that parenchymal
infarctions are more common in PE/GH preterm stillbirths
with significant overlap in lesions found in stillbirths and
PE/GH.
Stanek et al. 30 studied different grades of hypertension
and its effects on the placenta and concluded that the
preeclamptic groups showed the highest rates of decidual
arteriolopathy, which is comparable with our study. Salafia
et al. 31 concluded that placental infarction was associated
with increasing levels of proteinuria. Kovo M., et al. 21
compared pregnancy outcome and placental pathology in
pregnancies complicated by fetal growth restriction (FGR)
with and without preeclampsia and found higher rate of
maternal placental vascular lesions in hypertensive-FGR
compared with normotensive-FGR (82% versus 57.7%, p<
.001). |
Top
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
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The incidence of adverse fetal outcome and placental
changes suggestive of feto-maternal malperfusion shows a
linear trend with the grade of maternal hypertension.
CONFLICT of INTEREST
All authors declare that they have no conflict of interest.
ACKNOWLEDGEMENT
We thank Mrs Kamakshi and Mr Nalkar – Technicians who
processed the histopathology slides for the study. We thank
Dr Jamuna Kanakaraya for sharing the clinical details of the
cases that she sent to the department of pathology, KIMS,
Hubballi.
AUTHORSHIP CONTRIBUTIONS
Concept: PJ, PR, Design: PB, Data collection or processing:
PB, Analysis or Interpretation: PB, Literature search: PJ,
Writing: PB, Approval: PR. |
Top
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
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1) Brichant JF, Bonhomme V. Preeclampsia: An update. ActaAnaesthesiol Belg. 2014;65:137-49. 2) Salgado SS, Salgado MK. Structural changes in pre-eclamptic andeclamptic placentas—an ultrastructural study. J Coll PhysiciansSurg Pak. 2011;21:482-6. 3) Roberts JM, Pearson G, Cutler J, Lindheimer M. Summary ofthe NHLBI working group on research on hypertension duringpregnancy. Hypertension. 2003;41:437-45. 4) Weiner E, Mizrachi Y, Grinstein E, Feldstein O, Rymer‐Haskel N, Juravel E, Schreiber L, Bar J, Kovo M. The role ofplacental histopathological lesions in predicting recurrence ofpreeclampsia. Prenat Diagn. 2016;36:953-60. 5) Khong TY, Mooney EE, Ariel I, Balmus NC, Boyd TK, BrundlerMA, Derricott H, Evans MJ, Faye-Petersen OM, Gillan JE, HeazellAE. Sampling and definitions of placental lesions: Amsterdamplacental workshop group consensus statement. Arch Pathol LabMed. 2016;140:698-713. 6) Gestational Hypertension and Preeclampsia: ACOG PracticeBulletin, Number 222. Obstet Gynecol. 2020;135:e237-e60. 7) ACOG Committee on Practice Bulletins. ACOG PracticeBulletin. Chronic hypertension in pregnancy. ACOG Committeeon Practice Bulletins. Obstet Gynecol. 2001;98:Suppl 177-85. 8) Conrad KP, Benyo DF. Placental cytokines and the pathogenesisof preeclampsia. Am J Reprod Immunol. 1997;37:240-9. 9) Maynard SE, Min JY, Merchan J, Lim KH, Li J, Mondal S,Libermann TA, Morgan JP, Sellke FW, Stillman IE, EpsteinFH. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1)may contribute to endothelial dysfunction, hypertension, andproteinuria in preeclampsia. J Clin Invest. 2003;111:649-58. 10) Rinehart BK, Terrone DA, Lagoo-Deenadayalan S, Barber WH,Martin Jr JN, Bennett WA. Expression of the placental cytokinestumor necrosis factor α, interleukin 1β, and interleukin 10 isincreased in preeclampsia. Am J Obstet Gynecol. 1999;181:915-20. 11) Levine RJ, Maynard SE, Qian C, Lim KH, England LJ, Yu KF,Schisterman EF, Thadhani R, Sachs BP, Epstein FH, Sibai BM.Circulating angiogenic factors and the risk of preeclampsia. NEngl J Med. 2004;350:672-83. 12) Tsatsaris V, Goffin F, Munaut C, Brichant JF, Pignon MR, Noel A,Schaaps JP, Cabrol D, Frankenne F, Foidart JM. Overexpressionof the soluble vascular endothelial growth factor receptor inpreeclamptic patients: Pathophysiological consequences. J ClinEndocrinol Metab. 2003;88:5555-63. 13) Rana S, Karumanchi SA, Levine RJ, Venkatesha S, Rauh-HainJA, Tamez H, Thadhani R. Sequential changes in antiangiogenicfactors in early pregnancy and risk of developing preeclampsia.Hypertension. 2007;50:137-42. 14) Benirschke K, Kaufmann P, Baergen RN. Pathology of the humanplacenta. New York: Springer; 2006. 15) Redline RW, Boyd T, Campbell V, Hyde S, Kaplan C, KhongTY, Prashner HR, Waters BL, Society for Pediatric Pathology,Perinatal Section, Maternal Vascular Underperfusion NosologyCommittee. Maternal vascular underperfusion: Nosology andreproducibility of placental reaction patterns. Pediatr Dev Pathol.2004;7:237-49. 16) Salafia CM, Pezzullo JC, Ghidini A, Lopèz-Zeno JA, WhittingtonSS. Clinical correlations of patterns of placental pathology inpreterm pre-eclampsia. Placenta. 1998;19(1):67-72. 17) Van Oostwaard MF, Langenveld J, Schuit E, Papatsonis DN,Brown MA, Byaruhanga RN, Bhattacharya S, Campbell DM,Chappell LC, Chiaffarino F, Crippa I. Recurrence of hypertensivedisorders of pregnancy: An individual patient data metaanalysis.Am J Obstet Gynecol. 2015;212:624.e1-17. 18) Navbir P. Placental morphology and its co-relation with fetaloutcome in pregnancy induced hypertension. InternationalJournal of Basic and Applied Medical Sciences. 2012;2:120-5. 19) Roland MC, Friis CM, Voldner N, Godang K, Bollerslev J, HaugenG, Henriksen T. Fetal growth versus birthweight: The role ofplacenta versus other determinants. PLoS One. 2012;7(6):e39324. 20) Molteni RA, Stys SJ, Battaglia FC. Relationship of fetal andplacental weight in human beings: fetal/placental weight ratios atvarious gestational ages and birth weight distributions. J ReprodMed. 1978;21:327-34. 21) Kovo M, Schreiber L, Ben-Haroush A, Wand S, Golan A, BarJ. Placental vascular lesion differences in pregnancy-inducedhypertension and normotensive fetal growth restriction. Am JObstet Gynecol. 2010;202:561.e1-5. 22) Kher AV, Zawar MP. Study of placental pathology in toxaemia ofpregnancy and its fetal implications. Indian J Pathol Microbiol.1981;24:245-51. 23) Fox H, Sebire NJ. Pathology of the placenta. Major problems inpathology. 3rd ed. Saunders-Elsevier (London); 2007. 24) Fox GE, Van RW, Resau JH, Sun CC. The effect of immersionformaldehyde fixation on human placental weight. Arch PatholLab Med. 1991;115:726-8. 25) Ezeigwe CO, Okafor CI, Eleje GU, Udigwe GO, Anyiam DC.Placental Peripartum Pathologies in Women with Preeclampsiaand Eclampsia. Obstet Gynecol Int. 2018;2018:9462938. 26) Ruiz-Quiñonez G, Reza-López SA, Chávez-Corral DV, Sánchez-Ramírez B, Leal-Berumen I, Levario-Carrillo M. Placentalmaturity, hypertensive disorders of pregnancy and birth weight.Hypertens Pregnancy. 2014;33:132-44. 27) Devisme L, Merlot B, Ego A, Houfflin‐Debarge V, Deruelle P,Subtil D. A case–control study of placental lesions associatedwith pre‐eclampsia. Int J Gynaecol Obstet. 2013;120:165-8. 28) Falco ML, Sivanathan J, Laoreti A, Thilaganathan B, KhalilA. Placental histopathology associated with pre‐eclampsia:Systematic review and meta‐analysis. Ultrasound Obstet Gynecol.2017;50:295-301. 29) Gibbins KJ, Silver RM, Pinar H, Reddy UM, Parker CB, ThorstenV, Willinger M, Dudley DJ, Bukowski R, Saade GR, Koch MA.Stillbirth, hypertensive disorders of pregnancy, and placentalpathology. Placenta. 2016;43:61-8. 30) Stanek J. Placental pathology varies in hypertensive conditions ofpregnancy. Virchows Archiv. 2018;472(3):415-23. 31) Salafia CM, Xenophon J, Lerer T, Silberman L. Fetal growthand placental pathology in maternal hypertensive diseases. ClinExper Hyper Preg 1990;B9:27-41. |
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Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
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Copyright © 2023 The Author(s). This is an open-access article published by the Federation of Turkish Pathology Societies under the terms of the Creative Commons Attribution License that permits unrestricted use, distribution, and reproduction in any medium or format, provided the original work is properly cited. No use, distribution, or reproduction is permitted that does not comply with these terms. |
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