Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 9  |  Issue : 3  |  Page : 341-347  

Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension


1 Department of Pathology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, Maharashtra, India
2 Department of Pathology, Grant Medical College, Mumbai, Maharashtra, India
3 Department of Otorhinolaryngology, YCM Hospital, Pimpri, Pune, Maharashtra, India

Date of Web Publication17-May-2016

Correspondence Address:
Banyameen Iqbal
Department of Pathology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.182505

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  Abstract 

Background: Many disorders of pregnancy, which are associated with a high perinatal morbidity and mortality, are accompanied by gross pathological changes in placenta. Hypertensive disorders of pregnancy are common, and form one of the deadly triads along with hemorrhage and infection that greatly contribute to maternal mortality and morbidity. In addition, they are strongly associated with fetal growth restriction, prematurity, and contributing largely to perinatal mortality and morbidity. A study of placentae was done to find out the morbid and histological changes in placentae of hypertensive mothers and to correlate the findings with the birth weight of new born babies. Materials and Methods: Ninety placentae were studied. The weight of the placenta, placental fetal ratio, retroplacental hematoma, infarction, and histopathological findings were noted. Placental findings were correlated with fetal outcome. Results: The placental weight and fetoplacental weight ratio (5.38:1) was decreased in the hypertensive group. There was an increase in the incidence of infarction (28.8%) and retroplacental hematoma (15.5%) in the hypertensive group. Percentage of cytotrophoblastic proliferation of villi, >30% syncytial knots formation (64.5%), basement membrane thickening of villi (37.8%), and fibrinoid necrosis of villi (46.7%) increased in the placentae from pregnancy-induced hypertension group as compared to the normal group. Conclusions: Hypertensive disorders of pregnancy adversely influence the morphology of placenta. Fetal outcome is poor in the presence of infarction, retroplacental hematoma, basement membrane thickening of villi, and fibrinoid necrosis of villi. The pathological changes observed in the placentae of patients with hypertensive disorders of pregnancy adversely influence the perinatal outcome.

Keywords: Fetal outcome, hypertensive disorders of pregnancy, placenta


How to cite this article:
Kambale T, Iqbal B, Ramraje S, Swaimul K, Salve S. Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension. Med J DY Patil Univ 2016;9:341-7

How to cite this URL:
Kambale T, Iqbal B, Ramraje S, Swaimul K, Salve S. Placental morphology and fetal implications in pregnancies complicated by pregnancy-induced hypertension. Med J DY Patil Univ [serial online] 2016 [cited 2020 Jun 1];9:341-7. Available from: http://www.mjdrdypu.org/text.asp?2016/9/3/341/182505


  Introduction Top


The term placenta means flat cake in Latin. [1] The placenta is defined as a fusion of the fetal membranes to the uterine mucosa for the transfer of oxygen and metabolites between maternal and fetal blood. [2] It provides oxygen, nourishment, and protection to the fetus. It also has secretory and endocrine function. Preeclampsia is a major cause of maternal and neonatal morbidity and mortality. Recognized as a specific disorder since the time of Hippocrates, the only completely successful therapy remains delivery of the placenta. Microscopic examination of the placenta is important to determine the nature of the pathology, but many disorders show similar features.

Hereby, we made an attempt to find out the morbid and histological changes in the placentae of hypertensive mothers and its relation to perinatal outcome.


  Materials and Methods Top


Mothers with uncomplicated pregnancy and those with pregnancy-induced hypertension (PIH) were selected from indoor patients of a Tertiary Care Hospital. Treating obstetricians subdivided PIH cases using acclaimed criteria into mild PIH, severe PIH, and eclampsia. After delivery, the placenta was collected immediately for morbid and histopathological studies. The size, shape, and weight of the placentae were noted. Condition of membranes, site of insertion of umbilical cord, presence of infarction, calcification, and retroplacental hematoma were noted.

Tissue bits were taken from the implantation of the umbilical cord, marginal sections as 12, 3, 6, 9'o clock positions and center of the placenta, umbilical cord at the placental junction, and cut end and membranes. Additional placental sections are also taken if there is a presence of any fibrosis or infarct.

Tissue bits were processed and stained with routine hematoxylin and eosin stain and special stains, i.e., periodic acid-Schiff, reticulin, wherever required. Microscopic sections were studied by arbitrary criteria considering the area of histopathological sections. The newborn babies were inspected for congenital anomalies. Apgar score and birth weights were noted, and fetoplacental weight ratio was calculated in each case.


  Observation and Results Top


In the present study, maximum of 26 (57.7%) cases belonged to mild PIH, 15 (33.3%) cases belonged to severe PIH, and minimum of 4 (8.8%) cases were of eclampsia. Most cases belonged to 20-25 years age group, of which 16 cases were of mild PIH. Minimum numbers of cases were present in the age group of 30-35 years. There was only one case of eclampsia above 30 years of age. In the control group, 30 cases belonged to 20-25 age group and three cases were present in the age group of 30-35 years [Graph 1]. Primigravida being one of the etiologic factors of PIH, the number of cases of PIH were more in primigravida group (24 cases) wherein 14 cases were of mild PIH and seven and three cases of severe PIH and eclampsia, respectively. In the control group, 18 cases were primigravida and 13 were second gravida [Graph 2].





In the present study, the mean placental weight was more in the control group (489.1 g) than in the PIH group (405.2 g). These findings are statistically significant. In mild PIH, severe PIH, and eclampsia group, the mean placental weight was 424.8 g, 383 g, and 342 g, respectively. Placental weight decreased as the severity of disease progresses. The mean fetal birth weight in the control group was 2739.7 g, while that in PIH group it was 2079.6 g and also the fetal birth weight decreases with increasing grades of PIH. These findings were statistically significant. Normally, fetoplacental weight ratio varies between 6:1 and 8:1 and in the present study, the fetoplacental weight ratio in normal group was 5.68 and in PIH group it was 5.38.

On gross examination, 12 (26.6%) PIH group placentae showed calcification with an increase in incidence as the severity of disease progresses [Figure 1]. The control group showed calcification in 5 (11.1%) placentae. Retroplacental hemorrhage was seen in 7 (15.5%) cases of PIH group [Figure 2]a and b and in only three cases of control group. In the present study, no placenta from control group showed presence of placental infarction, while it was seen in 13 placentae from PIH group (28.8%) [Figure 3]. Statistically significant association of PIH group to placental infarct is present. However, no statistical significance is seen between PIH to calcification and retroplacental hematoma.
Figure 1: Photomicrograph showing intervillous calcification (H and E, ×100)

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Figure 2: (a) Gross picture showing maternal surface with crater formation due to retroplacental hematoma. (b) Photomicrograph showing retroplacental hemorrhage with underlying portion of decidua and villi (H and E, ×100)

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Figure 3: Photomicrograph showing placental infarction (H and E, ×200)

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On microscopy, cytotrophoblastic proliferation (>20%) was seen in all the severe PIH and eclampsia cases. Control group showed 7 (15.6%) cases with cytotrophoblastic proliferation of >20%, while 38 (84.4%) cases showed cytotrophoblastic proliferation of <20%. Excess cytotrophoblastic proliferation is directly proportional to the severity of the disease. Placental cytotrophoblastic proliferation of <20% was more in control group than in PIH. These findings were statistically significant. All the cases of severe PIH and eclampsia showed syncytial knots of >30%, while only 10 (38.4 %) cases of mild PIH showed the same [Figure 4]. Control group showed 36 (80%) placentae with <30% syncytial knots and only 9 (20%) placentae with >30% syncytial knots. In the PIH group, 16 (35.5%) cases showed presence of syncytial knots in <30% of villi, whereas 29 (64.5%) cases showed syncytial knots in >30% of villi. All the 4 (100%) cases of eclampsia showed >3% basement membrane thickening, while as 9 (60%) severe PIH and 4 (15.4%) mild PIH cases showed the same. No placenta from control group showed presence of basement membrane thickening in >3% of villi, while it is present in 17 (37.8%) placentae from PIH group. Basement membrane thickening in >3% of villi was seen in cases of PIH than the normal. These findings were statistically significant. 3 (75%) cases of eclampsia and 8 (53.3%) cases of severe PIH showed fibrinoid necrosis in >3% villi and only 10 (38.4%) cases of mild eclampsia showed this feature [Figure 5]. 2 (4.4%) placentae from control group showed presence of fibrinoid necrosis in >3% of villi, while it is present in 21 (46.7%) placentae from PIH group. Fibrinoid necrosis in <3% of villi was seen in 24 (53.3%) cases of PIH and in 43 (95.6%) patients of control group. These findings were statistically significant [Table 1].
Figure 4: Photomicrograph showing increase in syncytial knots composed of closely packed densely staining nuclei (H and E, ×100)

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Figure 5: Photomicrograph showing subchorionic fibrin deposition (H and E, ×100)

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Table 1: Histopathological findings in the different groups of placenta

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In normal deliveries, there is no perinatal loss; however, 10 (22.2%) low birth weight babies and 3 (6.6%) are having low Apgar score. In cases of eclampsia, all the babies are having low birth weight out of which 3 (75%) babies show low Apgar score and 2 (50%) show perinatal loss [Table 2]. Histopathological findings and their fetal outcome are shown in [Table 3].
Table 2: Fetal outcome in control group and PIH group

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Table 3: Histopathological findings of placenta and fetal outcome

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Comparison of the data using χ2 -test association among calcification, retroplacental hemorrhage, infarction, cytotropic proliferation, syncytial knots, basement membrane thickening, and fibrinoid necrosis in PIH placentae with fetal low birth weight, low Apgar score, and fetal loss is shown in [Table 4] and [Table 5].
Table 4: Association of histopathological findings of placenta with fetal outcome

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Table 5: Association of morphological findings of placenta with fetal outcome

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  Discussion Top


Placenta normally weighs 450-500 g. Fox have shown that placentae tend to be smaller in preeclampsia than those in uncomplicated pregnancies. [3] It is a well-established fact that blood flow to the placenta is reduced in PIH and this result in a small fetus with poor growth. Fox reported that placentae tend to be smaller in preeclampsia than those in uncomplicated pregnancies. [4] The mean placental weight in normal group was 489.1 g and in PIH group it was 383.2 g. The placentae were lighter in PIH and there was a reduction in weight with increasing grade of PIH. Placental weight decreases as the severity of disease progresses. The mean weight of placenta in eclampsia group was 342 g, in severe PIH group it was 383.3 g, and slightly more in mild PIH group which was 424.8 g.

Majumdar [5] and Kurdukar et al. [6] observed that fetal birth weights were lower in cases of preeclampsia; our findings correlated with these studies. The difference in the mean fetal birth weight observed by different researchers may be due to various factors such as socioeconomic status, races, and nutrition of mother. Fox [3] reported hypertrophy of placental mass in response to chronic hypoxia in hypertensive cases. This hypertrophy along with low birth weight of fetuses contributes to low fetoplacental weight ratio. In the present study, fetoplacental ratio was 5.38:1. Majumdar and Kurdukar et al. observed reduced fetoplacental weight ratio with increasing degree of PIH. Majumdar and Kurdukar et al. reported values of 6.23 ± 0.87:1 and 5.17:1, respectively. Chakravorty [7] also noted similar findings of 5.8:1, which correspond to the findings in the present study.

Dutta and Dutta [8] found calcification in 4 out of 32 (12.5%) cases of normal pregnancy and 26 (44.3%) placentae from PIH group of 59 cases. 4 out of 50 (8%) cases of normal pregnancy and 7 out of 49 (14.3%) cases showed calcification in a study by Kurdukar et al. [5] The incidence of calcification increases as the severity of the hypertension increases.

Fox [4] studied 195 cases of normal placentae out of which 48 (24.6%) showed calcification, and he observed that the incidence of calcification in 6 (6.6%) out of 92 cases was lesser in PIH than in the normal group. He explained that the incidence of calcification in PIH group was lesser than the normal group because he had included cases who delivered before term. In the present study, 12 out of 45 (26.6%) placentae from PIH showed calcification out of which 4 (100%) cases belong to eclampsia, 5 (33.3%) cases belong to severe PIH, and 3 (11.5%) cases belong to mild PIH. Therefore it is concluded that the incidence of placental calcification increases as the severity of the disease increase.

Page [9] observed 0.8% and 6.2% retroplacental hematoma in the normal and PIH groups, respectively, whereas Kurdukar et al. noted a percentage of 12% and 12.2%. [6] Present study showed an incidence of 15.5% that is 7 out of 45 placentae showed retroplacental hemorrhage in PIH, which is comparable to other studies. Thrombotic occlusion of maternal uteroplacental vessels is responsible for infarction. [3] Infarction involving more than 5% of placental parenchyma is clinically significant. Placental ischemia is caused, and a reduced amount of placental tissue is available for nutrition of the fetus causing untoward fetal outcome as suggested by Wigglesworth and Fox. [3],[6] The results of our study (28.8%) are comparable to the results of study done by Kurdukar et al. [6] (28.7%). In the present study, control group did not show any placental infarction [Table 5].

In the present study, cytotrophoblastic proliferation observed is comparable to the study done by Kurdukar et al. [6] In mild PIH cases with <20% cytotrophoblastic proliferation, there were 46% cases of low birth weight and 25% of low Apgar score cases and no fetal loss, while with >20% of cytotrophoblastic proliferation there were 70% cases of low birth weight, 30% cases of low Apgar score, and no fetal loss. Similarly, in severe PIH cases with >20% cytotrophoblastic proliferation, it shows 60% cases of low birth and 46.6% cases of low Apgar score with 20% fetal loss. Similarly, in eclampsia cases with >20% cytotrophoblastic proliferation, it shows 100% cases of low birth weight and 75% of low Apgar score cases with 50% of fetal loss [Table 3] and [Table 4].

The presence of >20% cytotrophoblastic proliferation was associated with low Apgar score in 14.75% and still birth in 35.2% in a study done by Avasthi and Micha, [2] in which term abnormal placentas were included in the sample, whereas in the present study of PIH placenta, low Apgar score was seen in 44.8% and fetal loss is 17.2% with the presence of >20% cytotrophoblastic proliferation. Similar findings were observed by Sodhi et al. [10] and Kher and Zawar. [11]

On microscopy, term placenta (37-40 weeks) showed an average of 28% syncytial knots. A drop-off to a mean of 22.5% was noted at 36 weeks. [12] Kurdukar et al. found an increase in the knot count with 84% cases of severe PIH and 100% cases of eclampsia, while in the present study, we found all the cases of severe PIH and eclampsia showing syncytial knot count more than 30% on low power view. Majumdar S et al. [5] found an increase in the number of syncytial knots. Furthermore, studies done by Kalra et al. [13] and Sodhi et al. [10] showed increased syncytial knots in their studies.

In the present study, mild PIH cases with <30% increase in syncytial knots, there were 50% cases of low birth weight, 25% of low Apgar score, and no fetal loss, while with >30% increase in syncytial knots, there were 60% cases of low birth weight, 30% of low Apgar score, and no fetal loss. Similarly, in severe PIH cases with >30% syncytial knots, there were 60% cases of low birth and 46.6% of low Apgar score cases with 20% fetal loss. Eclampsia cases with >30% increase in syncytial knots showed 100% low birth weight, 75% of low Apgar score cases, and 50% fetal loss. Kurdukar et al. [6] showed eclampsia cases with >30% increase in syncytial knots with 100% low birth weight, 100% of low Apgar score cases, and 40% fetal loss. There was no statistically significant association between the syncytial knot formation to fetal low birth weight, low Apgar score, and fetal loss [Table 3] and [Table 4].

Increase in the number of villi with thickened basement membrane is the result of ischemia of the uteroplacental circulation. It is due to the proliferation of cytotrophoblast and secretion of basement membrane material. This thickening is secondary to placental ischemia. [4]

In the present study, >3% thickening of basement membrane is seen in severe PIH (60% cases) and eclampsia (100% cases). In mild PIH cases with basement membrane thickening in <3% of villi, there were 50% cases of low birth weight, 22.7% of low Apgar score, and no fetal loss, while with basement membrane thickening >3%, there were 75% cases of low birth weight, 25% of low Apgar score, and no fetal loss. Similarly, in severe PIH with basement membrane thickening in <3% villi, there were 66.6% cases of low birth weight, 66.6% cases of low Apgar score, and no fetal loss, while with basement membrane thickening in >3% villi, there were 55.5% cases of low birth weight, 33.3% cases of low Apgar score, and 33.3% cases of fetal loss. Similarly, eclampsia cases with basement membrane thickening >3%, 100% cases show low birth weight, 75% show low Apgar score, and 50% show fetal loss. No statistical significant association was seen among basement membrane thickening, fetal birth weight, low Apgar score, and fetal loss [Table 3] and [Table 4].

The presence of >3% basement membrane thickening was associated with low Apgar score in 25% and still birth in 31.5% in a study done by Avasthi and Micha, [2] in which term abnormal placentae are included in the sample, whereas in the present study of PIH placenta, low Apgar score was in 41.1% cases and fetal loss in 29.41% with the presence of >3% basement membrane thickening. Kurdukar et al. [6] study showed eclampsia cases with >3% basement membrane thickening in which 100% were low birth weight, 100% low Apgar score cases, and 40% fetal loss.

Microscopic findings of localized fibrinoid necrosis, endothelial proliferation of arteries, and hyalinization depict the mosaicism of placenta and probably the aftermath of hypertension Teasdale [14] and Udainia et al. [15] Mosaicism of the placenta probably leads to placental insufficiency and ultimately to fetal growth retardation, thus creating a vicious cycle. [16] About 3% of the villi in mature placentae show fibrinoid necrosis. It is increased in PIH, diabetes mellitus, and Rh incompatibility. [1]

In mild PIH cases with fibrinoid necrosis in <3% of villi, there were 50% cases of low birth weight, 18.7% of low Apgar score, and no fetal loss, while with fibrinoid necrosis in >3% of villi, there were 60% cases of low birth weight, 40% of low Apgar score, and no fetal loss. Similarly, in severe PIH with fibrinoid necrosis in <3% of villi, there were 57.1% cases of low birth weight, 28.5% cases of low Apgar score, and no fetal loss, while with fibrinoid necrosis in >3%, there were 62.5% cases of low birth weight, 62.5% cases of low Apgar score, and 37.5% cases of fetal loss. Similarly, eclampsia cases with basement membrane thickening in >3% show 100% cases of low birth weight, 100% low Apgar score cases with 75% of fetal loss. Whereas in Kurdukar's et al. [6] study, in eclampsia cases with >3% fibrinoid necrosis, it showed 100% cases of low birth weight, 100% cases of low Apgar score, and 40% fetal loss. No statistically significant association was seen among fibrinoid necrosis, fetal low birth weight, low Apgar score, and fetal loss [Table 4] and [Table 5].


  Conclusions Top


From the present study, it can be concluded that the hypertensive disorders of pregnancy adversely influence the morphology of the placenta. The pathological changes observed in the placentae of patients with hypertensive disorders of pregnancy such as infarction, cytotrophoblastic proliferation, syncytial knots, basement membrane thickening, and fibrinoid necrosis are statistically significant when compared with control group and adversely influence the perinatal outcome. Though none of these pathological changes of PIH placentae are statistically significant to fetal outcome, they act collectively to determine fetal outcome.

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Conflicts of interest

There are no conflicts of interest.

 
  References Top

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Joshi VV. Handbook of Placental Pathology. Mishawaka, IN, USA: Igaku Shoin Medical Publisher; 1994.  Back to cited text no. 1
    
2.
Avasthi K, Micha U. Histopathology of placenta and its correlation with fetal outcome. J Obstet Gynaecol India 1991;41:317.  Back to cited text no. 2
    
3.
FOX H. White infarcts of the placenta. J Obstet Gynaecol Br Commonw 1963;70:980-91.  Back to cited text no. 3
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Fox H. Pathology of the Placenta. Philadelphia: Saunders; 1978.  Back to cited text no. 4
    
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Majumdar S. Study of placenta in normal and hypertensive pregnancies. J Anat Soc India 2005;54:34-8.  Back to cited text no. 5
    
6.
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Chakravorty AP. Foetal and placental weight changes in normal pregnancy and pre-eclampsia. J Obstet Gynaecol Br Commonw 1967;74:247-53.  Back to cited text no. 7
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Dutta DK, Dutta B. Study of human placentae associated with preeclampsia and essential hypertension in relation to foetal outcome. J Obstet Gynecol India 1989;39:757-63.  Back to cited text no. 8
    
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Page EW. On the pathogenesis of pre-eclampsia and eclampsia. J Obstet Gynecol 1972;79:883-94.  Back to cited text no. 9
    
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Sodhi S, Mohan H, Jaiswal TS, Mohan PS, Rathee S. Placental pathology in pre-eclampsia eclampsia syndrome. Indian J Pathol Microbiol 1990;33:11-6.  Back to cited text no. 10
    
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Kher AV, Zawar MP. Study of placental pathology in toxaemia of pregnancy and its fetal implications. Indian J Pathol Microbiol 1981;24:245-51.  Back to cited text no. 11
    
12.
Loukeris K, Sela R, Baergen RN. Syncytial knots as a reflection of placental maturity: Reference values for 20 to 40 weeks' gestational age. Pediatr Dev Pathol 2010;13:305-9.  Back to cited text no. 12
    
13.
Kalra VB, Agarwal A, Sareen PM, Kalra R. Histopathological changes in placenta in toxaemia of pregnancy. J Obstet Gynecol India 1985;35:86-90.  Back to cited text no. 13
    
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Teasdale F. Gestational changes in the functional structure of the human placenta in relation to fetal growth: A morphometric study. Am J Obstet Gynecol 1980;137:560-8.  Back to cited text no. 14
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Udainia A, Bhagwat SS, Mehta CD. Relation between placental surface area, infarction and foetal distress in pregnancy induced hypertension with clinical relevance. J Anat Soc India 2004;53:27-30.  Back to cited text no. 15
    
16.
Zacutti A, Borruto F, Bottacci G, Giannoni ML, Manzin A, Pallini M, et al. Umbilical blood flow and placental pathology. Clin Exp Obstet Gynecol 1992;19:63-9.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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