[Immunohistochemical study of the expression of receptors to steroid hormones in endometrial hyperplastic processes].
We examined 39 women with normal endometrium and 139 women with glandular-cystic hyperplasia of the endometrium (without atypia). According to clinical manifestations of hyperplasia, the patients were divided into 3 groups: 74 (53%) had reestablishing menstrual function after total curettage (group 1); 42 patients (30%) with glandular-cystic hyperplasia after curettage and hormonal therapy with progesterone and synthetic progestins (duration 3 to 6 months) had no repeated pathology of the endometrium (group 2); endometrial hyperplasia recurred 2 and 3 times as showed biopsies during 2-5 years of observation in 23 (17%) women (group 3). Immunohistochemical tests of normal endometrium revealed correlations between stages of menstrual cycle and steroid hormone receptors in nuclei of glandular epithelium and stromal cells. Maximum sensitivity of glandular epithelium to estrogen and pronounced expression of estrogenic receptors were observed at middle and late stages of proliferation. High sensitivity of glandular epithelium to progesterone was registered at middle and late stages of proliferation and early stage of secretion. Two types of hormone receptor expression were observed. Type 1 typical for the endometrium of middle and late stage of proliferation was characterised by a high content of receptors to E2 and P in glandular epithelium and stromal cells. Type 2 was observed in patients with recurring glandular hyperplasia and was characterised by a mosaic picture up to complete absence of receptor expression in nuclei of some glands and stromal cells. The detected zones free of receptors to estrogens and progesterone evidence for local disturbance of a regulating role of signal pathways of sexual steroids and can serve a substrate for formation of tissue autonomy.
Lysenko
O N
ON
State Medical University of Russia, 117198, Moscow.
Ashkhab
M Kh
MKh
Strizhova
N V
NV
Babichenko
I I
II
D000328:Adult; D002455:Cell Division; D004714:Endometrial Hyperplasia / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D004717:Endometrium / Q000378:metabolism; D004967:Estrogens / Q000378:metabolism*; D005260:Female; D005500:Follow-Up Studies; D020249:Hormone Replacement Therapy; D006801:Humans; D006965:Hyperplasia / Q000473:pathology; D007150:Immunohistochemistry; D008597:Menstrual Cycle; D008875:Middle Aged; D011374:Progesterone / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000276:immunology / Q000378:metabolism; D011980:Receptors, Progesterone / Q000276:immunology / Q000378:metabolism; D011987:Receptors, Steroid / Q000276:immunology / Q000378:metabolism*
D004967:Estrogens; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D011987:Receptors, Steroid; D011374:Progesterone