Endometrial Hyperplasia Specialists
CIGC physicians will discuss all options available to ensure you receive the best treatment for your endometrial hyperplasia.
Endometrial Hyperplasia Treatment Options
Endometrial hyperplasia is an overgrowth of the endometrium, the lining of the uterus, that may progress to or coexist with endometrial cancer.
Uterine Hyperplasia and Cancer. Hyperplasia is an overgrowth of the uterine lining that in some cases can develop into uterine cancer.
Types 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:
- Simple without atypia: One percent risk of ovarian cancer
- Complex without atypia: Three percent risk of ovarian cancer
- Simple with atypia: Eight percent risk of ovarian cancer
- Complex with atypia: The most significant type of endometrial hyperplasia
- Twenty-nine percent of cases progress to uterine cancer and 17 to 59 percent of cases have a coexistent uterine cancer
- Alternatively, EIN (endometrial intraepithelial neoplasia) is also used to classify hyperplasia1
Endometrial Hyperplasia Symptoms
Endometrial hyperplasia typically causes abnormal uterine bleeding and most commonly occurs in postmenopausal women.
Additional symptoms include:
- Shorter menstrual cycles (less than 21 days)
- Bleeding during menstrual cycle that is heavier and longer than usual
Endometrial Hyperplasia Causes
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.
Endometrial Hyperplasia Diagnosis
Biopsy 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.
- Polycystic ovary syndrome (PCOS)
- Estrogen therapy without progesterone
- Estrogen-secreting ovarian tumors
- Age 35 or older
- Never having been pregnant
- First period at an early age
- Menopause at an older age
- History of conditions such as diabetes mellitus, gallbladder disease, or thyroid disease
- Cigarette smoking
- Family history of ovarian, colon, or uterine cancer
Endometrial Hyperplasia Treatments
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.
The CIGC Difference
After 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.
Endometrial Hyperplasia FAQs
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.
A hormone “mismatch” means that too much of one hormone is being produced, and not enough of another. Polycystic ovary syndrome is an example of a hormone mismatch or imbalance. As a result, too much estrogen leads to overstimulation of the lining and hyperplasia. The use of hormone therapy can also result in an overstimulation of the lining. Menopausal patients using estrogen-only therapy with the uterus in place can develop hyperplasia. There are many other causes of estrogen imbalance. Whatever the cause, typically abnormal uterine bleeding will occur and needs to be evaluated by your physician.
Endometrial hyperplasia can progress to or coexist with uterine cancer, however there are various stages that lead to cancer development. Hyperplasia can be simple, meaning pathological evaluation of the lining reveals just simple overgrowth. It can also be complex, meaning that the glands are more crowded and complicated. Neither simple nor complex hyperplasia are worrisome, with only a three to five percent incidence of malignancy. However, persistent stimulation of the lining leads to hyperplasia with atypia. Atypia means the cells have developed changes to the nuclei and other parts of the cell that are more consistent with malignancy. Note that 30 to 40 percent of patients with complex atypical hyperplasia actually have cancer in the uterus when that diagnosis is made. Eventually, uterine cancer can occur at a high rate over time from atypical hyperplasia with continued estrogen stimulation.
The main symptom is bleeding. In premenopausal patients, hyperplasia can lead to heavy bleeding during the period with clots, or irregular or prolonged bleeding. Bleeding can also occur between periods, called irregular bleeding. In menopausal patients, any bleeding is of concern regardless of how light or heavy. Postmenopausal bleeding needs to be further evaluated with a biopsy of the uterine lining.
The diagnosis of endometrial hyperplasia often includes an endometrial biopsy or hysteroscopy and biopsy. Endometrial biopsy is an office procedure, and is relatively sensitive, meaning the results obtained are accurate, but not as accurate as hysteroscopy. Hysteroscopy and biopsy is a more accurate test, in that the entire lining of the uterus can be evaluated with a camera and light, and areas that are more suspicious can be seen and biopsied. Whereas an endometrial biopsy is a “blind” procedure, hysteroscopy allows for an increased specificity for diagnosing uterine hyperplasia and malignancy. In patients with persistent bleeding and repeat negative endometrial biopsies, a hysteroscopy and biopsy may be recommended.
Hyperplasia treatment depends on the type of hyperplasia and whether the patient desires to preserve the uterus for fertility. Patients with non-atypical hyperplasia who desire fertility can usually be treated with hormone therapy with resolution of the condition. It does not matter whether the hyperplasia is simple of complex — as long as there is no atypia present, the use of progesterone in many different forms will treat the condition. Oral pills, injections, and IUDs are examples of progesterone therapy. Atypical hyperplasia is more worrisome since there is a higher incidence of malignancy. For patients with atypia who are not interested in future childbearing, hysterectomy is usually recommended. This should be performed laparoscopically, and does not need to be performed as an open or robotic procedure. CIGC surgeons make laparoscopic hysterectomy a very easy procedure for patients to recover from, usually only requiring a seven-day recovery time back to work, thereby allowing for a very reasonable treatment option.
After extensive counseling, if fertility is desired, then a trial of higher dose progesterone therapy is usually given to treat the atypical hyperplasia, followed by suppressive therapy to prevent its return. This process can be long and involves multiple biopsies of the uterus as well as ultrasounds. If, after several biopsies, it appears that the hyperplasia with atypia has resolved, pregnancy can be initiated with close follow-up required. Atypical hyperplasia has a 30 to 40 percent incidence of malignancy when it is diagnosed. This means that the diagnosis is atypical hyperplasia, but up to 40 percent of patients will actually have cancer in the uterus. This means that out of 100 patients with a diagnosis of atypical hyperplasia, 40 will have cancer. For these reasons, the issue of fertility needs to be clearly defined.
Simple or complex hyperplasia without atypia can be treated with hysterectomy if medical therapy does not resolve the condition and the patient does not require fertility. Laparoscopic hysterectomy should always be performed. DualPortGYN hysterectomy, for example, results in a much faster recovery with less complications that either open or robotic procedures, and becomes an excellent option for recurrent non-atypical hyperplasia. For atypical hyperplasia, hysterectomy — sometimes with node dissection — is recommended since there is a much higher chance that malignancy may be present.
Ready for a Consultation
If 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.
1 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.