Endometrial hyperplasia occurs in both pre- and postmenopausal women, but is most common in women in their early 50s, during perimenopause. The diagnosis is rare in women younger than 30. Endometrial hyperplasia diagnosed after age 60 is more likely to be EIN.
Abnormal uterine bleeding or postmenopausal bleeding is the only symptom for the vast majority of patients.
Most risk factors for endometrial hyperplasia are conditions that expose the uterus to sustained estrogen without opposing progesterone. As such, obesity, polycystic ovarian syndrome (PCOS), anovulation, nulliparity, tamoxifen use, estrogen therapy without progesterone, and early menarche or late menopause are all well-defined risk factors for endometrial hyperplasia.
There are genetic syndromes that predispose women to endometrial hyperplasia, particularly Lynch syndrome (hereditary nonpolyposis colorectal cancer), which should be suspected when a woman has a family history of endometrial, colorectal, ovarian, intestinal, or renal cancers.
Nearly 40% of women diagnosed with EIN will be found to have endometrial adenocarcinoma at the time of hysterectomy. Of women diagnosed with endometrial hyperplasia who subsequently develop endometrial adenocarcinoma, time to progression is usually between 2.5 and 6 years, depending on the degree of histologic derangement.
There are 2 major systems for classifying endometrial hyperplasia, and pathologists may report results using either.
1) EIN schema (preferred, but less commonly used):
- Benign endometrial hyperplasia (benign)
- EIN (precancerous)
- Hyperplasia without atypia (benign)
- Atypical hyperplasia (precancerous)
