Endometrial hyperplasia describes a condition where the lining of the uterus, known as the endometrium, becomes unusually thick. This overgrowth of cells is not cancer, but it can increase the likelihood of developing endometrial cancer, a type of uterine cancer.
Understanding Endometrial Hyperplasia
Endometrial hyperplasia involves an excessive proliferation of the cells that form the inner lining of the uterus. This condition primarily stems from an imbalance of hormones, specifically too much estrogen and insufficient progesterone. Estrogen promotes the growth of the endometrial lining, while progesterone helps to regulate this growth and ensures the lining sheds during menstruation. Without enough progesterone to counteract estrogen’s effects, the endometrium continues to thicken.
Healthcare providers classify endometrial hyperplasia based on the appearance of the cells under a microscope. Hyperplasia without atypia means the cells appear normal, and this type has a very low chance of becoming cancerous. Conversely, hyperplasia with atypia involves abnormal cell changes, which indicates a higher risk of progression to cancer. This type is considered precancerous.
Factors Influencing Progression
The timeline for endometrial hyperplasia to potentially turn into cancer is not fixed and varies considerably among individuals. The presence of atypical cells is the most significant factor, as atypical hyperplasia progresses to cancer much more frequently than non-atypical types. For hyperplasia without atypia, the long-term risk of progression to cancer is typically less than 5%. In contrast, atypical hyperplasia carries a substantial risk, with studies estimating a progression rate to cancer that can range from 20% to 50% if left untreated.
Hormonal imbalances, particularly prolonged exposure to unopposed estrogen, are a primary cause of endometrial hyperplasia and influence its progression. This can occur if the body produces too much estrogen or if there is not enough progesterone to balance it. Age also plays a role, as endometrial hyperplasia is more common in women transitioning to or who have completed menopause, although it can occur in younger individuals. During perimenopause and after menopause, a woman’s body may produce less progesterone, leading to unopposed estrogen effects.
Obesity is another significant factor because fat cells can produce estrogen, leading to elevated levels that stimulate endometrial growth. Certain medical conditions, such as Polycystic Ovary Syndrome (PCOS), also increase the risk due to chronic anovulation, which results in prolonged exposure to estrogen without the counteracting effect of progesterone. Medications like Tamoxifen, used in breast cancer treatment, can also increase the risk of endometrial hyperplasia and cancer because of their estrogen-like effects on the uterus.
Managing Endometrial Hyperplasia
Diagnosis of endometrial hyperplasia typically begins with evaluating symptoms such as abnormal uterine bleeding, which may include heavy or prolonged periods, bleeding between periods, or any bleeding after menopause. A transvaginal ultrasound can measure the thickness of the uterine lining, and if it appears too thick, an endometrial biopsy is often performed to collect tissue samples for microscopic examination. This biopsy is crucial for classifying the type of hyperplasia. Hysteroscopy, a procedure where a thin, lighted tool is used to view the inside of the uterus, may also be performed to examine the lining and take targeted biopsies.
Treatment options are tailored to the type of hyperplasia, the presence of atypical cells, and individual factors like a desire for future fertility. Hormonal therapy is a common approach, primarily using progestins, which are synthetic forms of progesterone. Progestins work by counteracting the effects of estrogen, helping to thin the endometrial lining and promote its shedding. This can be administered orally, via injection, or through a progestin-releasing intrauterine device (IUD). Progestin therapy is often effective in achieving regression of hyperplasia, especially for types without atypia.
Lifestyle modifications can also play a supportive role in managing endometrial hyperplasia. Maintaining a healthy weight through diet and regular exercise is beneficial, as excess body fat contributes to higher estrogen levels. Weight loss can help reduce estrogen and lower the risk of progression.
For atypical hyperplasia, or when hormonal therapy is unsuccessful, surgery may be considered. Hysterectomy, the surgical removal of the uterus, is a definitive treatment option, especially for women who have completed childbearing or have a high risk of cancer. Regular follow-up and monitoring, including repeat biopsies, are essential to ensure the condition is managed effectively and to detect any progression.