History of Endometriosis: A 20th‐Century Disease

Ivo Brosens, Giuseppe Benagiano
In: Endometriosis · 2011 · pp. 1–18 · doi:10.1002/9781444398519.ch1 · W2116676490
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This paper reviews the 20th-century evolution of endometriosis diagnosis, pathogenesis theories, classification systems, surgical and hormonal treatments, and current research directions.

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Abstract

The process of identifying the presence of epithelial invasions in the peritoneal cavity, but outside the uterine cavity, proceeded in steps over a period of 60 years until, in 1920, Cullen established that uterine adenomyoma, ovarian and deep endometriosis were one disease characterized by the presence of "adenomyomatous tissue" outside the uterine cavity. Sampson then gave the condition a name and provided the first theory on the pathogenesis of the disease, observing that the peritoneal lesions were bleeding at menstruation. A true revolution in the management of endometriosis occurred when, in the 1940s, new pelvic endoscopic techniques were introduced, allowing differentiation between causes of intra-abdominal bleeding, appendicitis, and salpingitis. The American Fertility Society stratified endometriosis into mild, moderate, severe, and extensive disease, using a weighted point score; this classification has now been revised twice and a "stage 5" proposed. The most important localization is in the peritoneum, with early lesions appearing and disappearing. In the ovary, endometriosis forms pseudocysts, the inside of which is constituted by invaginated ovarian cortex and a thin layer of endometriotic tissue. Hormonal treatment was started in the 1940s using, in sequence, androgens, estrogens, estrogen-progestins ("pseudo-pregnancy regimen"), antigonadotropic and antiprogestin agents. Conservative surgery gained popularity in the 1970s when laparoscopic techniques were introduced; in the 1980s the use of intraperitoneal adjuncts was added to reduce postoperative adhesion formation. Pathogenesis is still hotly debated: Sampson's retrograde menstruation theory remains valid, but the role of a modified peritoneal environment is today widely accepted, explaining reduced fecundability even in the presence of minimal endometriosis. Finally, the initial role of possible endometrial dysfunction is now being investigated.

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endometriosis

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