HYPERPLASIA (overgrowth of the endometrium).
Endometrial hyperplasia occurs when there is an
imbalance between estrogens and PROGESTERONEin
the woman’s BLOODcirculation. Researchers do not
know what sets the stage for this imbalance. Ele-
vated estrogens cause the endometrium to thicken
and engorge with blood, and diminished proges-
terone fails to initiate adequate sloughing of the
endometrial tissue (such as during MENSTRUATION).
The tissue continues to accumulate, and over time
its cells become abnormal.
Symptoms and Diagnostic Path
Because endometrial cancer usually develops later
in life, its symptoms sometimes blend with those
of MENOPAUSE. Because of this a doctor should
evaluate symptoms that persist, even when the
symptoms do not seem especially serious. Early
symptoms of endometrial cancer include
- unusually long or severe menstrual periods
- spotting or bleeding between menstrual periods
- watery, blood-tinged vaginal discharge
- PAINduring SEXUAL INTERCOURSE
- pelvic or lower abdominal pain
The diagnostic path includes a comprehensive
medical examination with PELVIC EXAMINATION, dur-
ing which the doctor often can palpate (feel) a
growth within the uterus or detect abnormalities
in the uterus’s size or shape. Diagnostic imaging
procedures such as COMPUTED TOMOGRAPHY (CT)
SCANor ULTRASOUNDmay provide further informa-
tion. However, only endometrial biopsy can pro-
vide a certain diagnosis. The doctor may obtain a
tissue sample for biopsy by inserting a narrow
catheter through the VAGINAand CERVIXinto the
uterus and aspirating (suctioning) cells from the
endometrium. HYSTEROSCOPYor the surgical OPERA-
TION DILATION AND CURETTAGE(D&C) may also provide
endometrial cells for pathology analysis.
When confirming the diagnosis, the pathologist
assigns a grade and stage to the cancer that char-
acterize its aggressiveness and the extent to which
it has grown or metastasized (spread to other loca-
tions in the body). Additional pathology tests
determine whether the cancer cells have estrogen
receptors (are estrogen positive). CANCER STAGING
AND GRADINGand estrogen reception provide guid-
ance for CANCER TREATMENT OPTIONS AND DECISIONS.Treatment Options and Outlook
TotalHYSTERECTOMY, a surgical operation to remove
the uterus and cervix, is nearly always the first
treatment of choice for stage 0, 1, and 2 endome-
trial cancers. Women who have stage 1 or stage 2
endometrial cancer subsequently undergo adju-
vant (follow-up) treatment such as HORMONE THER-
APYor RADIATION THERAPY. Very early endometrial
cancer (stage 0, also called carcinoma in situ, and
stage 1) is nearly always curable.
For stage 3 and 4 endometrial cancer, the first
treatment of choice is radiation therapy to shrink
the cancer, with follow-up surgery and hormonal
therapy (stage 3) or hormonal therapy alone.
Surgery may be total hysterectomy with salpingo-
oophorectomy (removal of the uterus, cervix, FAL-
LOPIAN TUBES, and OVARIES) or radical hysterectomy
(removal of all the organs of reproduction, the fatty
layer covering them called the omentum, and
nearby LY M P Hnodes). Radiation therapy may be
external beam (targeted at the pelvis from a
machine outside the body) or brachytherapy
(implanted radioactive pellets). Though other treat-
ment options are more effective for stage 0, 1, and
2 endometrial cancers, combination CHEMOTHERAPY
becomes a treatment option for metastasized
endometrial cancer (stage 3 and stage 4).
Most endometrial cancers are hormone sensi-
tive. Hormonal therapy, such as progestins or
estrogen antagonists, effectively shrinks cancer
tumors in women by depriving their cells of the
hormones they need to thrive. Progestin causes
endometrial atrophy (shrinkage of the endo-
metrium) and is an option for younger women
with stage 0 or stage 1 endometrial cancer who
wish to preserve their FERTILITY. Among the estro-
gen antagonists currently available are aromatase
inhibitors and tamoxifen; these therapies require
the cessation of ovarian function. Most women
who have stage 2 and more advanced endometrial
cancer undergo oophorectomy (surgical removal
of the ovaries). Aromatase inhibitors block the
conversion of TESTOSTERONEto estrogen in adipose
(fat) cells throughout the body, the primary means
of estrogen production in a woman’s body after
MENOPAUSE.274 The Reproductive System