A hostile endometrial environment will impede embryonic implantation as shown by the placement of an intrauterine device into the endometrial cavity for contraception. This hostile effect is postulated to be reproduced by endometrial polyps and submucous fibroids. In addition, hormonal, immune and biochemical factors have been postulated to result in a hostile endometrial environment.
Poor progesterone effect resulting in delayed maturation of the endometrial lining, commonly referred to as the luteal phase defect, has been considered as hostile to implantation. Indeed, luteal phase defect has been demonstrated in a case of trisomy 16, suggesting that the defect is a secondary phenomenon of an primary defect, namely, genetic abnormality of an oocyte and its follicular apparatus resulting in abnormally low hormonal stimulation and finally, poor endometrial maturation (18). Teleologically, this would prevent pregnancy with abnormal embryos. Theoretically, this mechanism may go astray during genetically normal cycles and result in failed implantation, but has never been proved to be a cause of infertility, per se.
Other factors, which have been implicated in the development of a hostile environment for implantation, are autoimmune factors such as lupus anticoagulant and Integrin IIIß (19). It has been shown that antiphospholipid antibodies are not a factor in implantation but the effects of Integrin III ß are yet to be determined (20).
Patients with endometrial polyps and submucous fibroids may have premenstrual spotting or heavy menstrual bleeding. A luteal phase defect is not detected by any medical history.
Endometrial polyps and submucous fibroids are detected by either hysterosalpingography, sonohysterography, or hysteroscopy (Figure 4). A dilation and curettage (D&C) may be performed and histology of the curettings will confirm the diagnosis. Submucous fibroids are often felt as an irregularity while curetting the endometrial cavity.
Abnormal autoimmune factors do not cause infertility and need not be diagnosed. Integrin IIIß is still a research tool and diagnosis of an abnormal concentration should be left to research protocols.
The luteal phase defect is not a documented cause of infertility (21,22). Because its role in spontaneous abortion is not known, some physicians prefer to make the diagnosis in infertile patients. The diagnosis is made by performing an endometrial biopsy in the luteal phase. A histological dating lagging more than 2 days behind the actual postovulatory date diagnoses the defect.
Endometrial polyps may be removed by a uterine curettage and removal confirmed by hysteroscopy. Submucous fibroids may be removed through hysteroscopic surgery. Depending upon the depth of myometrial invasion, laparoscopy or laparotomy may be necessary. Pritts et al recently performed a meta analysis of women undergoing hysteroscopic myomectomy and found a modest improvement in pregnancy outcome (relative risk of 1.72 with a confidence interval of 1.13-2.58)(23).
As mentioned, other causes of endometrial hostility have not been proven to be related to infertility and, thus, treatment is not warranted.