The limited efficacy of hormone therapy for endometrial proliferative process (EPP) in postmenopausal patients and its side effects on the immune system functionalities have not been studied in detail. Here we assess the feasibility of hormone therapy for EPP in postmenopausal patients through evaluation of estradiol and progesterone receptor gene expression in endometrial tissue and peripheral blood mononuclear cells (PBMC). The study enrolled 92 postmenopausal patients with EPP, including 37 pts with glandular-fibrous polyps, 7 pts with non-atypical endometrial hyperplasia (EH), 8 pts with atypical endometrial hyperplasia (AEH), 31 pts with moderately differentiated adenocarcinoma and 9 pts with highly differentiated adenocarcinoma. The PBMC isolates and endometrial samples were tested for ER⍺, ERβ, mER, PRA, PRB, mPR and PGRmC1 expression by reverse real time polymerase chain reaction (RT–PCR). Differential changes in PBMC receptor profiles upon in vitro exposure to progesterone or mifepristone were determined for patients with endometrial polyps and healthy women. The results indicate elevated expression of ERα, ERβ, PRA, PRB, mPR and PGRmC1 by endometrial tissues in EH and elevated expression of mER, ER⍺ and PRA by PBMC in AEH, apparently reflecting suppressed functionalities of monocytes, macrophages, Т-cells and natural killer cells. Unaltered expression of the studied genes by PBMC in endometrial adenocarcinoma may reflect the incrementing tumor autonomy. In vitro, mifepristone inhibited ER⍺, ERβ, mPR, PGRmC1, PRA and PRB expression in PBMC isolated from patients with endometrial polyps. We suppose that such effects can mitigate the negative influence of sex steroid hormones on immunocompetent cells.

Microscopic colitis is an inflammatory bowel disease of unknown etiology that presents as chronic watery diarrhea with no endoscopic evidence of the bowel involvement but with the microscopic changes. Diagnosis of microscopic colitis is based on the histological examination of the intestinal biopsy and requires a highly qualified gastroenterologist, endoscopist and histologist. The article presents a clinical case of microscopic colitis in a 42-year-old patient, reflects the main stages of diagnosis and treatment of the patient.

Chronic heart failure (CHF) occurs in 4.3-28% of patients with diabetes mellitus and is most often associated with the presence of coronary heart disease, arterial hypertension and the direct adverse effects of insulin-resistance, hyperinsulinemia and hyperglycemia on the myocardium. Diabetes mellitus occurs in 12-47% of patients with CHF and can develop within several years after a diagnosis of HF in 22% of patients due to insulin-resistance of failure tissues. The presence of diabetes mellitus leads to a greater severity of clinical symptoms and hospitalization rate, worsening of quality of life and prognosis in CHF. A decreased left ventricular ejection fraction is an independent predictor of the poor prognosis in the patients with diabetes mellitus. The algorithm of the treatment of CHF in the patients with and without diabetes mellitus is not fundamentally different, but it requires taking into account the metabolic effects of the prescribed drugs. Angiotensin receptor-neprilysin inhibitor are increasingly used in clinical practice and are gradually replacing angiotensin-converting enzyme inhibitors and sartans in CHF both without diabetes mellitus and in its presence. Recently, the effectiveness of type 2 sodium glucose cotransporter inhibitors has been proven in patients with CHF with and without diabetes mellitus. This review is devoted to the relationship of diabetes mellitus and CHF, as well as the approaches to the management of such comorbid patients.

Objective. Immunohistochemical analysis of the efficacy of progestin therapy for endometrial hyperplasia (EH) without atypia in female patients of reproductive age. Patients and methods. The study included 101 female patients of reproductive age with abnormal uterine bleeding who were diagnosed with EH without atypia after histological examination of the endometrium. These patients were treated with standard doses of progestins between days 5 and 25 of their menstrual cycle for 6 months. After the end of hormone therapy, aspiration biopsy of the endometrium was performed. Immunohistochemical examination of endometrial biopsy was performed in addition to histological examination in 54 patients before and after therapy: the expression of progesterone (PR-A, PR-B) and estrogen receptors (ERα) and the Ki-67 proliferative index were determined. The control group included 18 women without endometrial pathology. Results. Therapy was effective in 77 patients with EH (the menstrual cycle was normalized, the endometrium corresponded to the menstrual phase at pelvic ultrasound and histological examination of uterine aspirate); EH was still present in 24 patients. Immunohistochemical examination of the endometrium in patients without the effect of progestin therapy initially revealed lower expression of ERα in endometrial glands, PR-A and PR-B in endometrial stroma and glands, and a higher Ki-67 proliferative index in endometrial stroma; their expression did not change after therapy. In patients with a positive effect of hormone therapy, the expression of ERα in endometrial glands, PR-A and PR-B in endometrial stroma and glands increased and approached the values of healthy women in the control group. Conclusion. Patients with EH and positive effect of progestin therapy had higher values of the expression of ERα in endometrial glands, PR-A and PR-B in endometrial stroma and glands, and a lower Ki-67 proliferative index in endometrial stroma, which suggests that these parameters may serve as predictors of the efficacy of therapy for EH with gestagen-containing medications. Key words: abnormal uterine bleeding, progestagens, endometrial hyperplasia, immunohisto-chemical examination, Ki-67 proliferative index, endometrial pathomorphology, progesterone receptors, estrogen receptors