Endometrial hyperplasia occurs when the endometrium, the lining of the uterus, becomes too thick. It is not cancer, but in some cases, it can lead to cancer of the uterus. It is best considered a “pre-cancer” at this stage.
It can be classified as simple or complex, which refers to how abnormal the tissue look under a microscope.
Endometrial hyperplasia most often is caused by excess estrogen without 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. If ovulation from the ovaries each month does not occur, progesterone is not made, and the lining is not shed. The endometrium may continue to grow in response to estrogen. The cells that make up the lining may crowd together and may become abnormal. This condition, called hyperplasia, may lead to cancer in some women.
Endometrial hyperplasia usually occurs after menopause, when ovulation stops and progesterone is no longer made. It also can occur during peri-menopause, when ovulation may not occur regularly. Sometimes it occurs in younger women, particularly in those who have polycystic ovarian syndrome.
Endometrial hyperplasia is more likely to occur in women with the following risk factors:
- Age older than 35 years
- Never having been pregnant or used the oral contraceptive pill
- Personal history of certain conditions, such as diabetes mellitus, polycystic ovary syndrome.
- Cigarette smoking
- Family history of ovarian, colon, or uterine cancer
The most common symptom of endometrial hyperplasia is:
- Bleeding during the menstrual period that is heavier or lasts longer than usual
Irregular bleeding around the time before menopause- this should always be investigated and not just put down to “a change in hormones”
- Any bleeding after menopause
- The type of hyperplasia differs based on the characteristics of the cells found in the biopsy sample. It is important to identify the type because some patients will have a significant risk of coexistent uterine cancer.
There are different types of endometrial hyperplasia:
- Simple without atypia: One percent risk of uterine cancer.
- Complex without atypia: Three percent risk of uterine cancer.
- Simple with atypia: Eight percent risk of uterine 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 coexistent uterine cancer at the time of diagnosis.
Endometrial hyperplasia can be seen on a transvaginal ultrasound. Women with abnormal bleeding should initially be evaluated with a transvaginal ultrasound. In post-menopausal women, the ultrasound is used to assess the thickness of the lining. Lining thickness of greater than four mm is suspicious for hyperplasia or malignancy and this must be ruled out (other benign conditions, such as polyps, can also cause this appearance). Biopsy of the uterine lining is the definitive test for diagnosis of hyperplasia. The can be done in the rooms via a pipelle biopsy, or via hysteroscopy with D & C under a general aneasthetic.
Progesterone therapy can be used to treat endometrial hyperplasia without atypia. Oral progesterone, Depo Provera (injection) or the MIrena 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.
If you have atypical hyperplasia, especially complex atypical hyperplasia, the risk of cancer is increased. Hysterectomy usually is the best treatment option if you do not want to have any more children. If you are hoping to have children, you may be suitable for a trial of progesterone treatment and if your endometrium responds you may be able to delay having a hysterectomy.
Dr Farrell has extensive experience in managing women with hyperplasia and discussing the best options of investigation and treatment for you.