Endometrial hyperplastic process (EHP) is non-cyclical proliferation of endometrial glands with a predominance of the glandular component over the stromal [WHO Classification of Tumours of Female Reproductive Organs. 4th ed. (Lyon): IARC; 2014].
EHP is characterized by a high prevalence in the structure of gynecological morbidity, poses the risk of malignancy and development of endometrial cancer.
WHO classification of EHP [WHO Classification of Tumours of Female Reproductive Organs, 2014]: hyperplasia without atypia and atypical endomet-rial hyperplasia.
Symptoms and diagnostics. The clinical presentation of endometrial hyperplasia is non-specific and most often manifests with abnormal uterine bleeding.
Ultrasound is an effective tool for the first stage of EHP diagnostics (fig. 8.1). The conventional ultrasound risk limit for excluding endometrial cancer is 3-4 mm, that is, the probability of cancer is reduced to 1% if the thickness of the endometrium is less than this value. However, it should be kept in mind that the thickness of the normal and pathological endometrium on ultrasound may have identical parameters.
The final diagnosis of EHP is based on a morphological examination of the biopsy sample, which is usually obtained by aspiration biopsy, less often by uterine curettage.
Hysteroscopy is able to detect local endometrial pathological processes, such as polyps that were missed during aspiration biopsy. Hysteroscopy has a greater diagnostic value in detecting endometrial cancer than endometrial hyperplasia.
The use of CT or MRI in establishing EHP diagnosis is impractical.
Fig. 8.1. Ultrasound image of endometrial hyperplasia (endometrial thickness 19 mm)
Pathogenesis. EHP develops in case of excessive estrogen effect on the endometrium and in the absence of compensatory effect of progesterone. In addition to estrogenic stimulation of the endometrium, immunosuppression and infection, suppression of apoptosis, increased proliferation and neoangio-genesis may be a significant factor in EHP development.