The endometrium is the mucosal lining of the uterus, a dynamic tissue that prepares monthly for the possibility of pregnancy. When this lining becomes too thick, the condition is commonly referred to as endometrial hyperplasia or, more simply, thickened endometrium. This cellular overgrowth is a medical finding that requires professional evaluation because it can be associated with an increased risk of uterine health concerns. While the term may sound alarming, a thickened endometrium is frequently benign and treatable, but it serves as an important signal for further investigation.
The Endometrial Lining and Normal Cyclical Changes
The endometrium constantly changes throughout the reproductive years in response to fluctuating hormone levels. The menstrual cycle is divided into two primary phases that dictate the lining’s thickness. During the proliferative phase, estrogen stimulates the growth of the endometrial tissue, causing it to thicken in preparation for a potential fertilized egg.
Following ovulation, the secretory phase begins, where progesterone is released, maturing the lining and stabilizing its structure. If pregnancy does not occur, the levels of both hormones drop, triggering the shedding of the functional layer of the endometrium, which is menstruation.
For example, in pre-menopausal women, the thickness can range from 5 millimeters (mm) during the early proliferative phase to as much as 16 mm during the secretory phase. In contrast, for post-menopausal women not taking hormone replacement therapy, a thickness of 5 mm or less is considered the expected range. Any measurement exceeding this threshold in a post-menopausal person warrants closer medical attention.
Primary Causes of Endometrial Thickening
The primary underlying cause of endometrial thickening is chronic, uninterrupted stimulation by the hormone estrogen, often without the balancing effect of progesterone. This hormonal imbalance, known as unopposed estrogen, drives the continuous growth of endometrial cells.
Conditions that disrupt regular ovulation are a frequent cause of this imbalance because ovulation is necessary for progesterone production. Polycystic Ovary Syndrome (PCOS), which often involves anovulation, leads to prolonged estrogen exposure and is a known risk factor for developing hyperplasia. Obesity is also a contributing factor, as fat tissue produces its own form of estrogen (estrone), which leads to excessive stimulation of the uterine lining.
Certain medical treatments can also cause the endometrium to thicken. Hormone replacement therapy (HRT) that provides estrogen without adequate progesterone supplementation can directly lead to hyperplasia. Tamoxifen, a medication used in the treatment of breast cancer, acts like a weak estrogen on the uterus, which can also result in significant endometrial thickening.
Recognizing Symptoms and Diagnostic Procedures
The most common symptom that prompts an evaluation for thickened endometrium is Abnormal Uterine Bleeding (AUB). For pre-menopausal women, this manifests as periods that are heavier, more frequent, or longer lasting than usual, or bleeding between cycles. In post-menopausal women, any vaginal bleeding or spotting must be investigated immediately, as it is the most frequent sign of a potentially concerning endometrial change.
The initial step in diagnosis is typically a Transvaginal Ultrasound (TVUS), which uses sound waves to measure the exact thickness of the endometrial lining. While this measurement provides a strong indication of a potential problem, especially in post-menopausal individuals, it cannot determine the cellular composition of the tissue. If the TVUS shows a concerning thickness, further diagnostic steps are often necessary.
Advanced Diagnostic Procedures
A Saline Infusion Sonography (SIS), also called a sonohysterogram, involves injecting sterile saline fluid into the uterus during a TVUS. The saline distends the uterine cavity, allowing for clearer visualization of the lining and helping to distinguish between diffuse thickening and focal lesions like polyps or fibroids.
The definitive diagnostic tool is the Endometrial Biopsy, where a small tissue sample is collected and sent to a lab for microscopic examination. This procedure provides a clear cellular diagnosis, determining whether the thickening is benign or if it involves abnormal cells.
Understanding Hyperplasia, Cancer Risk, and Treatment Options
The microscopic analysis of the endometrial biopsy classifies the tissue into distinct categories, which dictates the level of concern and subsequent treatment plan. The simplest form is benign endometrial thickening, which can resolve spontaneously or with minimal intervention.
The classification system differentiates between hyperplasia without atypia and hyperplasia with atypia, with the latter carrying a higher risk of progression to cancer. Hyperplasia without atypia rarely progresses to cancer and is most often managed conservatively with hormone therapy. Atypical hyperplasia, which involves abnormal-looking cells, is considered a precancerous condition, with a significant percentage of cases potentially leading to endometrial carcinoma if left untreated.
The management of hyperplasia without atypia typically involves medical treatment with progestin therapy, which reverses the effects of unopposed estrogen. This can be administered orally or locally via a hormonal intrauterine device. For atypical hyperplasia, treatment options are more aggressive, ranging from high-dose progestin therapy with close monitoring (for those preserving fertility) to a hysterectomy, which surgically removes the uterus and eliminates the cancer risk entirely.