A proliferative endometrium is a descriptive term for the state of the tissue lining the inside of the uterus. The endometrium’s primary function is to prepare for the implantation of a fertilized egg each month. The word “proliferative” indicates that the cells of this lining are actively multiplying and growing. A diagnosis can describe a normal, healthy phase of the menstrual cycle or point toward a condition involving excessive, abnormal cell growth. The distinction determines whether this finding is a sign of normal reproductive health or a pathology.
The Normal Menstrual Cycle and the Proliferative Phase
The proliferative phase represents the first stage of endometrial preparation in the menstrual cycle, immediately following the shedding of the previous lining during menstruation. This phase is also known as the follicular phase. It typically spans from day five until ovulation, lasting approximately 14 to 18 days.
The process is driven by the hormone estrogen, released by the developing follicles in the ovaries. Estrogen stimulates the cells of the endometrium to multiply, causing the uterine lining to thicken. The endometrium regenerates from its basal layer during this time.
This growth is necessary to create a thick, highly vascularized tissue suitable to host a potential pregnancy. The lining typically grows from about 4.5 millimeters to a thickness of up to 10 millimeters by the time of ovulation. The term “proliferative endometrium” on a pathology report for a premenopausal woman is usually an expected finding, confirming that the hormonal cycle is proceeding normally.
Understanding Endometrial Hyperplasia
The term “proliferative” becomes concerning when the cell growth is excessive or uncontrolled, a condition known as endometrial hyperplasia. This occurs when the endometrium is exposed to continuous, unopposed estrogen without the balancing effect of the hormone progesterone. Without progesterone to signal maturation and eventual shedding, the cells continue to proliferate, leading to an abnormally thickened lining.
Endometrial hyperplasia is not cancer, but it is considered a precancerous condition. The risk it poses is stratified based on the microscopic appearance of the cells, specifically the presence of cellular atypia. The World Health Organization classifies the condition into two main categories: hyperplasia without atypia and atypical hyperplasia.
Hyperplasia without atypia involves an overgrowth of cells that appear essentially normal and has a low risk of progressing to cancer, estimated at less than 5% over 20 years. Conversely, atypical hyperplasia, also called endometrial intraepithelial neoplasia, features cells that look and act abnormally. This form carries a much higher risk, with progression to endometrial cancer ranging from 20% to 50% if left untreated. Up to 42% of women diagnosed with atypical hyperplasia are found to already have coexisting endometrial cancer when the uterus is surgically removed.
Evaluation and Management of Abnormal Proliferation
The suspicion of abnormal proliferation, often due to symptoms like abnormal or heavy uterine bleeding, triggers a diagnostic workup. The first step involves a transvaginal ultrasound, which measures the thickness of the endometrial lining. This imaging is followed by a procedure to obtain a tissue sample for definitive diagnosis.
Diagnosis requires histological examination of the tissue, usually obtained through an outpatient endometrial biopsy or a hysteroscopy with dilation and curettage. Hysteroscopy allows for direct visualization of the uterine cavity and is often used when an office biopsy is inconclusive or to evaluate a focal lesion.
Management is dictated by the presence of cellular atypia and the patient’s desire for future fertility. For hyperplasia without atypia, treatment involves hormonal therapy using progestins, which can be administered orally or delivered directly to the uterus via a levonorgestrel-releasing intrauterine system (LNG-IUS). Progestin treatment aims to reverse the effects of unopposed estrogen, with a high success rate in resolving the hyperplasia.
For patients with atypical hyperplasia, especially those who have completed childbearing, the preferred treatment is a hysterectomy to eliminate the risk of cancer. If fertility preservation is desired, conservative management with high-dose progestin therapy is an option, but it requires rigorous and frequent monitoring with follow-up endometrial biopsies to confirm regression.