I had prolonged uterine bleeding. My gynecologist performed an endometrial curettage (DD&C) and confirmed findings of endometrial hyperplasia.
Endometrial hyperplasia is a condition due to abnormal thickening of the endometrium (womb lining) because of unopposed estrogen hormone stimulation. The commonest etiology of this condition is anovulation (failure to ovulate).
Women usually present with prolonged menstrual bleeding, which can be mild spotting to heavy menstrual flow. These symptoms can cause personal distress and inconvenience to anemia (pallor) due to chronic blood loss.
Making the diagnosis
The pelvic ultrasound usually shows a thickened endometrium characterized by an echogenic endometrium. Curettage of the endometrium provides opportunity to remove the abnormal endometrium as well as tissue assessment. A hysteroscopy examination of the uterine cavity provides further opportunity to exclude polyps or sinister uterine growth.
The diagnosis of endometrial hyperplasia depends on the histopathology results. The endometrium examination may reveal findings of a simple or complex hyperplasia (types of thickening based on cellular layering). This is further classified depending on the presence of atypia (abnormality of cell structure). The final diagnosis will appear as a simple or complex hyperplasia with or without atypia. However, for purpose of uniformity, WHO (2014) has recommended the use of Endometrial Hyperplasia without atypia and Atypical Hyperplasia to describe these pathologies.
The concern: Endometrial hyperplasia and endometrial (womb) cancer
The presence of endometrial hyperplasia is a precursor to endometrial (womb) cancer. However, the risk of malignant transformation is less than 5% over 20 years for endometrial hyperplasia without atypia.
On the other hand, the risk of developing endometrial cancer is highest in atypical hyperplasia. The reported cumulative risk of cancer in 4 years is 8%, which increases to 12.4 after 9 years and to 27.5% after 19 years (Lacey JV 2010). About 43% of this atypical hyperplasia has also been associated with a concomitant endometrium cancer at time of hysterectomy (Trimble 2006).
In view of low risk of endometrial cancer in women who have endometrial hyperplasia without atypia, an option of observation alone with follow-up biopsies can be considered. The majority of these cases regress spontaneous during follow- up. However, treatment with progestogens has a higher disease regression rate over observation alone. Progestogen treatment is indicated in women who fail to regress following observation alone and in symptomatic women with abnormal uterine bleeding.
Progestogen can be administered orally or by injections. The other alternative is the use of medicated IUCD. The recommended duration of treatment is 6 months and this is followed by a endometrial biopsy confirm endometrial regression. Two negative biopsies over six months interval are required to complete the treatment. Any vaginal bleeding should be assessed and a relapse excluded.
Surgery is rarely indicated unless the women opted for it and do not wants medical treatment. Other indications for surgery include failure of endometrial regression following medical treatment, persistent uterine bleeding and relapse after a completed progestogen treatment. A hysterectomy (complete removal of the womb) is the recommended surgical option.
The treatment of endometrial hyperplasia with atypia is hysterectomy. This is due to the high likelihood of progression to endometrial cancer. For women who prefer to keep the uterus, medical treatment in the forms of progestogen or medicated IUD can be used for women who want to preserve their uterus until a later date.
Lacey JV et al., J Clin. Oncol 2010
RCOG Greentop guideline 2016
Trimble CL et al., Cancer 2006