ASSOCIATION OF PLACENTA PREVIA WITH A HISTORY OF PREVIOUS CESARIAN DELIVERIES AND INDICATIONS FOR A POSSIBLE ROLE OF A GENETIC COMPONENT
Matalliotakis M, Velegrakis A, Goulielmos GN, Niraki E, Patelarou AE, Matalliotakis I
*Corresponding Author: Dr. Michail Matalliotakis, Venizeleio & Pananio General Hospital of Heraklion, Knossos Avenue, 71409 Heraklion, Greece. Tel: +30-281-036-8304. Mobile: +30-694-386-1582. Fax: +30-281-036-8305. E-mail: mihalismat@hotmail.com
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DISCUSSION

In the current study, we investigated pregnancies associated with a placental dysfunction, placenta previa, in the genetically and environmentally homogeneous population of Crete, Greece. Placenta previa represents the placenta that partially or wholly covers the internal cervical os. Our data indicate that the frequency of observed placenta previa is slightly higher than the one reported so far, which ranges between 0.3 and 0.5% [6,7].Thus, 76 cases out of 5200 live births had placenta previa (1.46%). As a possible explanation, this inconsistency may be considered to be due to the very low number of specialized tertiary centers that are available for a large population. Placenta previa is subdivided into three main types that can be confirmed by a transvaginal scan. Complete form means that the placenta totally covers the cervical os, partial that the edge of the placenta partially covers the birth canal and marginal indicates that the placenta lies close to the cervical os [8]. Several studies suggested that a previous history of C-section is the primary risk factor for developing placenta previa. Data show up to 37.5% increased risk due to previous history [9,10]. In the present study, 50 out of 76 women (66.0%) had a history of previous C-sections, a situation that can be explained by the fact that the endometrial cells located close to the scar are unable to differentiate properly resulting in a defective implantation mechanism. Interestingly, it has been reported that the rate of placenta previa increases proportionally with the history of previous C-sections, which is also consistent in our case [11]. Placenta percreta is a potentially lethal complication. It is a result of failure of decidua basalis after a repair of a previous uterine scar, and as a consequence, the chorionic villi invade the myometrium. Hudon et al. [12] stated that women who have both placenta previa and previous uterine scarring are susceptible to develop placenta acreta. In a total of 76 patients with placenta previa, six of them developed placenta percreta. In this group, all women were older than 36 and had a history of more than one previous C-section. According to the literature, placenta previa is more common among increased age group (>30 years old), which is in line with the data of the present study. Although, there is not any statistically difference between ultrasound and magnetic resonance imaging (MRI) for diagnosing placenta percreta, high risk cases should be carefully evaluated by MRI in order to determine the degree of the invasion to adjacent organs. It was suggested in the literature to use MRI imaging when the placenta is located in the posterior wall of the uterus [13,14]. In the evaluation of the related complications in our series, we reported that seven cases were transferred to the ICU, 14 cases needed blood transfusions and eight underwent hysterectomy due to placenta invasion into the bladder, which was confirmed by MRI. As far as the time of delivery is concerned, each case should be individualized depending on the patient’s preferences and risks. A planned preterm hysterectomy after 34 weeks where fetal lungs have matured is recommended, with the placenta being left in situ, to avoid massive bleeding in cases where invasion of the chorionic villi is prominent. However, if the mother has a desire for future fertilization, surgical management should be individualized [15]. Upon now, a few studies have linked the male gender with placenta previa formation. The gender at birth seems to be influenced by variable factors such as parental age, race, psychological status, exposure to hormonal treatment for subfertility and the time of the insemination within the menstrual cycle. The quality of these series is limited because of the incompleteness of the information presented in the reports and the small number of cases [16]. Notably, Jakobovits and Zubek [17] reported an association between male gender and placenta previa at the extreme ends of maternal age. Moreover, it has been proposed that early and late insemination during the menstrual cycle may contribute to male conceptions and also leads to a change in the site of implantation [4]. It is postulated that a male fetus is more likely to develop from late fertilization during the cycle, as a result in a delay in the creation and implantation of blastocyst in the lower uterine segment. Our results suggest that, our results suggest that male gender dominance has become obvious. Out of 76 cases, we reported 49 (65.0%) male newborns. In a population based study in Canada, 433,031 pregnancy outcomes were collected. The male-to-female ratio was higher in cases complicated by a placenta previa than in those without [18]. It has been suggested that the male embryo is a possible risk factor that we should take into consideration, especially in cases with a history of previous C-sections that may be associated with invasion of the placenta further to other organs. Although the risk factors for placenta previa are well defined, much less is known about its etiology and the possible enrolment of genetic factors in the development of this condition. In the present study, a woman gave birth to three children and placenta previa was observed in all cases. Moreover, three out of six women with placenta percreta were related to each other. Altogether, these observations indicate that both conditions could be genetically influenced, although no clear genetic contributions to susceptibility have thus far been defined. Placenta previa has an overall prevalence in North America of 2.9/1000 pregnancies, compared with a global prevalence of 5.2/ 1000 pregnancies [19], while the highest prevalence internationally was found in Asian women, appearing an overall prevalence is 12.2/1000 pregnancies. These regional differences in these rates have not been explained in depth, although Iyasu et al. [20] reported that in the United States, women of Asian ethnicity had twice the risk of placenta previa compared with women of other ethnicities. This latter finding strengthens the role of genetics rather than the effect of environmental factors as regards the development of placenta previa in Asian women. Interestingly, the role of genetics in placenta previa has now been demonstrated. Studies aiming to identify differentially expressed genes, which may impair placentation resulting in placenta previa increta/percreta (I/P), have shown that the metastasis associated lung adenocarcinoma transcript 1 (MALAT-1) (also known as HCN, NEAT2 and PRO2853) gene expression in placenta previa I/P is increased and its down-regulation inhibits trophoblast-like cell invasion in vitro. Placenta previa increta/percreta, a severe form of invasive placentation (a collective term for placenta accreta, increta and percreta), is associated with potentially life-threatening hemorrhage, which often requires a Cesarean hysterectomy. Therefore, it has been assumed that MALAT-1 might be involved in regulating trophoblast invasion during the development of advanced invasive placentation [21]. Additionally, the role of epigenetics in pregnancies associated with placental dysfunction including placenta previa has been also pointed out, indicating that the contribution of epigenetic alterations can be detected in susceptible subjects before the onset of clinical disease. In particular, the involvement of “hypermethylation” has also been reported in placenta previa. Thus, it has been demonstrated that an increased concentration of fetal-derived hypermethylated sequences of RASSF1A (Ras association domain-containing protein 1) tumor suppressor gene according to advancing gestation and before the onset of placenta previa [22]. Additionally, and contrarily to placenta previa, a remarkable genetic predisposition has been reported for other placentationassociated obstetric complications such as placental abruption and postpartum hemorrhage [6,23].



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