What causes thick uterine wall? Estrogen is to blame

The thick uterine wall in women is an abnormal phenomenon, which is often caused by the action of estrogen. Moreover, thick uterine wall can easily lead to obesity in women, or cause endocrine functional tumors, complex endometrial formation and other hazards.

Estrogen effects

For most women, the thick uterine wall is mostly a temporary phenomenon and mostly appears before ovulation. Experts remind these women that this is a normal physiological phenomenon and usually this symptom disappears after ovulation. The reason why the endometrium becomes thick at this time is mainly because follicles develop in the ovaries during the ovarian cycle. When they mature, under the action of estrogen secreted by the ovaries, the endometrium will gradually thicken.

This phenomenon is to allow the fertilized egg to implant better. In addition, it is also for the better growth of the embryo. Only the thickening of the endometrium can provide good conditions for the embryo. It can also be said that thick endometrium is often a symptom of pregnancy.

1. Obesity: In obese women, androstenedione secreted by the adrenal glands is converted into estrone by aromatase in adipose tissue. The more adipose tissue there is, the stronger the conversion capacity is, and the higher the estrone level in the plasma is, thus causing a persistent estrogen effect.

2. Endocrine functional tumors: Endocrine functional tumors are rare tumors, accounting for 7.5%. The gonadotropin function of the pituitary gland is abnormal, and ovarian granulosa cell tumors are also tumors that continuously secrete estrogen.

3. Simple endometrial hyperplasia: The affected uterus is slightly larger, the endometrium is significantly thickened, and sometimes appears diffusely polyp-like. The amount of curettage material is large and may be mixed with red, smooth, polyp-like tissue. Microscopically, the lesions are diffuse, involving the functional layer and basal layer of the endometrium, and because of the simultaneous proliferation of the stroma and glands, there is no appearance of glandular crowding. The glands vary in size and have smooth contours. The morphology of glandular epithelial cells is similar to that of normal late proliferative phase and has no atypia.

4. Complex endometrial hyperplasia: The etiology of complex hyperplasia is roughly similar to that of simple hyperplasia, but because the lesions are focal, it may also be related to the distribution of hormone receptors in the tissue. A small number of complex hyperplasias may develop into atypical hyperplasia, thus affecting the prognosis. The diseased endometrium can be thickened or very thin, or it can be polyp-like. Unlike simple hyperplasia, the lesion is a focal proliferation of glandular components without involving the stroma. The amount of curettage material can be large or small, and is often mixed with normal, atrophic, or other types of hyperplastic endometrium.