Table of Contents
Definitin of Endometrial Hyperplasia
An overgrowth of the endometrium, the tissue that lines the uterus. the thickened endometrium fails to slough during menstruation, thus continuing to accumulate. Often menstruation is minimal or intermittent.
Endometrial hyperplasia in which cell DNA remains normal nearly always remains benign (does not become cancerous). Endometrial hyperplasia that consists of both abnormal cells and abnormal cell organization (architecture), though itself benign, is precancerous.
There are four types:
- Simple endometrial hyperplasia (also called cystic glandular or mild hyperplasia) is the earliest stage of endometrial hyperplasia. There is excessive growth of the cells of the endometrium in confined locations though the cells and their architecture (structure and arrangement) are normal. The risk for progression to endometrial cancer is minimal; simple endometrial hyperplasia often resolves (goes away) without treatment.
- Complex endometrial hyperplasia features excessive growth of normal cells with irregular architecture, presenting a somewhat higher, though still relatively low, risk for developing into endometrial cancer without treatment. For most women, doctors recommend treatment with progestin, a synthetic form of progesterone, to halt the actions of estrogen and cause the endometrium to wither and slough. The endometrium generally returns to normal within two or three menstrual cycles.
- Simple endometrial hyperplasia with atypia is a moderate stage of endometrial hyperplasia in which patches of endometrial cells are not only replicating more frequently than normal but have also become abnormal in their DNA (called nuclear atypia). However, the cellular architecture still follows the normal pattern for endometrial tissue. Untreated simple endometrial hyperplasia with atypia progresses to endometrial cancer in about 10 percent of women. Treatment with progestin often resolves the hyperplasia.
- Complex endometrial hyperplasia with atypia is the most serious stage of endometrial hyperplasia. The endometrial cells have abnormal DNA, instructing them to replicate in unstructured and dysfunctional ways. As well, the endometrial tissue that contains the atypical cells is disorganized and erratic. Without treatment, this stage of endometrial hyperplasia progresses to endometrial cancer in a third or more of women. Treatment with progestin usually, though not always, resolves the hyperplasia.
Symptoms and Diagnostic Path
Symptoms of hyperplasia may include bleeding between menstrual periods, anovulatory periods (menstrual cycles without ovulation), heavy or prolonged menstrual periods, and pain during sexual intercourse.
Some women may experience amenorrhea (absence of menstrual periods). Endometrial biopsy, as an independent procedure or after dilatation and curettage (d&c), confirms the diagnosis. Imaging procedures are not usually helpful as they cannot conclusively distinguish between noncancerous and cancerous tumors in the uterus.
Treatment Options and Outlook
In addition to progestin therapy, other treatment options include the surgical operations D&C and hysterectomy. In D&C the surgeon gently scrapes away the overgrown endometrium; in hysterectomy the surgeon removes the uterus.
In most situations, hysterectomy is appropriate only when complex endometrial hyperplasia with atypia recurs after other treatments or when the risk for endometrial cancer is high for other reasons, though women who are past menopause and have persistent symptoms may opt for hysterectomy to permanently end the hyperplasia.
Risk Factors and Preventive Measures
Any circumstance that increases the presence of estrogen in the blood circulation underlies the development of endometrial hyperplasia. The risk for endometrial hyperplasia is highest in women who have anovulatory periods (menstrual cycles without ovulation), who take unopposed estrogen therapy (estrogen alone), or who take long-term tamoxifen to treat breast cancer.
Other factors that increase estrogen within the body are obesity, insulin resistance, and type 2 diabetes. nutritional eating habits that emphasize foods low in fats, especially saturated fats, and daily physical exercise are the key lifestyle measures that reduce the risk for endometrial hyperplasia.
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