BACKGROUND
The pathogenetic features of the effect of intestinal dysbiosis on the development of diseases of the female reproductive system are still insufficiently investigated. Today there is a hypothesis that intestinal dysbiosis may be important in the etiopathogenesis of endometriosis.
OBJECTIVE
To identify on the basis of morphological and microbiological methods whether there is a relationship between infection of peritoneal fluid and macrophage cell population in endometrioid ovarian cysts.
MATERIAL AND METHODS
The collection of biological material was carried out in the gynecological departments of the Clinical Hospital of Emergency Medical Care (Smolensk). The experimental group consisted of 23 patients with a histologically verified diagnosis of endometrioid ovarian cyst. The following material was taken from each patient: a fragment of ovarian cyst tissue — for pathohistological examination (hematoxylin-eosin staining) and immunohistochemical examination using CD68, Ki-67 and p53 markers; peritoneal fluid and feces — for microbiological examination. Morphological evaluation of endometrioid ovarian cysts was carried out on the basis of their division into ‘immature’, ‘mature’ and ‘old’. Based on the results of microbiological examination, the patients were divided into two groups with infected and sterile peritoneal fluid.
RESULTS
Microbiological signs of intestinal dysbiosis are present in all patients, regardless of the presence of microorganisms in the peritoneal fluid. However, the most pronounced differences between the subgroups are determined in relation to mycotic flora. In the subgroup of patients with infected peritoneal fluid, mycelial fungi in the feces were present in 54.5% of cases in an amount higher than acceptable for the normal composition of the intestinal microflora (<104). In the subgroup with uninfected peritoneal fluid, mycelial fungi were detected in feces only in 16.6% of cases, not always going beyond the norm. Candida pseudotropicalis (kefyr), Pseudomonas aeruginosa and Enterococcus faecalis were found in the peritoneal fluid. It was also noticed that the subgroup with infected peritoneal fluid mainly consisted of patients with ‘immature’ and ‘mature’ endometrioid cysts, whereas the group with uninfected peritoneal fluid was represented mainly by ‘old’ endometrioid ovarian cysts in the complete absence of ‘immature’. The expression of immunohistochemical markers CD68, Ki-67 and p53 in the endometrioid cyst wall was significantly higher in the group with infected peritoneal fluid.
CONCLUSIONS
The pilot data obtained by us give the right to talk about the presence of a connection between the etiopathogenesis of endometriosis and the syndrome of increased intestinal permeability, which requires further research. Based on the results obtained, it can be assumed that the significance is not a specific microorganism located in the peritoneal fluid, but the possibility of its intramacrophagal parasitization with subsequent influence on the system of mononuclear phagocytes.
