Preeklamtik ve normal plasentaların histopatolojik ve klinik bulgular eşiliğinde değerlendirilmesi

Abstract

AMAÇ: Preeklampsi (PE) maternal ve neonat morbidite ve mortalitenin en önemli nedenleri arasında yer alan bir hastalıktır. PE’nin patofizyolojisi tam olarak aydınlatılamamıştır. Hipoperfüzyon, hipoksi ve iskemi PE’nin etiyopatogenezinde kritik bileşenlerdir. Bu çalışmanın amacı PE’li ve sağlıklı gebelerin plesantalarındaki kronik villitis, infarkt, ödem, kalsifikasyon, korangiozis, perivillöz fibrin depoziti, villüslerde fibrozis, sinsityal knot artışı, retroplasental dekolman, plasental ağırlık ortalaması, yaş, gravite, parite, abortus, hemoglobin, platelet, LDH, D-Dimer ve Protein 24 düzeyleri ile klinik sonuçlarının incelenmesidir.

MATERYAL YÖNTEM: Çalışmamızda 2015-2018 yılları arasında patoloji bölümümüze tanı almış yaş, gravite, abortus, parite değerlerinde anlamlı farklılık bulunmayan preeklamptik ve kontrol grubu gebe plasentalarında 91 PE tanılı gebe ve kontrol grubu olarak ise 92 normal sağlıklı gebe alındı. Hastaların ve bebeklerin verileri dosyalarından, laboratuvar verileri hastane otomasyon sisteminden elde edildi. Plasentaya ait hematoksilen ve eozin boyalı preperatlar arşivden çıkarılarak tekrar değerlendirildi. Veriler sayı, yüzde, ortalama, standart sapma, korelasyon testleri ile analiz edildi. Sayısal değişkenler arası ilişkiler bağımsız gruplarda t testi ile ve kategorik veriler arası ilişkiler Ki-kare testi ile araştırılmıştır. P<0,05 olan test sonuçları, istatistiksel açıdan anlamlı kabul edilmiştir.

BULGULAR: Yaş, gravite, parite, abortus, hemoglobin, platelet, LDH, D-Dimer ve Protein 24 düzeyleri vaka ve kontrol grupları arasında istatistiksel olarak farklı bulunmadı (p>0,05). Çalışma grubunda plasental ağırlık ortalaması 330,8±89g 342 iken kontrol grubunda plasental ağırlık ortalaması 431±59g bulunmuştur. Retroplasental dekolman ise çalışma grubunda 6 olguda 7% (6/85) oranında bulunmuşken kontrol grubunda 1 olguda 1% (1/92) oranında izlenmiştir. Analiz ettiğimiz olgularda gebelik haftaları ortalamaları çalışma grubu hastalarında 33±3, kontrol grubu olgularında ise 38±1 bulunmuştur. Gravite, abortus, korangiozis, villitis, ödem, korioamnionit, kalsifikasyon, perivillöz fibrin ve sinsityal knot artışı için vaka ve kontrol grupları arasında istatistiksel olarak anlamlı ilişki belirlenmedi (p>0,05).

SONUÇ: Bulgularımıza göre preklamptik hastalarda plasental histopatolojide bazı parametrelerde farklılıklar mevcuttur bu farklılıklar plasental yetmezlik ile ilişkili olabilir. Ancak bir kısım plasental histopatolojik parametrelerde de farklılık olmaması her perinatal sorunun plasental bir anormallikle ilişkili olmadığı gibi her plasental patolojinin de perinatal kötü sonuçla ilişkili olmadığını desteklemektedir.

Keywords

• Preeklampsi
• Koranjiozis
• Plasenta
• Retroplasental dekolman
• Hipoksi

Comparison of Preeclamptic and Normal Placentas with Histopathological and Clinical Findings

Abstract

OBJECTIVE: Preeclampsia (PE) is one of the most important reasons leading to maternal, and neonate morbidity and mortality. The pathophysiology of PE has yet to be fully elucidated. Hypoperfusion, hypoxia and ischemia are the critical components in the etiopathogenesis of PE. Here, we aimed to investigate the association between chronic villitis, infarction, edema, calcification, chorangiosis, perivillous fibrin deposits, fibrosis in villi, syncytial knot increase, retroplacental detachment, average placental weight, age, gravity, parity, abortion, hemoglobin, platelet, lactate dehydrogenase (LDH), D-dimer and protein 24 levels, and the clinical results.

MATERIAL and METHOD: With no significant differences in age, gravity, abortion and parity values, 91 pregnant women diagnosed with PE in the preeclamptic placentae in our pathology department between 2015 and 2018, and 92 normal healthy pregnant women were included as the study and the control groups. Patients and babies’ data were obtained from their files, and the laboratory data were obtained from the hospital automation records. Hematoxylin and eosin-stained preparations of the placentae were removed and re-evaluated from the archive. The data were analyzed by number, percentage, mean, standard deviation, and correlation tests. Numeric variables were investigated by t test in independent groups whiler categorical data were assessed by chi-square test. Results with p<0.05 were considered statistically significant.

RESULTS: As to age, gravity, parity, abortion, hemoglobin, platelet, LDH, D-dimer and protein 24 levels, no statistical difference was found between the study and control groups (p>0.05). Mean placental weight was 330.8±89 g and 431±59 g in the study and control groups. Retroplacental detachment was 7% in six cases (6/85) in the study group, while 1% in one case (1/92) in the controls. Mean gestational weeks were found as 33±3 and 38±1 weeks in the study and control groups. No statistically significant association was determined between the study and control groups for gravity, abortion, chorangiosis, villitis, edema, chorioamnionitis, calcification, perivillous fibrin and syncytial knot increase (p>0.05).

CONCLUSION: Based on our findings, there were some differences in placental histopathology of preeclamptic patients; the differences may be related to placental insufficiency. However, the absence of differences in various placental histopathological parameters also supports that every perinatal problem is not associated with a placental abnormality, nor is every placental pathology associated with a perinatal malfunction.

Keywords

• Chorangiosis
• hypoxia
• placenta
• preeclampsia
• retroplacental detachment

References

1. 1. Henderson JT, Thompson JH, Burda BU, Cantor A, Beil T, Whitlock EP. Screening for Preeclampsia. 2017.
2. 2. Brown HL, Small MJ. Overview of Maternal mortality & morbidity. Pub Med. 2014.
3. 3. Woelkers D, Barton J, von Dadelszen P, Sibai B. [71-OR]: The revised 2013 ACOG definitions of hypertensive disorders of pregnancy significantly increase the diagnostic prevalence of preeclampsia. Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health. 2015;5(1):38.
4. 4. Laresgoiti‐Servitje E. A leading role for the immune system in the pathophysiology of preeclampsia. Journal of leukocyte biology. 2013;94(2):247-57.
5. 5. Jauniaux E, Watson AL, Hempstock J, Bao Y-P, Skepper JN, Burton GJ. Onset of maternal arterial blood flow and placental oxidative stress: a possible factor in human early pregnancy failure. The American journal of pathology. 2000;157(6):2111-22.
6. 6. BURTON GJ, HUNG T-H. Hypoxia-reoxygenation; a potential source of placental oxidative stress in normal pregnancy and preeclampsia. Fetal and Maternal Medicine Review. 2003;14(2):97-117.
7. 7. Chen A, Li C, Wang J, Sha H, Piao S, Liu S. Role of toll-like receptor 3 gene polymorphisms in preeclampsia. Cellular Physiology and Biochemistry. 2015;37(5):1927-33.
8. 8. Myatt L, Roberts JM. Preeclampsia: syndrome or disease? Current hypertension reports. 2015;17(11):83.

9. 9. Harmon AC, Cornelius DC, Amaral LM, Faulkner JL, Cunningham Jr MW, Wallace K, et al. The role of inflammation in the pathology of preeclampsia. Clinical science. 2016;130(6):409-19.
10. 10. Nelson DB, Ziadie MS, McIntire DD, Rogers BB, Leveno KJ. Placental pathology suggesting that preeclampsia is more than one disease. American journal of obstetrics and gynecology. 2014;210(1):66. e1-. e7.
11. 11. Suzuki K, Itoh H, Kimura S, Sugihara K, Yaguchi C, Kobayashi Y, et al. Chorangiosis and placental oxygenation. Congenital anomalies. 2009;49(2):71-6.
12. 12. Papageorghiou A, Yu C, Bindra R, Pandis G, Nicolaides KJUiO, Obstetrics GTOJotISoUi, et al. Multicenter screening for pre‐eclampsia and fetal growth restriction by transvaginal uterine artery Doppler at 23 weeks of gestation. 2001;18(5):441-9.
13. 13. Soma H, Yoshida K, Mukaida T, Tabuchi YJCtg, obstetrics. Morphologic changes in the hypertensive placenta. 1982;9:58-75.
14. 14. Choudhury M, Friedman JEJC, hypertension e. Epigenetics and microRNAs in preeclampsia. 2012;34(5):334-41.
15. 15. Chhatwal J, Chaudhary DN, Chauhan NJIJoR, Contraception, Obstetrics, Gynecology. Placental changes in hypertensive pregnancy: a comparison with normotensive pregnancy.7(9):3809.
16. 16. Ogge G, Chaiworapongsa T, Romero R, Hussein Y, Kusanovic JP, Yeo L, et al. Placental lesions associated with maternal underperfusion are more frequent in early-onset than in late-onset preeclampsia. 2011;39(6):641-52.
17. 17. Kaplan C, Lowell D, Salafia CJAop, medicine l. College of American Pathologists Conference XIX on the examination of the placenta: report of the working group on the definition of structural changes associated with abnormal function in the maternal/fetal/placental unit in the second and third trimesters. 1991;115(7):709.
18. 18. Altshuler GJAop, medicine l. Chorangiosis. An important placental sign of neonatal morbidity and mortality. 1984;108(1):71-4.
19. 19. Ogino S, Redline RWJHp. Villous capillary lesions of the placenta: distinctions between chorangioma, chorangiomatosis, and chorangiosis. 2000;31(8):945-54.
20. 20. Sevinç A. Plasentasyon bozukluğu ile birlikte olan gebeliklerde plasentanın histopatolojik incelenmesi. 2016.
21. 21. İskender-Mazman D, Akçören Z, Yiğit Ş, Kale G, Korkmaz A, Yurdakök M, et al. Placental findings of IUGR and non-IUGR. 2014;56(4).
22. 22. Eren S, Kuyumcuoğlu U, Aydoğmuş H, Okay İ, Alkan A, Ertekin K. PREEKLAMPTİK VE NORMAL GEBELERDE PLASENTANIN IŞIK VE ELEKTRON MİKROSKOBU İLE İNCELENMESİ.
23. 23. Ahmed M, Daver RGJIJRCOG. Study of placental changes in pregnancy induced hypertension. 2013;2(4):524-7.
24. 24. Baergen RN. Manual of Benirschke and Kaufmann's pathology of the human placenta: Springer Science & Business Media; 2005.