Abstract

BACKGROUND: Uterine anomalies are a cause of female reproductive failure. Originally, malformations of the Mllerian ducts are believed to be the main reason for uterus abnormalities. There is an assumption that anti-Mllerian hormone (AMH) or AMH receptor (AMHR2) gene mutation may lead to alterations in the formation of the Mllerian ducts in female fetuses resulting in uterine anomalies.
 AIM: The aim of this study was to assess the AMHR2 expression in the endometrium of patients with uterine anomalies and a history of reproductive failure.
 MATERIALS AND METHODS: The present study included 112 women, of whom 92 patients were diagnosed with uterine anomalies (main groups): arcuate uterus (n = 30), septated uterus (n = 30), bicornuate uterus (n = 12), unicornuate uterus (n = 10), didelphys uterus (n = 10); and 20 patients had normal uterine anatomy (control group), with the secretory phase (n = 10) and the proliferative phase (n = 10) of menstrual cycle evaluated. Histological and immunohistochemical studies of the endometrium were carried out according to the standard technique with an assessment of AMHR2 marker expression in the biopsy samples.
 RESULTS: The AMHR2 area expression in the endometrial stroma was significantly lower in patients with septated uterus compared to those with arcuate uterus (р 0.001). The same tendency was noted when compared to other uterine anomalies and healthy controls. AMHR2 expression in the endometrial stroma of patients with arcuate uterus was significantly higher compared to unicornuate uterus (p 0.05).
 CONCLUSIONS: The data obtained suggest that morphofunctional characteristics of the endometrium in patients with uterine anomalies have no specific pathognomonic features. The decline in AMHR2 expression in the endometrial stroma seems to be related to chronic endometritis, as an inverse correlation exists between the AMHR2 area expression and chronic endometritis, compromising pregnancy occurrence.

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