ABSTRACT
Objectives: Maternal age has been increasing for several decades with many of these late pregnancies between 40 and 45 years old. The main objective of this study is to assess whether maternal age is an independent factor of obstetric, fetal, and neonatal complications. Patients and methods: A monocentric, French study "exposed-unexposed" was conducted during 11 years in a maternity level IIB. Maternal and perinatal outcomes were studied using univariates and multivariate analysis. We compared women aged 40 and above in a 1:1 ratio with women of 25-35 years old. Results: One thousand nine hundred eighty-two women were 40 or older (mean age: 41.9) on the day of their delivery and compared to other 1,982 women who were aged between 25 and 35 years old (mean age: 30.7) Preeclampsia, gestational diabetes, were significantly higher in the study group (4.6 vs. 1.5% and 14.5 vs. 6.9%, respectively, p < 0.001). We found also a significant difference for gestational hypertension (3.1 vs. 1.1% p < 0.001), preterm birth (10.4 vs. 6.5% p < 0.001), cesarean (16.6 vs. 5.4% for scheduled cesarean, and 50.4 vs. 13.9% for emergency cesarean, p < 0.001) and fetal death in utero (2.1 vs. 0.5% in the study group, p < 0.001). These results were also significantly different in multivariate analysis. Conclusion: A pregnancy after 40 years old is worth considering today as far as the risk factors are controlled and understand by the patient and the obstetrician. However, they have a significantly higher risks of cesarean, preterm delivery, pre-eclampsia, gestational diabetes, and fetal death in utero (FDIU). It is therefore the responsibility of the obstetrician to inform correctly these women in a detailed way, to reassure them and to adapt the monitoring of their pregnancy accordingly.
ABSTRACT
Endometriosis is a benign disease with high prevalence in women of reproductive age estimated between 10 and 15% and is associated with considerable morbidity. Its etiology and pathogenesis are controversial but it is believed to involve multiple genetic, environmental, immunological, angiogenic, and endocrine processes. Altered expressions of growth factors, cytokines, adhesion molecules, matrix metalloproteinases, and enzymes for estrogen synthesis and metabolism have been frequently observed in this condition. The possibility of genetic basis of endometriosis is demonstrated in studies of familial disease, in which the incidence of endometriosis is higher for first-degree relatives of probands as compared to controls. This review describes mainly the cellular, cytochemical, cytogenetic, and molecular genetic features of endometriotic lesions and cultured endometriotic cells. In attempts to identify candidate gene (s) involved in the pathogenesis of endometriosis, a tissue-based approaches including conventional cytogenetics (RHG-banding), loss of heterozygosity (LOH), and comparative genomic hybridization (CGH) were employed. In addition to the karyotypic anomalies, consistent chromosome instability was confirmed by CGH and fluorescence in situ hybridization (FISH). The nature and significance of the molecular genetic aberrations in relation to the locations and function of oncogenes and tumor suppressor genes will be discussed. At last, a possible pathogenic role of embryonic duct remnants was observed in seven female fetal reproductive tract in endometriosis and may induce a discussion about the beginning of ovarian tumors and malignant proliferations.
