Postmenopausal vaginal bleeding is reported by 90% of patients with a diagnosis of endometrial cancer. Risk factors for endometrial cancer include obesity, increasing age, type 2 diabetes, use of unopposed estrogen, polycystic ovary syndrome, chronic anovulation, and family history of gynecologic cancers. Evaluation includes a detailed history and physical examination, focusing on bleeding characteristics, pain, and vaginal discharge. First-line diagnostic tests include transvaginal ultrasonography to measure endometrial thickness and endometrial biopsy. If thickening or irregularities are observed on ultrasonography, further workup is indicated. In postmenopausal patients, an endometrial thickness of 4 mm or less has a negative predictive value greater than 99% for endometrial cancer. The risks and benefits of deferring endometrial biopsy should be discussed with the patient because some type 2 endometrial cancers can develop from atrophic endometrium and may progress more aggressively. Persistent uterine bleeding or a change in menstrual bleeding warrants inclusion of biopsy in the workup. Endometrial intraepithelial neoplasia, previously atypical endometrial hyperplasia, is clinically significant on pathology reports because it is considered a precursor for endometrioid adenocarcinoma, requiring urgent referral to gynecologic oncology. Family physicians play a critical role in early identification of endometrial cancer, clearing patients for surgery, and long-term surveillance.
Case 2. JM is a 58-year-old Black cisgender woman who presents because of menstrual bleeding. She has not had a period in 2 years, and in the past 3 months, she has had bleeding for 4 days every month that resolves spontaneously. Her medical conditions include hypertension, diabetes, and obesity. Her family history is significant for a sister and mother who had hysterectomies for suspected fibroids. She is asking today whether she needs a hysterectomy because her family members required surgery.
Background, Epidemiology, and Risk Factors
The number of new cases of endometrial cancer in the United States among patients with a uterus is 67,880 annually, with a peak age at diagnosis of 60 years.1 Compared with other cancers, endometrial cancer is increasing in incidence and associated mortality.1 This is largely attributed to the obesity epidemic. The rate of endometrial cancer is also disproportionately higher in Black women compared with those in other racial and ethnic groups.2–4 Additional risk factors include but are not limited to increasing age, type 2 diabetes, use of unopposed estrogen, polycystic ovary syndrome, and a family history of gynecologic cancers.5,6 Diagnoses associated with chronic anovulation, which leads to prolonged and unopposed estrogenic stimulation of the endometrial lining, also increase a patient’s risk of developing endometrial cancer.
Factors protecting against endometrial cancer include parity and use of oral contraceptives. There is an inverse relationship between the number of pregnancies and the risk of developing this malignancy. Additionally, use of oral contraceptives reduces the risk of endometrial cancer by 30% to 40%, with longer durations of use providing greater protection and benefits lasting decades after discontinuation.7
The most common type of endometrial cancer is endometrial carcinoma, which arises from the uterine lining. Endometrial carcinoma is generally further divided into two types: type 1 (endometrioid) and type 2 (nonendometrioid), which includes serous and clear cell carcinomas. The types are further delineated by their histologic characteristics, grade, and hormone receptor expression. Type 1 affects approximately 80% of patients and is clinically associated with metabolic syndrome and obesity. Survival rates for type 1 are up to 85% at 5 years5; however, the prognosis for patients with type 2 is poor with an overall survival rate of 55% at 5 years.3,4 It should be noted that Black patients have a higher and disproportionate rate of type 2 endometrial carcinoma and more extensive disease at the time of diagnosis.8
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