Defective myometrial spiral artery remodelling as a cause of major obstetrical syndromes in endometriosis and adenomyosis

被引:106
作者
Brosens, I. [1 ]
Pijnenborg, R. [2 ]
Benagiano, G. [3 ]
机构
[1] Leuven Inst Fertil & Embryol, Louvain, Belgium
[2] Katholieke Univ Leuven Hosp, Dept Dev & Regenerat, Louvain, Belgium
[3] Univ Rome, Dept Gynecol Obstet & Urol, Rome, Italy
关键词
Endometriosis; Adenomyosis; Deep placentation; Spiral arteries; Obstetrical syndromes; UTERINE JUNCTIONAL ZONE; IN-VITRO FERTILIZATION; PLACENTAL BED; PHYSIOLOGICAL TRANSFORMATION; MENSTRUAL-CYCLE; WOMEN; RISK; TROPHOBLAST; SUBENDOMETRIAL; PREECLAMPSIA;
D O I
10.1016/j.placenta.2012.11.017
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Endometriosis and adenomyosis are characterized by the presence of ectopic endometrium, but are also associated with functional and structural changes in the eutopic endometrium and inner myometrium. Alterations in the inner myometrium occurring in women with endometriosis and adenomyosis may be at the root of a defective remodelling of the myometrial spiral arteries from the onset of decidualization and result in vascular resistance and increased risk of defective deep placentation. The association of major obstetrical syndromes and different types of defective remodelling of the myometrial spiral arteries has been well documented. The possibility of a link between both endometriosis and adenomyosis and some major obstetric syndromes remains controversial because of at least two factors: first, changes of the inner myometrium are frequently present in women with endometriosis but the diagnosis requires high-resolution imaging such as magnetic resonance which is not routinely performed and second, patients with endometriosis are frequently subjected to prolonged hormone suppressive therapy. Indeed, there is evidence that pre-treatment with a Gonadotropin Releasing-Hormone analogue can improve the uterine microenvironment and implantation rate following IVF in infertile patients with endometriosis. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:100 / 105
页数:6
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