Endometrial hyperplasia is an overgrowth or thickening of part or all of the lining of the uterus.
Hyperplasia usually develops in the presence of continuous estrogen stimulation unopposed by progesterone. During adolescence and in the years before menopause women may have numerous cycles without ovulation during which there is continuous unopposed estrogen activity. Similarly, hormone replacement therapy consisting of estrogen without progesterone may lead to endometrial hyperplasia.
Diagnosis can only be made by a pathologist who examines a sample of tissue removed from the thickened lining by a sampling procedure such as endometrial biopsy or dilatation and curettage (D&C). By microscopic exam it can be determined if hyperplasia with or without atypical cells is present.
Conventional medicine uses progestins such as Provera, given continuously, either by mouth or long acting injections. A D&C is repeated after 3-4 months of treatment to demonstrate resolution of the hyperplasia. Failure of hyperplasia without atypia to resolve in a repeat D&C is cause for alarm.
Endometrial hyperplasia is currently the reason for 5% of all hysterectomies performed in the U.S.
Hyperplasia without atypia may resolve spontaneously or following a D&C. On the other hand, hyperplasia with atypia tends to persist (in 75% of cases) even after multiple D&Cs and hormone treatment.
Hyperplasia without atypia rarely progresses to endometrial cancer while hyperplasia with atypia is a precancerous condition that may progress to overt malignancy.
Endometrial hyperplasia usually occurs after menopause, when ovulation stops and progesterone is no longer made.
The addition of progesterone or resumption of ovulation (which produces progesterone) can eliminate the hyperplasia.
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