Endometriosis is a complex condition where, the lack or relative absence of an overt anatomical barrier to fertility often belies the true extent of reproductive problem(s). All too often the view is expounded that the severity of endometriosis-related infertility is inevitably directly proportionate to the anatomical severity of the disease itself, thereby implying that endometriosis causes infertility primarily by virtue of creating anatomical barriers to fertilization. This over-simplistic and erroneous view is often used to support the performance of many unnecessary surgeries for the removal of small innocuous endometriotic lesions, on the basis of such “treatment” evoking an improvement in subsequent fertility. The annual birth rate for normally ovulating women, free of any pelvic pathology (including mild endometriosis), who are having regular intercourse with fertile male partners, timed to coincide with ovulation differs with the age of the woman. For women under 35yrs it is about 80%.For those 35-40yrs of age, is about 50-60% and for women in their early 40’s the comparable annual rate is approximately 20-25% In contrast women in similar age categories who have even the mildest degree of endometriosis can expect a 3-4 fold reduction in annual birth rate. It is indeed indisputable that even the mildest form of endometriosis can compromise fertility. It is equally true that, mild to moderate endometriosis is by no means a cause of absolute “sterility.” Rather, 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. Two important reasons for such reduction in fertility potential are:

  • The existence of endometriotic deposits in the pelvis is associated (in all cases) with the presence “toxins” in the pelvic secretions. This significantly reduces the fertilization potential of eggs as they pass from the ovary to the fallopian tube via the pelvic cavity, and…..
  • In about one third (1/3) of cases, endometriosis almost certainly involves an immune implantation dysfunction (IID), such that the uteri of such women tends to reject the embryo (fertilized egg) as it attempts to gain attachment to the uterine lining (endometrium).

What about Surgery, ovulation induction with fertility agents and intrauterine (artificial) insemination- IUI for treating women who have early endometriosis? All women with endometriosis have toxins in their pelvic secretions that, compromise the ability of sperm to fertilize eggs that pass through this environment from the ovary (ies) to reach sperm in the fallopian tube(s).This dramatically reduces fertilization potential of such eggs (by a factor of 4-6 fold) It serves to explain why potentially all women with endometriosis have reduced fecundity (reproductive potential) and. It also serves to explain why the use of tubal surgery, fertility drugs and/or intrauterine insemination (IUI) will likely not improve fecundity over no treatment at all and why in normally ovulating women, when pregnancy ensues following such approaches it in all likelihood occurred  in spite of, rather than due to such treatment. The only way to avoid this effect is through by-passing this toxic pelvic environment by extracting the eggs before they are exposed to the toxic pelvic secretions…IOW, IVF. Endometriosis and an immunologic implantation dysfunction (IID): The second factor that must be carefully evaluated in women with early endometriosis is the possibility that she might have an immunologic implantation dysfunction (IID) linked to activation of uterine natural killer cells (NKa). Accordingly, in my opinion, all women who have symptoms suggestive of endometriosis (heavy and painful menstruation, pain with ovulation, pain with deep penetration during intercourse, unexplained infertility and failure to conceive after repeated attempts at IUI or IVF) should be tested for NKa using the K-562 target cell test and if this indicated NKa, the treatment would involve Intralipid infusions, steroids and possible heparinoids (e.g. Clexane and Lovenox). Tests for IID should only be done in a reproductive immunology reference lab capable of performing these tests with the required sensitivity currently exist in the U.S.A. There are to my knowledge fewer than a half dozen such reference laboratories in the United states.. How should fertility treatment be planned for in women with Early Endometriosis? Since in the absence of an IID, women ovulating women who have early endometriosis (and fertile partners) can and do conceive spontaneously albeit much more difficult to succeed. Thus, since alternatives such as ovulation induction, surgery and/or IUI offer little if any advantage over no treatment at all, younger women (under 35y) who have no diminished ovarian reserve (normal AMH) and no IID, can elect to take a “wait and see approach for a year or two at which time if no pregnancy occurs IVF would become the treatment of choice. However, if there is an associated IID or a male infertility component to boot, they are best advised to go directly to IVF which is much likely to be successful”. However, if such women, in addition have diminished ovarian reserve (such that time3 might be running out on their fecundity), and IID or a concomitant male factor component they Are best advised to go directly to IVF. Older women (over 35yrs) who have endometriosis-related infertility, do not have time to waste, and should, in my opinion, regard IVF as a first line approach, regardless of their immunologic status.