Pathophysiology

A. Simple hyperplasia without atypia is least likely to progress to endometrial carcinoma, whereas complex hyperplasia with atypia is most likely to progress to carcinoma. The presence of nuclear atypia is the most worrisome finding. Progression to endometrial carcinoma was more than tenfold higher in women with atypical hyperplasia (simple or complex) than in women with no atypia (23 and 1.6 percent, respectively). Approximately 25 percent of women with atypical hyperplasia have coexistent endometrial cancer.

B. Risk factors for endometrial hyperplasia are the same as those for endometrial cancer. The risk for both disorders is increased tenfold in women who use unopposed estrogen-replacement therapy.

Risk factors for Endometrial Cancer

Risk factor

Relative risk (RR)

Increasing age Unopposed estrogen therapy

Late menopause (after age 55)

Nulliparity

Polycystic ovary syndrome (chronic anovulation) Obesity Diabetes

3

Hereditary nonpolyposis colorectal cancer Tamoxifen

22-50 percent lifetime risk 2/1000

Early menarche Estrogen secreting tumor Family history of endometrial, ovarian, breast, or colon cancer

NA NA NA

C. Etiology. Exposure of the endometrium to continuous estrogen unopposed by progesterone can lead to endometrial hyperplasia.

1. Endogenous estrogen. One source of endogenous unopposed estrogen is chronic anovulation is associated with polycystic ovary syndrome (PCOS) and the perimenopausal period. Secretion of excessive estradiol from an ovarian tumor (eg, granulosa cell tumor) may also result in endometrial hyperplasia.

2. Exogenous estrogen. Continuous exposure to unopposed estrogen results in endometrial hyperplasia.

II. Clinical manifestations. Endometrial hyperplasia should be suspected in women with heavy, prolonged, frequent, or irregular uterine bleeding. Abnormal uterine bleeding in perimenopausal or menopausal women is the most common clinical symptom of endometrial neoplasia, although such bleeding is usually (80 percent) due to a benign condition.

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