[Study on pathogenesis of adhesions in endometriosis (author's transl)].

In order to clarify the pathogenesis of adhesions in external endometriosis, visceral peritoneum with lesions and its surroundings was collected directly after laparotomy. The histological changes of the peritoneum were observed with scanning and transmission electron microscopes. Local fibrinolytic activity was also examined by peritoneal and tissue plasminogen activator activity (PAA). 1) The surface of early lesions of endometriosis was always covered with the peritoneum, one layer of mesothelial cells which were somewhat degenerated. Normal peritoneum (about 5 cm away from adhesions) possessed one layer of mesothelial cells. The surface of the cells appeared slightly bulged and covered with numerous long microvilli. Degeneration of the mesothelial cells increased with proximity to adherent lesions. The surface of the degenerated cells was extremely swollen and the shortened, club-shaped microvilli were irregularly distributed. A part of the peritoneum was denuded, and it was difficult to observe the mesothelial cells. These changes increased gradually with proximity to adhesions and fibrin deposits were also observed. 2) The peritoneal PAA of lesions of endometriosis appeared decreased in comparison with the normal peritoneum. Compared with normal myometrium, the tissue PAA of internal endometriosis was also decreased. In conclusion, the pathogenetic mechanism of adhesions was presumed to be as follows: Early lesions of endometriosis were always covered with peritoneum, so adhesions could not be observed. However, enlargement of lesions produced a damage of the peritoneum and out pouring of fibrins, causing fibrinous adhesions to other peritoneum. Fibrous adhesions were promoted by a decrease of fibrinolytic activity in the lesions.