Why do patients with polycystic ovaries develop endometrial cancer? Our study found that young patients with endometrial cancer often have primary infertility, irregular menstruation, polycystic ovaries and endometrial hyperplasia, aligning with the findings here at Antai Hospital. The survey also showed higher rates of non-pregnancy, a history of infertility, irregular menstrual cycles, and simultaneous primary tumors in the endometrium and ovaries. These findings suggest that chronic hormonal imbalance and polycystic ovary syndrome (PCOS) may be associated with the occurence of endometrial cancer in young normal-weighted women.
Polycystic ovary syndrome (PCOS) contains all or most of the risk factors that leads to endometrial cancer:
Chronic hyperinsulinemia, low IGFBP-1, SHBG, hyperandrogenemia, lack of luteal progesterone production. Due to ovulation disorder, the endometrium of patients with polycystic ovary syndrome (PCOS) is stimulated by single low concentration estrogen, and lacks regulation of progesterone and periodic endometrium shedding. Moreover, the level of androgen in patients is about 3 ~ 4 times higher than that of normal women, and androgen can be converted into estrone, leading to changes in the proliferation of endometrium. Various degrees of hyperplasia, and then develop atypical hyperplasia, and even endometrial cancer.
In untreated patients with polycystic ovary syndrome (PCOS), endometrial hyperplasia occurs in 35 percent of patients and endometrial cancer in 8 percent of patients, according to the study. Women with polycystic ovary syndrome (PCOS) are four times more likely to develop endometrial cancer later in life than women of the same age with normal menstruation. Polycystic ovary syndrome (PCOS) occurs in 19% to 25% of endometrial cancer patients under the age of 40.
There may be a correlation between endometrial cancer and abnormal metabolism of PCOS, and excessive production of ovarian androgens may be the main reason for the development of endometrial cancer. In vitro experiments with ovarian cancer and ovarian interstitial tissue of PCOS patients have shown increased responsiveness to insulin stimulation, resulting in androgen overproduction, similar to that in PCOS patients. Patients with endometrial cancer have increased ovarian venous androgen concentration and LH, which are key hormones that stimulate ovarian androgen synthesis. Because steroid hormones affect the transcription of cell cycle related genes, resulting in endometrial hyperplasia. There are steroidal plastin receptor co-activators in the endometrium. When such substances increase, the endometrium may be sensitive to estrogen, which is associated with low pregnancy rate and endometrium hyperplasia or even cancer.
Changes in the endometrium vary with different levels of estrogen secreted by the ovary. When follicular dysplasia occurs, the endometrium is proliferative. When the ovary continues to secrete a small amount or a large amount of estrogen, it can stimulate the endometrium, leading to hyperplasia of the endometrium glands.
Clinical findings of Antai Hospital show the abundantly clear relationship between endometrial thickness under ultrasound and endometrial hyperplasia in patients with non-ovulatory infertility. Amongst them, 60% endometrial has a proliferative stage membrane and 35% have endometrial growth, including atypical growth. When the endometrial thickness is less than 7mm or the menstrual period was less than 3 months, no endometrial hyperplasia was found, and the endometrial only showed proliferative changes. For patients who have never received treatment, whose menstrual period is more than 3 months, whose endometrial thickness is 27mm, or who have recurrent irregular vaginal bleeding, Antai Hospital recommends routine curettage. For patients with endometrial thickening indicated by ultrasound, curettage should be performed first to determine whether there is endometrial hyperplasia, even if there is no irregular vaginal bleeding.
- A reminder: if PCOS patients have not been treated, before menopause, progesterone deficiency in PCOS women is a major risk factor for PCOS endometrial lesions. Therefore, PCOS should be detected and treated as soon as possible. Dr. Chen Fenglin from Antai-Tai Hospital believes that the cause of this disease is actually gonadal malstructure, that is, the remaining testicular tissue (ovaltestis) in the ovarian differentiation stage. Therefore, Antai-tai treatment does not stop at changing the clinical symptoms of the disease, but terminates the testicular tissue in the ovary through minimally invasive technology (altering the gonadal malstructure gene). Then according to the type supplemented by drug regulation.