ABSTRACT

Telomerase is a ribonucleoprotein DNA polymerase elongating the telomeres and playing a crucial role in cell division. Its reactivation has been paralleled with immortalization and malignancy. Telomerase activity has been detected in a broad range of human cancers and its expression could be an important step in tumor progression. Here the relation between endometrial telomerase activity, endometrial thickness, endometrial histopathology and BMI was tested. The endometrial telomerase expression as a molecular marker in malignant transformation was questioned and revized. From all premenopausal patients complaining of menometrorragia (n:39) endometrial biopsies were taken for histopathologic and telomerase activity analysis; endometrial thickness and BMI was noted. Patients with endometrial hyperplasia without atipia (n:20) were treated with didrogesterone (Duphaston® 10 mg) 2x1 for 6 months. And endometrial biopsies were taken again. In patients with BMI above 30 the telomerase activity was statistically significantly higher (p:0.001). After progestin treatment there was a statistically significant decrease in telomerase activity (p:0.001) and endometrial thickness (p:0.0001). No statistically significant difference in telomerase activity before treatment between the endometrial hyperplasia group and the control group was found. In conclusion, the telomerase activity, being clinically usefull in the postmenopausal period, was found to be of no value in endometrial pathology prediction in premenopausal women. Gestagen treatment meaningfully decreased telomerase activity and endometrial thickness in hyperplastic patients and proved that is the cornerstone in the treatment of endometrial hyperplasia without atipia.