Issue: 2025, Vol. 30, No. 4

A. M. Gerasimov, L. V. Kulida, G. N. Kuz’menko, L. V. Posiseyeva

PROTEOLYTIC ACTIVITY PROFILING IN EXTERNAL ENDOMETRIOSIS AT SYSTEMIC AND LOCAL LEVELS

Keywords

external endometriosis, ptoteases, fibrosis

Abstarct

Endometriosis is currently considered a classic inflammatory disease. Systemic inflammation plays a leading role in the development of chronic pain, reproductive dysfunction, fibrosis, and immunological disorders in endometriosis. Fibrosis is assigned a central position in the pathogenesis of endometriosis. Objective – to assess protease activity at systemic and local levels, the morphofunctional state of the endometrium in patients with endometriosis, and to evaluate the possible correlation between their activity and the severity of fibrosis. Material and Мethods. 436 women were under observation. Patients in the control group (I) (n = 117) were admitted to the endoscopic surgery department for elective surgical sterilization due to social indications. Group II (n = 319) involved women with external genital endometriosis of varying stages of progression, admitted to the clinic for elective laparoscopy to clarify the causes of infertility (n = 265) or for surgical treatment of endometriosis (n = 54). The levels of cathepsin D, plasminogen, protein C, α2-macroglobulin, haptoglobin, antitrypsin, and D-dimer were investigated in the serum and peritoneal fluid of patients, the activity of cathepsin D and its morphofunctional characteristics being assessed In the endometrium. Results and Discussion. The main changes in proteolytic activity in genital endometriosis primarily affect peritoneal fluid. Levels of cathepsin D, plasminogen, protein C, and haptoglobin were significantly reduced, while α2-macroglobulin and D-dimer levels being increased. Hormonal level and sex hormone receptor dissonance, decreased cathepsin D activity, and the presence of chronic inflammation and fibrosis foci in both the stroma and the walls of spiral arteries characterized the endometrium in patients of Group II. The severity of fibrosis worsened, especially in the arterial walls with the spread of the endometriotic process. The following parameters also indicated endometriosis spread: plasminogen – r = 0.56 (p < 0.05); AT III – r = 0.6 (p < 0.05); acidic α1-antitrypsin – r = 0.31 (p < 0.05); D-dimer – r = 0.34 (p < 0.05); and haptoglobin – r = 0.52 (p < 0.05). It can be hypothesized that changes in proteolytic activity at the local level (PF, endometrium) may contribute to the formation of fibrosis in endometriosis.

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