Molecular mechanisms of resistance of endometrial hyperplasia to progestogen therapy based on the study of the expression of estrogen and progesterone receptors and paracrine cellular markers of cellular interaction

The problem of resistance non atypical endometrial hyperplasia (NEH) to traditionally accepted, pathogenetically sound therapy with different types progestins is currently an unsolved problem. In about 17-20% cases there a recurrence or even progression forms (AEH), which required the use surgical treatments. aim study was investigate results hormone for treatment in women expression estrogen and progesterone receptors combination intercellular adhesion molecules E-cadherin β-catenin determine cause hormonal resistance, formation groups progestogen-sensitive (EH) type NEH (+), can progestogens treatment, progestogen-resistant (-), should be offered alternative therapy. performed on morphological material endometrium obtained by diagnostic biopsy abnormal uterine bleeding who were diagnosed histological examination. For immunohistochemical study, 80 samples taken from (AUВ) same after without atypia 3 6 months control group (CG) consisted 20 followed-up tactics. All divided into used treatment: I – continuous intake 100 mg micronized per os twice day months, II dihydrogesterone III LNG-IUD used. state proliferation differentiation studied tissues assessed their key molecular participants (ERα) (PGR), transmembrane glycoproteins β-catenin. ERα PGR determined immu­nohistochemistry calculated semi-quantitative H-index method. Evaluation determining percentage IHH-positive cells these antigens depending degree color. criterion effectiveness considered absence pathological changes endometrium. showed that change secretory 45% cases, dydrogesterone 55% reduction EH normal picture. intrauterine system levonorgestrel (LNG-IUD) greatest efficiency, 75% normalization structure observed. 32% normalized. After gestagens, both oral (micronized progesterone, dydrogesterone) LNG-IUDs positive effect use; therapeutic form gestagens not significant reducing excessive proliferation. patients did receive discontinued various reasons, it shown 47% had spontaneous regression EH. overall no 20% I, III. Determination all pronounced glands stroma, differ significantly (+) (-). Analysis (-) glandular (50.82±0.73) stroma (47.34±0.82) lower than (gland 187±3.1; 166.4±2.3; p<0.05), as well unchanged proliferative phase (glands 193.2±8.5; 178.7±6.3; p<0.05) 140.2±4.4; 116.6±3.1; p<0.05). A 86.4% absent 13.6% decreased. women, 49.2% weak, 34.4% moderate, 16.4% negative, indicating association between expression. marked cytoplasmic up 80%, interpreted potentially threatening relapses. Thus, mechanisms progestogen will help develop differential approach its diagnosis treatment.