Whether or not so-called “mild” endometriosis affects fertility has remained controversial, but it appears that any stage of endometriosis, even mild, can negatively affect a woman’s fertility for a variety of reasons.
When compared with normally ovulating women of a similar age who do not have endometriosis, women with mild to moderate endometriosis are about three to four times less likely to have a successful pregnancy.
Endometriosis may adversely affect fertility in several different ways:
Anatomical pelvic/tubal adhesions (tubal infertility)
Diminished ovarian reserve (reduced egg supply)
Toxic pelvic peritoneal factors (toxic pelvic environment)
Autoimmune implantation dysfunction
ANATOMICAL PELVIC/TUBAL ADHESIONS (TUBAL INFERTILITY)
Endometriosis and scar tissue can have adverse effects on normal tubal function, which then interferes with “egg pickup.” It is easy to understand how adhesions can negatively impact a woman’s fertility if the tubes have problems picking up an egg. With this type of problem, the degree of infertility is directly proportional to the anatomical severity of the endometriosis and adhesions. This type of infertility can often be overcome with surgery and/or medical manipulation (fertility drugs and intrauterine inseminations, also known as IUIs).
DIMINISHED OVARIAN RESERVE
More advanced stages of endometriosis (stages III and IV) are associated with large ovarian cysts, called endometriomas, as well as more severe pelvic adhesions. The large invasively growing endometriomas may destroy much of the normal ovarian tissue. More importantly, women with these advanced stages of endometriosis have often needed multiple extensive surgeries due to chronic pelvic pain. Multiple ovarian surgeries can often lead to a considerable reduction in the number of eggs remaining, as well as decreased ovarian blood flow due to adhesions following the surgeries. If an infertility patient has endometriomas that are not symptomatic, we will leave them alone so as to not compromise their ovarian reserve of eggs, in anticipation of doing in vitro fertilizaton (IVF).
TOXIC PELVIC PERITONEAL FACTORS (TOXIC PELVIC ENVIRONMENT)
Reactionary types of autoimmunity may occur with medical conditions such as endometriosis in which there is widespread tissue damage. Patients may have an “altered peritoneal environment” due to an inflammatory reaction triggered by the tissue damage from the endometriosis. This inflammatory reaction in the pelvis may result in the production and release of “toxic substances” and activation of specific white blood cells. In this situation, endometriosis results in the release of these local pelvic toxins and white cells that may interfere with the fertilization of eggs as the eggs pass through the pelvis from the ovary into the fallopian tube. In addition to the eggs being exposed to various pelvic inflammatory cells and toxins, sperm waiting in the tubes may also be adversely affected, leading to decreased fertilization potential. Some experts believe that virtually all women with endometriosis have an underlying toxic peritoneal factor to some extent, which can interfere with normal fertilization and reduce fertility. This may explain why pregnancy rates are reduced more than 4-fold in women with even the mildest stages of endometriosis.
Unfortunately, the use of fertility drugs with IUIs, and even surgery to remove some of the endometriotic tissue or tubal adhesions, will usually not be enough to overcome infertility due to a toxic pelvic peritoneal environment. IVF can bypass this problem of the toxic pelvic environment by transferring the embryo(s) directly into the uterine cavity.
AUTOIMMUNE IMPLANTATION DYSFUNCTION
In some women, tissue damage from endometriosis may lead to alterations in cell membrane phospholipids, resulting in the “autoimmune” production of antiphospholipid antibodies (APAs). This may occasionally result in the “activation” of specialized immune cells in the uterine lining known as Natural Killer (NK) Cells and Cytotoxic Lymphocytes (CTL). This type of reaction is referred to as autoimmune implantation dysfunction. Some researchers claim that up to one-third of women with endometriosis (any stage) have these immune barriers to implantation. The autoimmune NK/CTL “activation” results in a lethal reaction against the implanting embryo. These women may not be able to conceive with IVF until the underlying autoimmune implantation problem has been identified and treated with immunotherapy. For some women, could this be a cause of so-called unexplained infertility or perhaps repeated IVF failures. Women with endometriosis may benefit from an evaluation for immunologic factors, such as antiphospholipid antibodies (APA) and Natural Killer cell activation.
Several reports have demonstrated that women with endometriosis-related autoimmune implantation failure may benefit from Intralipid or IVIG treatments, as well as steroids or Lovenox, if administered prior to an IVF embryo transfer, depending on their abnormality. Without treatment, these women are not as likely to conceive.
Laurence A.Jacobs, M.D.