Endometrial hyperplasia is a benign proliferation of the cells lining the uterus (the endometrium), usually triggered by an imbalance of estrogen and progesterone. When this imbalance persists, the lining thickens beyond normal limits, setting the stage for bleeding problems and, in some cases, cancer.
The endometrium is the inner mucosal layer of the uterus that sheds each month during menstruation. Its thickness naturally oscillates between 3mm (menstrual phase) and 14mm (mid‑secretory phase). Any sustained stimulus that pushes the endometrium to stay in the proliferative state leads to endometrial hyperplasia.
Two hormones dominate endometrial behavior:
The combination of high estrogen and low progesterone creates the perfect storm for the endometrium to overgrow.
Clinicians distinguish three main categories based on architectural patterns and cytologic atypia. The most critical split is between typical (low‑risk) and atypical (high‑risk) forms.
| Feature | Typical Hyperplasia | Atypical Hyperplasia |
|---|---|---|
| Architectural pattern | Gland crowding without irregular shapes | Glandular irregularities, cribriform patterns |
| Cytologic atypia | Absent or mild | Marked nuclear enlargement, loss of polarity |
| Risk of progression to cancer | ~2% | ~30% over 5years |
| Management focus | Progestin therapy, surveillance | High‑dose progestins or hysterectomy |
When atypical hyperplasia persists, genetic mutations accumulate-most commonly in PTEN and DNA mismatch‑repair pathways. These alterations can transform the hyperplastic tissue into endometrial carcinoma, the most common gynecologic cancer in developed nations. Early detection of atypia therefore cuts the pathway to invasive disease.
Two tools dominate the workup:
Both tests are quick, outpatient procedures and together achieve >90% sensitivity for detecting significant hyperplasia.
Therapeutic choices aim to restore hormonal balance and, when needed, remove abnormal tissue.
Several health issues share the same estrogen‑dominant environment:
Screening women with these conditions for endometrial thickness is a cost‑effective way to catch hyperplasia early.
While the link between estrogen excess and hyperplasia is well‑established, gaps remain:
Ongoing trials are expected to refine risk‑stratification tools, making personalized treatment possible within the next few years.
The most common sign is abnormal uterine bleeding-either heavy, prolonged, or spotting between periods. Some women notice pelvic pressure or a feeling of fullness, but many are asymptomatic and are diagnosed during routine screening.
First, a transvaginal ultrasound measures endometrial thickness. If the measurement exceeds the normal threshold (5mm post‑menopause) or bleeding patterns are abnormal, an office‑based endometrial biopsy is performed. The tissue sample is examined under a microscope and graded as typical or atypical hyperplasia.
Yes-weight loss of about 5% of body weight can lower estrogen production from fat, improving hormone balance. Regular aerobic exercise, a Mediterranean‑style diet, and smoking cessation also reduce the risk of progression.
The IUS is widely used and effective, but it’s contraindicated in women with active pelvic infection, unexplained vaginal bleeding, or uterine anomalies. A quick ultrasound helps rule out these issues before insertion.
Surgery (hysterectomy) is advised for persistent atypical hyperplasia that does not respond to high‑dose progestins, for women who have completed childbearing, or when an invasive cancer is suspected based on biopsy results.
Tamoxifen blocks estrogen receptors in breast tissue but mimics estrogen in the uterus. This partial agonist effect can stimulate the endometrium, increasing the risk of hyperplasia and, over time, carcinoma. Regular ultrasound monitoring is advised for long‑term users.
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