New Understanding of Diagnosis, Treatment and Prevention of Endometriosis

Abstract

For 100 years, pelvic endometriosis has been considered to originate from the implantation of endometrial cells following retrograde menstruation or metaplasia. Since some observations, such as the clonal aspect, the biochemical variability of lesions and endometriosis in women without endometrium, the genetic-epigenetic (G-E) theory describes that endometriosis only begins after a series of cumulative G-E cellular changes. This explains that the endometriotic may originate from any pluripotent cell apart from the endometrium, that 'endometrium-like cells' can harbour important G-E differences, and that the risk is higher in predisposed women with more inherited incidents. A consequence is a high risk after puberty which decreases progressively thereafter. Considering a 10-year delay between initiation and performing a laparoscopy, this was observed in the United Arab Emirates, Belgium, France and USA. The subsequent growth varies with the G-E changes and the environment but is self-limiting probably because of the immunologic reaction and fibrosis. That each lesion has a different set of G-E incidents explains the variability of pain and the response to hormonal treatment. New lesions may develop, but recurrences after surgical excision are rare. The fibrosis around endometriosis belongs to the body and does not need to be removed. This suggests conservative excision or minimal bowel without safety margins and superficial treatment of ovarian endometriosis. This G-E concept also suggests prevention by decreasing oxidative stress from retrograde menstruation or the peritoneal microbiome. This suggests the prevention of vaginal infections and changes in the gastrointestinal microbiota through food intake and exercise. In conclusion, a higher risk of initiating endometriosis during adolescence was observed in UAE, France, Belgium and USA. This new understanding and the limited growth opens perspectives for earlier diagnosis and better treatment.

Keywords: adenomyoisis; endeometriosis; genetic and epgigenetic; medical therapy; surgery.

Figure 1

Deep endometriosis initiating more than 10 years after menopause in women not taking estrogens (reprinted from [11] with permission) suggests monitoring the growth of endometriosis during medical treatment.

Figure 2

Origin and development of endometriosis: a combination of G-E events, with further growth, immune response, inflammation and fibrosis (figure from [7]).

Figure 3

During adolescence the risk of initiating endometriosis is highest with a progressive decline thereafter. After puberty the endocrinology, and the oxidative stress of retrograde menstruation and the peritoneal microbiome change. Susceptible women will initiate endometriosis earlier while the remaining group will have a lower risk. Considering a 5 to 10 years delay between the initiation of endometriosis and the laparoscopy explains that most laparoscopies for endometriosis were performed between 25 and 30 years of age with an exponential decline thereafter (reproduced with permission [8]).

Figure 4

Incidence of laparoscopies and type of endometriosis In Latifa, United Arab Emirates, in France and Belgium. The severity of deep (>2 cm) and cystic (>3 cm) endometriosis is indicated by darker colours.

Figure 5

Endometriotic lesions as a cause of pain and infertility. Adenomyosis, peritoneal pockets and Müllerianosis are not discussed.

Figure 6

Images of conservative excision of short bowel resection in deep endometriosis in the bowel. Note the fibrosis around the endometriosis.

Figure 7

Transvaginal hydro laparoscopy images of an endometrioma before (A) and after (B) surgery of endometriosis. (A,B) ovarioscopic view: note neoangiogenesis and endometrium-like tissue. (C) superficial coagulation using 5Fr bipolar probe. (D) Final result after coagulation: minimal trauma, no carbonization [67].