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DOI: 10.1055/s-0039-1692716
Placental Findings in Postpartum Preeclampsia: A Comparative Retrospective Study
Funding A.D. received a grant from the Swiss National Science Foundation.![](https://www.thieme-connect.de/media/ajp/202012/lookinside/thumbnails/10-1055-s-0039-1692716_180655-1.jpg)
Abstract
Objective Preeclampsia is a multifactorial placental disease that can occur after delivery. The pathophysiology of postpartum preeclampsia remains unknown. The objective was to describe placental findings in postpartum preeclampsia.
Study Design This is a case–control study, comparing the placental histologic findings in four groups of 30 patients with postpartum preeclampsia, early-onset preeclampsia, late-onset preeclampsia, and normotensive controls.
Results Placentas of postpartum preeclampsia had a mean placental weight not different from that of late-onset preeclampsia at a similar gestational age (479.0 ± 152.7 vs. 521.3 ± 144.1 g, p = 0.07); they showed a higher rate of acute deciduitis of 42.4% than early preeclampsia (5.7%, p < 0.01) or in controls (3.2%, p < 0.01); 18.2% had decidual arteriolopathy, with no significant difference with other groups. These placentas had fewer villous infarcts as compared with early preeclampsia (9.1 vs. 62.9%, p < 0.01) and less accelerated maturation of villi (24.2 vs. 74.3%, p < 0.01).
Conclusion There were no significant differences for decidual arteriolopathy and villous infarcts among postpartum preeclampsia, late-onset preeclampsia, and the controls. This suggests that postpartum preeclampsia is more of a maternal disease in which the placenta may act as a priming effect in predisposed mothers and becomes clinically apparent after delivery.
Keywords
postpartum period - preeclampsia - pregnancy - hypertension - placental findings - placental diseaseNote
This work has been presented to the fall meeting of the Society for Pediatric Pathology 2016, Honolulu, Hawaii.
Publication History
Received: 19 December 2018
Accepted: 14 May 2019
Article published online:
02 July 2019
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References
- 1 Sibai B, Dekker G, Kupferminc M. Pre-eclampsia. Lancet 2005; 365 (9461): 785-799
- 2 Chaiworapongsa T, Chaemsaithong P, Yeo L, Romero R. Pre-eclampsia part 1: current understanding of its pathophysiology. Nat Rev Nephrol 2014; 10 (08) 466-480
- 3 Maynard SE, Min JY, Merchan J. , et al. Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) may contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia. J Clin Invest 2003; 111 (05) 649-658
- 4 Wikström AK, Larsson A, Eriksson UJ, Nash P, Olovsson M. Early postpartum changes in circulating pro- and anti-angiogenic factors in early-onset and late-onset pre-eclampsia. Acta Obstet Gynecol Scand 2008; 87 (02) 146-153
- 5 Sibai BM. Etiology and management of postpartum hypertension-preeclampsia. Am J Obstet Gynecol 2012; 206 (06) 470-475
- 6 Filetti LC, Imudia AN, Al-Safi Z, Hobson DT, Awonuga AO, Bahado-Singh RO. New onset delayed postpartum preeclampsia: different disorders?. J Matern Fetal Neonatal Med 2012; 25 (07) 957-960
- 7 Bigelow CA, Pereira GA, Warmsley A. , et al. Risk factors for new-onset late postpartum preeclampsia in women without a history of preeclampsia. Am J Obstet Gynecol 2014; 210 (04) 338.e1-338.e8
- 8 Larsen WI, Strong JE, Farley JH. Risk factors for late postpartum preeclampsia. J Reprod Med 2012; 57 (1-2): 35-38
- 9 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 (04) 1173-1177
- 10 Roberts JM, August PA, Bakris G. et al. Report of the American College of Obstetricians and Gynecologists’ Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013; 122 (05) 1122-1131
- 11 Khong TY, Mooney EE, Ariel I. , et al. Sampling and definitions of placental lesions: Amsterdam Placental Workshop Group Consensus statement. Arch Pathol Lab Med 2016; 140 (07) 698-713
- 12 Redline RW. Classification of placental lesions. Am J Obstet Gynecol 2015; 213 (4, Suppl): S21-S28
- 13 Staff AC, Benton SJ, von Dadelszen P. , et al. Redefining preeclampsia using placenta-derived biomarkers. Hypertension 2013; 61 (05) 932-942
- 14 Redman CW, Sargent IL. Placental debris, oxidative stress and pre-eclampsia. Placenta 2000; 21 (07) 597-602
- 15 Magee L, von Dadelszen P. Prevention and treatment of postpartum hypertension. Cochrane Database Syst Rev 2013; (04) CD004351
- 16 Falco ML, Sivanathan J, Laoreti A, Thilaganathan B, Khalil A. Placental histopathology associated with pre-eclampsia: systematic review and meta-analysis. Ultrasound Obstet Gynecol 2017; 50 (03) 295-301
- 17 Aardema MW, Oosterhof H, Timmer A, van Rooy I, Aarnoudse JG. Uterine artery Doppler flow and uteroplacental vascular pathology in normal pregnancies and pregnancies complicated by pre-eclampsia and small for gestational age fetuses. Placenta 2001; 22 (05) 405-411
- 18 Cox LS, Redman C. The role of cellular senescence in ageing of the placenta. Placenta 2017; 52: 139-145
- 19 Sultana Z, Maiti K, Aitken J, Morris J, Dedman L, Smith R. Oxidative stress, placental ageing-related pathologies and adverse pregnancy outcomes. Am J Reprod Immunol 2017; 77 (05) DOI: 10.1111/aji.12653.
- 20 Stanek J. Hypoxic patterns of placental injury: a review. Arch Pathol Lab Med 2013; 137 (05) 706-720
- 21 Stanek J. Histological features of shallow placental implantation unify early-onset and late-onset preeclampsia. Pediatr Dev Pathol 2019; 22 (02) 112-122
- 22 Chen Y, Huang Y, Jiang R, Teng Y. Syncytiotrophoblast-derived microparticle shedding in early-onset and late-onset severe pre-eclampsia. Int J Gynaecol Obstet 2012; 119 (03) 234-238
- 23 Knight M, Redman CW, Linton EA, Sargent IL. Shedding of syncytiotrophoblast microvilli into the maternal circulation in pre-eclamptic pregnancies. Br J Obstet Gynaecol 1998; 105 (06) 632-640
- 24 Petrozella L, Mahendroo M, Timmons B, Roberts S, McIntire D, Alexander JM. Endothelial microparticles and the antiangiogenic state in preeclampsia and the postpartum period. Am J Obstet Gynecol 2012; 207 (02) 140.e20-140.e26
- 25 Southcombe J, Tannetta D, Redman C, Sargent I. The immunomodulatory role of syncytiotrophoblast microvesicles. PLoS One 2011; 6 (05) e20245
- 26 Conde-Agudelo A, Villar J, Lindheimer M. Maternal infection and risk of preeclampsia: systematic review and metaanalysis. Am J Obstet Gynecol 2008; 198 (01) 7-22
- 27 von Dadelszen P, Magee LA. Could an infectious trigger explain the differential maternal response to the shared placental pathology of preeclampsia and normotensive intrauterine growth restriction?. Acta Obstet Gynecol Scand 2002; 81 (07) 642-648
- 28 Lemichez E, Lecuit M, Nassif X, Bourdoulous S. Breaking the wall: targeting of the endothelium by pathogenic bacteria. Nat Rev Microbiol 2010; 8 (02) 93-104
- 29 Keski-Nisula L, Aalto ML, Katila ML, Kirkinen P. Intrauterine inflammation at term: a histopathologic study. Hum Pathol 2000; 31 (07) 841-846
- 30 Salafia CM, Weigl C, Silberman L. The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies. Obstet Gynecol 1989; 73 (3 Pt 1): 383-389
- 31 Faye-Petersen OM, Heller DS, Joshi VV. Handbook of Placental Pathology, 2nd ed. Boca Raton, FL: CRC Press, Taylor & Francis Group; 2006
- 32 Romero R, Gotsch F, Pineles B, Kusanovic JP. Inflammation in pregnancy: its roles in reproductive physiology, obstetrical complications, and fetal injury. Nutr Rev 2007; 65 (12 Pt 2): S194-S202
- 33 Stanek J. Decidual arteriolopathy with or without associated hypertension modifies the underlying histomorphology in placentas from diabetic mothers. J Obstet Gynaecol Res 2017; 43 (05) 839-847
- 34 Stanek J. Placental pathology varies in hypertensive conditions of pregnancy. Virchows Arch 2018; 472 (03) 415-423