Causes of Infertility: IMPLANTATION FAILURE
Causes of Infertility: IMPLANTATION FAILURE
In normal and stimulated cycles, pre-ovulatory endometrial (uterine lining) thickness and ultrasound appearance is predictive of potential embryo implantation (pregnancy) following In Vitro Fertilization/Embryo Transfer (IVF/ET). It has been shown that with “conventional” IVF/ET (where the woman receives fertility drugs and has her own fresh embryos transferred to her uterus), optimum implantation potential requires that on the day of the hCG trigger the endometrium should measure ≥ 9.0mm and ideally (although less important than thickness) should have a “triple line appearance”. While some viable pregnancies may occur with a lining of 8-9mm, very few will occur when the endometrium measures <8mm. For some reason that remains unclear at present, this rule of thumb might not apply to third party embryo recipients (ovum donation, IVF-surrogacy) and to women undergoing Frozen Embryo Transfers (FET). In this case, the recipient receives estrogen (but not gonadotropins) to prepare the uterine lining. Here, a lining measuring ≥8mm on the day that progesterone supplementation is started may be adequate.
A “poor” endometrial lining more commonly occurs when the basal or “germinal” endometrium, from which the full endometrial layer develops, is compromised in its response to estrogen. This most commonly occurs as a result of:
1. Permanent damage to the basal endometrium:
a) Due to inflammation of the uterine lining (endometrium), i.e., endometritis (an infection occurring following a delivery, abortion or miscarriage)
b) Following repeated or over-aggressive D&C procedures
c) Following uterine surgery that causes excessive endometrial scarring.
2. Endometrial resistance to estrogen:
a) Due to overuse of clomiphene citrate
b) Developmental – as sometimes occurs following prenatal in-utero exposure to diethylstilbestrol (DES).
3. Reduced blood flow to the basal endometrium:
a) Due to multiple uterine fibroids – especially when present immediately under the endometrium (submucosal).
b) Following extensive uterine surgery
c) As a result of Adenomyosis
4. Over-exposure to ovarian testosterone:
a) Due to overgrowth of ovarian connective tissue (stromal hyperplasia) that produces testosterone in response to luteinizing Hormone (LH). This occurs more commonly in older women (beyond 40 years);
b) In poor responders to gonadotropins (especially when they are given large amounts of LH-containing gonadotropins, e.g., Repronex, Menopur)
c) In very high responders to gonadotropin stimulation, e.g., women with Polycystic Ovarian Syndrome (PCOS).
Over-exposure of endometrial cells to increased testosterone production (as might occur in all such cases, especially when high doses of LH-containing gonadotropins are administered) reduces endometrial receptivity to estrogen. This might explain why, when the same women ultimately resort to ovum donation or undergo FET’s where no ovarian stimulation with gonadotropins is undertaken, the uterine lining subsequently thickens normally following treatment with estrogen.
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