Diagnosis Of Endometriosis and Treatment With a Sher Reproductive Endocrinologist

Endometriosis is a condition where the uterine lining (endometrium) grows on pelvic structures outside the uterine cavity. In early-stage endometriosis there is usually little, if any, visible evidence of anatomical distortion sufficient to compromise the release of an egg (ovulation) or its transportation from the ovary to the fallopian tube. In contrast, advanced endometriosis is characterized by the presence of pelvic adhesions sufficient to distort normal pelvic anatomy and interfere with fertilization as well as egg/embryo transportation mechanisms. Women who have endometriosis should speak with a Reproductive Endocrinologist, since they are much more likely to experience infertility. There are several reasons for this:

• In its most severe form, the condition is associated with scarring and adhesions in the pelvis, resulting in damage to, or blockage of, the fallopian tubes, thereby preventing the union of sperm and eggs.
• Endometriosis is associated with the presence of toxins in peritoneal secretions. As sperm and egg(s) travel towards the fallopian tubes they are exposed to these toxins which compromise the fertilization process.
• Endometriosis is associated with abnormalities of the woman's immune system which interfere with the ability of the fertilized egg to attach (implant) to the uterine wall
• In about 25-30% of cases, endometriosis is associated with ovulation dysfunction.
• There is even evidence that endometriosis itself is a symptom of an underlying hormonal imbalance which may be impacting fertility.

Until quite recently, we really had no clue as to how reproductive problems associated with endometriosis evolve. Recent medical research has helped shed light on the subject and offers promise with regard to the future treatment of infertility/reproductive failure associated with this condition.

Grading Endometriosis

Since the diagnosis of endometriosis can only be made by identifying it at the time of surgery, the extent of the disease is based upon where it is located and the extent of the damage it has caused. One perplexing issue is that there is poor correlation between the severity of this illness and the resulting symptoms. There is correlation however with the "stage" of endometriosis and its impact upon fertility. Reproductive specialists divide patients into one of four levels based upon what is seen at the time of their surgery:

Stage I: This is the lowest severity of endometriosis and is also referred to as minimal. It involves the presence of a few lesions or even microscopic presence noted on a biopsy specimen.

Stage II: Mild endometriosis is a more obvious disease with obvious implants of endometrium on anatomic structure but no distortion of the anatomy and minimal scarring.

Stage III: Referred to as moderate endometriosis, Stage III indicates a more extensive problem but without complete obstruction of fallopian tubes. Additionally, women with moderate endometriosis are more likely to have implants upon the ovary and sometimes even within it as well.

Stage IV: Severe endometriosis can be a devastating illness and is often associated with complete hysterectomy and removal of the ovaries to relieve symptoms. The extent of scarring obstructs one or both tubes.

Over the last thirty years, endometriosis has been diagnosed with ever-increasing frequency. It is also being seen in younger women today and tends to recur more rapidly after treatment. Over the same time, medical science has become ever more effective in identifying the condition and better at treating its devastating effects on fertility.

Factors Influencing Outcome Following Fertility Treatment

In cases of severe endometriosis, pelvic/tubal adhesions that interfere with egg transportation to the fallopian tube and/or ovarian "chocolate" endometriotic cysts (endometriomas) of the ovary certainly contribute to infertility. However, this does not explain the reduced fecundity (chance of conceiving) in women with mild to moderately severe endometriosis, where anatomical barriers to fertility are usually absent. We believe that the two key factors that explain the obstacles created by infertility are those related to its toxicity and its relationship with the immune system.

"Toxins" in the peritoneal fluid. "Toxins" that impair fertilization of the egg are present in the peritoneal secretions of most women who have endometriosis. Impaired fertilization is a feature of endometriosis regardless of its severity. This explains why women with endometriosis are about three times less likely to conceive per month of trying and why procedures such as intrauterine insemination do not substantially increase the chances of pregnancy over no treatment at all. It also explains why in vitro fertilization (which relies upon removing eggs through aspiration of the ovarian follicles before they can be affected by peritoneal toxins), by bypassing this handicap improves pregnancy rates dramatically, making it the treatment of choice for most endometriosis patients with infertility.

The immunology connection. More than half of women with endometriosis (regardless of its severity) have immunologic implantation dysfunction. The most common of these involves the presence of antiphospholipid antibodies (APA) and about 2/5 of these APA+ women (i.e., 30% of all women with endometriosis) in addition have evidence of activated Natural Killer (NKa) cells in their uterine linings (endometria). It is this NKa activity that represents the most significant reason for immunologic implantation dysfunction in women with endometriosis. The exact reason for the NKa in women with endometriosis remains at best speculative. If present, NKa usually leads to destruction of the embryo's implanting "root system" (the trophoblast), leading to early rejection of the embryo even before there is clinical evidence of a pregnancy. In fact, in most such cases the woman will not even know that she in fact had a "mini-miscarriage".  Less often, the damaged embryo miscarries early in the first trimester.