Shared Molecular Features Linking Endometriosis and Obstetric Complications

Recent epidemiological research has shown the increased risk of adverse pregnancy outcomes in women with endometriosis compared with the general population. The aim of this review is to explore common pathophysiologic mechanisms between endometriosis and obstetric complications. A computerized literature search was performed to identify relevant studies. The search covered the period between January 2008 and October 2018. One of the potential mechanisms driving the initiation and progression of endometriosis is the accumulation of a variety of epigenetic changes in endometrial cells. Epigenetic control of gene expression which is considered to be responsible for the development of endometriosis is commonly seen in patients with preeclampsia, small for gestational age (SGA), or preterm birth. DLX5 and GATA3, paternally imprinted genes, and CDKN1C, a maternally imprinted gene, were aberrantly expressed in placenta tissues of the preeclampsia; CDKN1C, the growth inhibitor gene, was upregulated in human SGA placentas; and hypomethylation of PTGER2 would be associated with preterm birth. Preeclampsia, SGA, or preterm birth may share common epigenetic alterations with endometriosis, which raises the possibility that the occurrence of two conditions might be nonrandom. To date, however, there is a lack of evidence that links endometriosis and other obstetric complications, such as postpartum hemorrhage or placental abruption, at the epigenetic level. In conclusion, epigenetic changes may be a common hallmark of two conditions: endometriosis and obstetrical complications, such as preeclampsia, SGA, or preterm birth.