Complex hyperplasia is a condition characterized by an excessive proliferation of cells within the endometrium, the inner lining of the uterus. This overgrowth causes the endometrial tissue to become unusually thick.
Causes and Risk Factors
Complex hyperplasia develops primarily due to a hormonal imbalance, specifically prolonged exposure to estrogen without sufficient progesterone to counteract its effects. This situation is often referred to as “unopposed estrogen.” Estrogen stimulates the growth of the uterine lining, while progesterone helps to stabilize it and prepare it for shedding. When there is an excess of estrogen or too little progesterone, the endometrial cells continue to grow unchecked, leading to thickening.
Several factors can contribute to this hormonal imbalance. Obesity is a common risk factor, as fat cells can produce estrogen, increasing estrogen levels. Conditions like polycystic ovary syndrome (PCOS) often lead to irregular ovulation or anovulation, meaning progesterone is not produced regularly, resulting in sustained estrogen exposure. Certain types of hormone replacement therapy that provide estrogen without adequate progesterone can also contribute to complex hyperplasia. Other factors include never having been pregnant, early onset of menstruation, late menopause, diabetes, and a family history of uterine or colon cancer.
Symptoms and Diagnosis
The most common sign of complex hyperplasia is abnormal uterine bleeding. This can manifest as heavier or longer menstrual periods, bleeding between periods, or any bleeding after menopause. While these bleeding patterns can be indicative of complex hyperplasia, they are also associated with other gynecological conditions, making medical evaluation important.
When complex hyperplasia is suspected, a doctor typically begins with a transvaginal ultrasound. This imaging technique measures endometrial lining thickness. An endometrial thickness greater than 5 millimeters in postmenopausal women is often considered abnormal and warrants further investigation. The definitive diagnostic step is an endometrial biopsy, where a small tissue sample is collected from the uterine lining. A pathologist then examines this sample under a microscope to identify specific cellular changes and confirm the diagnosis.
The Role of Atypia in Cancer Risk
The presence or absence of “atypia” is a key factor in determining the potential for complex hyperplasia to progress to cancer. Atypia refers to the presence of abnormal-looking cells within the endometrial tissue that indicate precancerous development. Pathologists examine these cells for characteristics like altered cell stratification, enlarged nuclei, and increased mitotic activity.
Complex hyperplasia without atypia indicates an overgrowth of endometrial glands that are crowded and show architectural complexity, but the individual cells do not display precancerous features. While still an abnormal condition, the risk of complex hyperplasia without atypia progressing to endometrial cancer is relatively low, typically cited as less than 5% over 20 years. This type of hyperplasia may sometimes regress on its own or with medical intervention.
Complex hyperplasia with atypia, however, is a more serious diagnosis. This form involves not only architectural crowding of glands but also the presence of abnormal, precancerous cells within the glandular lining. This condition is considered a direct precursor to endometrial cancer, specifically endometrioid adenocarcinoma. The risk of complex hyperplasia with atypia progressing to endometrial cancer is substantially higher, with estimates ranging from 20% to 50% or even higher, and a significant portion of cases, around 25-40%, may already have an underlying cancer at the time of diagnosis.
Medical Management and Treatment
Treatment strategies for complex hyperplasia are tailored based on atypia presence and the patient’s individual circumstances, including fertility desires. For complex hyperplasia without atypia, conservative medical management is typically the first approach. This often involves progestin therapy, which counteracts estrogen’s proliferative effects on the endometrium. Progestins can be administered orally or through a levonorgestrel-releasing intrauterine system (LNG-IUS), delivering the hormone directly to the uterus. Treatment with progestins aims to induce regression of the hyperplasia, and follow-up endometrial biopsies usually monitor the response.
For complex hyperplasia with atypia, the standard treatment is often a hysterectomy, the surgical removal of the uterus. This is recommended due to the higher risk of progression to endometrial cancer or the possibility of undetected cancer. For individuals who wish to preserve their fertility, high-dose progestin therapy can sometimes be considered under close medical supervision. This fertility-sparing approach requires diligent follow-up with repeated biopsies to ensure the condition responds and to monitor for progression.