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Endometrial hyperplasia

1 What causes endometrial hyperplasia?

Endometrial hyperplasia most often is caused by excess estrogen without progesterone. If ovulation does not occur, progesterone is not made, and the lining is not shed. The endometrium may continue to grow in response to estrogen. The cells that make up the lining may crowd together and may become abnormal. This condition, called hyperplasia, may lead to cancer in some women.
 

When does endometrial hyperplasia occur?

Endometrial hyperplasia usually occurs after menopause, when ovulation stops and progesterone is no longer made. It also can occur during perimenopause, when ovulation may not occur regularly. Listed as follows are other situations in which women may have high levels of estrogen and not enough progesterone:

·         Use of medications that act like estrogen

·         Long-term use of high doses of estrogen after menopause (in women who have not had a hysterectomy)

·         Irregular menstrual periods, especially associated with polycystic ovary syndrome or infertility

·         Obesity

·         Most cases of endometrial hyperplasia are benign, or noncancerous. Because of the associated hormonal changes, this condition is most common among women who are nearing menopause or have reached menopause. Endometrial hyperplasia may also occur because of chronic disorders, such as diabetes, obesity, or polycystic ovarian syndrome.

·         Symptoms of endometrial hyperplasia include abnormal vaginal bleeding, including bleeding or spotting between menstrual periods, dramatic changes in the duration of menstrual periods, postmenopausal bleeding, or heavier menstrual blood flow. In some instances, endometrial hyperplasia may precede cancer of the uterus. Menstruating women with endometrial hyperplasia also have a risk for developing anemia (low red blood cell count).

 Treatment:
1. Progesterone

2. Drugs to decrease bleeding

3. Estrogen Progesterone combination therapy

4. Progesterone Receptor Modulator With Primarily Antagonistic Properties It binds strongly to endometrial progesterone receptors, minimally to estrogen receptors and upregulates androgen receptors. In a placebo controlled trial low dose mifepristone  has been shown to decrease fibroid size as well as symptoms as decrease in size ans bleeding and in mst cases need for surgery is avoided. Reduction in size with mifepristone might be due to the direct effect in reducing number of progesterone receptors. Besides, because of ovarian acyclicity seen with mifepristone, hormonal milieu similar to early follicular phase may also inhibit steroid dependent growth of myoma. Increase in androgen receptors also contributes to antiproliferative effects. Mifepristone also delays or inhibits ovulation, which may produce amenorrhoea. Direct suppressive effects on endometrial vasculature as well as on reducing stromal vascular endothelial growth factor (VEGF) has also been suggested for reducing menstrual blood loss.Mifepristone, on the other hand, is administered orally, has a few side effects and is less expensive than GnRH analogues.

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