Endometrial hyperplasia is an overgrowth of the endometrium, the lining of the uterus, that may progress to or coexist with endometrial cancer. In general, estrogen causes stimulation or growth of the lining, while progesterone — the anti-estrogen hormone — causes the uterine lining to shed, resulting in a menstrual period. “Unopposed” estrogen stimulation leads to hyperplasia. Unopposed means that estrogen only is acting on the lining, either because there is no progesterone, or too little progesterone to shed the lining.
Back to TopTypes of endometrial hyperplasia differ based on the characteristics of the cells found in the biopsy sample. It is important to identify the type of hyperplasia because some patients will have a significant risk of coexistent uterine cancer.
Types of endometrial hyperplasia include:
Twenty-nine percent of Complex Hyperplasia with atypia cases progress to uterine cancer and 17 to 59 percent of cases have a coexistent uterine cancer
Endometrial hyperplasia typically causes abnormal uterine bleeding and most commonly occurs in postmenopausal women.
Additional symptoms include:
Causes of endometrial hyperplasia can either be too much estrogen or not enough progesterone. Estrogen and progesterone are hormones secreted by the ovaries that control the growth and shedding of the uterine lining. Estrogen causes the growth of the uterine lining and progesterone counterbalances this growth. Long-term unopposed estrogen production causes overgrowth of the uterine lining and results in endometrial hyperplasia. The absence of progesterone production is caused by the absence of ovulation.
Back to TopBiopsy of the uterine lining is the definitive test for the diagnosis of hyperplasia. Women with abnormal bleeding should be evaluated with a pelvic ultrasound. In postmenopausal women, the ultrasound is used to assess the thickness of the lining. Lining thickness of greater than 4 mm is suspicious for hyperplasia or malignancy. Biopsy can be performed in the office or in the operating room using anesthesia.
Types of Biopsy
An office biopsy without hysteroscopy is considered a blind biopsy. A thin plastic tube is inserted into the uterus, and a small sample of the lining is obtained. This procedure is performed without anesthesia and can cause significant discomfort. In some cases, an adequate amount of sample cannot be obtained, and a different procedure needs to be performed. The benefit of this procedure is that it is very fast and does not require preparation or special equipment.
Office biopsy with hysteroscopy involves a thin camera being guided into the uterine cavity and a small biopsy obtained. A numbing injection to the cervix is used to decrease discomfort. The benefit of this procedure is that the entire cavity is visualized with the camera and the likelihood of insufficient sample is less than with the blind biopsy. This procedure does require special equipment and may require premedication to decrease the discomfort.
Hysteroscopy with Dilation and Curettage (D&C) is performed in the operating room under anesthesia. A scraping of the uterine lining (curettage) is performed with a special instrument. Since discomfort is not an issue, the majority of the thickened lining can be removed and a large sample of the lining obtained for analysis.
Back to TopRisk factors for endometrial hyperplasia include2:
Endometrial hyperplasia treatment depends on the type of hyperplasia and whether the patient desires to preserve the uterus for fertility. Hysterectomy (removal of the uterus) is recommended for patients who are postmenopausal or patients who have completed childbearing.
Nonsurgical Treatments for Hyperplasia without Atypia
Progesterone therapy is a potential endometrial hyperplasia treatment option for patients without atypia. Oral progesterone, Depo-Provera (injection), or an Intrauterine Device (IUD) are all possible treatment options. Progesterone counteracts the effects of estrogen and thins the uterine lining. Endometrial sampling after the progesterone treatment should be used to assess resolution. Resolution of hyperplasia occurs in almost 80 percent of cases. If hyperplasia persists or atypia develops, hysterectomy should be the next step.
Nonsurgical Treatments for Hyperplasia with Atypia2,3
If the tissue biopsy was obtained in the office, a D&C should be performed to confirm the absence of cancer before considering nonsurgical treatment. High-dose oral progesterone therapy (Megace) should only be offered to women who have not completed childbearing or women who cannot undergo surgery for medical reasons. Side effects of high dose progesterone include increased appetite and weight gain. Three months after the initiation of treatment, a D&C is performed to evaluate the response to treatment. If hyperplasia is still present, the dose of progesterone is increased and another D&C is performed in three months.
Progesterone treatment is considered ineffective if hyperplasia persists after nine months, and then a hysterectomy should be considered. If hyperplasia resolves, the patient should proceed with childbearing as soon as possible. If childbearing is delayed, maintenance progesterone therapy and endometrial biopsy every six to 12 months is recommended.
Surgical Treatment for Endometrial Hyperplasia with Atypia2,4
Partial hysterectomy (removal of the uterus and cervix) is the treatment of choice for hyperplasia with atypia in patients who have completed childbearing. Supracervical hysterectomy should not be performed because the abnormal uterine cells can be present in the cervix.
Removal of bilateral tubes and ovaries should be performed in postmenopausal women. Five percent of postmenopausal women with uterine cancers have cancer cells in the ovaries. Since 17 to 59 percent of complex hyperplasia with atypia cases are coexistent with cancer, removal of the ovaries is necessary.
In premenopausal women, the decision to remove the ovaries at the time of the hysterectomy is more difficult. Twenty-five percent of uterine cancers in premenopausal women have cancer cells in the ovaries. In some cases, it is reasonable to remove the uterus only and wait for the final pathology to identify whether the uterus contains cancer. If cancer is found, a second surgery will be required to remove the ovaries.
Post Surgery Follow-Up
If the pathology evaluation of the uterus confirms hyperplasia only and no uterine cancer, no further follow-up is required. Estrogen replacement therapy is not contraindicated in women with hyperplasia after the removal of the uterus.
Back to TopAfter receiving an endometrial hyperplasia diagnosis, it is important to find a physician who will discuss all of the options available to you.
Physicians at The Center for Innovative GYN Care® (CIGC®) are specialists in minimally invasive GYN surgery. Patients diagnosed with hyperplasia without atypia who require nonsurgical treatments are offered the best medical solutions available. They are handled with the same advanced and focused care as those patients diagnosed with hyperplasia with atypia who require surgery.
CIGC physicians are laparoscopic surgical specialists who have dedicated their careers to the performance of minimally invasive GYN care. Additionally, our commitment to gynecological surgery means that we have worked on a higher volume of cases, more difficult cases, and use advanced techniques and procedures learned during extensive training sessions. We strive to complete even the most complex surgeries with low complication rates.
If you do require a hysterectomy for endometrial hyperplasia, you should know that GYN care is the sole medicine practiced by CIGC surgical specialists. We partner with OBGYNs to ensure patients have the best possible care. Increased surgical volume is important to develop and maintain surgical expertise.
CIGC surgeons do not perform open hysterectomies on patients with endometrial hyperplasia. Open surgeries are known to be painful, have a relatively high risk of complications, and have an extended recovery period. CIGC surgeons also do not perform robotic surgeries. Surgeries in which robotic technology performs the procedure are extremely expensive and have a high risk of complications.
Specialists Not OBGYNs
Your OBGYN may be a good doctor, but an OBGYN is a generalist, not a surgical specialist. The majority of the practice of an OBGYN is dedicated to obstetrics care, so your doctor does not get nearly enough patient volume or practice to learn the best surgical techniques. The average OBGYN performs only 10 to 15 hysterectomies per year, while our surgeons average 400 per year. Since a heavy surgical volume is necessary to develop and maintain surgical expertise, it is easy to see why you should see a CIGC surgeon for endometrial hyperplasia surgery.
At CIGC, our endometrial hyperplasia surgeons perform a higher volume of cases, see a wider range of case types, and undergo comprehensive training in advanced laparoscopic techniques. Whether you are undergoing a definitive surgery or a conservative surgery for your endometrial hyperplasia, when you have it done at CIGC, you know you are working with specialists who concentrate only on this type of procedure.
Using the advanced DualPortGYN® technique, CIGC procedures leave you with minimal cosmetic scarring, a shorter recovery period of only a few days, and a lower risk of complications.
Back to TopIf you think you have endometrial hyperplasia, our specialists are ready to provide an evaluation of your symptoms and condition(s) and recommend an appropriate solution.
Back to Top1 Mutter GL. Endometrial intraepithelial neoplasia (EIN): will it bring order to chaos? The Endometrial Collaborative Group. Gynecol Oncol. 2000;76:287–290.
2 Armstrong A, Hurd W, Elguero S. Diagnosis and management of endometrial hyperplasia. J Minim Invasive Gynecol. 2012 Sept-Oct;19(5):562-71.
3 Byun JM, Jeong DH, Kim YN, et al. Endometrial cancer arising from atypical complex hyperplasia: The significance in an endometrial biopsy and a diagnostic challenge. Obstet Gynecol Sci. 2015;58(6):468–474.
4 Reed SD, Newton KM, Garcia RL, et al. Complex hyperplasia with and without atypia: clinical outcomes and implications of progestin therapy. Obstet Gynecol. 2010;116(2 Pt 1):365–373.
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