JMT: Beware of irregular menstruation and beware of endometrial cancer
- What are NK (Natural killer) cell biological characteristics?
- The first DMD gene therapy SRP-9001 may cost 4 million US dollars
- Can drinking red wine soften blood vessels?
- The new era of nanomedicine+mRNA is coming
- Moderna cooperates to develop non-viral gene therapy
- Subversive discovery: Can lymph nodes promote the success of cancer immunotherapy?
JMT: Beware of irregular menstruation and beware of endometrial cancer
JMT: Beware of irregular menstruation and beware of endometrial cancer. The cause of endometrial cancer is not very clear. Most doctors believe that there are two types of endometrial cancer, and there may be two pathogenesis. One is younger. Under the long-term action of estrogen that is not antagonized by progesterone, the endometrium will undergo proliferative changes, which will eventually lead to cancer, but the tumor is well differentiated. The pathogenesis of the other is not clear and may be related to gene mutation. It is more common in postmenopausal elderly people with thin body and low estrogen levels. Around the cancer focus may be atrophic endometrium, the tumor is highly malignant, poorly differentiated, and has a poor prognosis.
The former type accounts for the majority of endometrial cancers, and long-term estrogen stimulation without progesterone antagonism may be the main pathogenic factor. Many years ago, people have known that giving estrogen to experimental animals and observing increased mitosis of endometrial cells can cause the endometrium to evolve from hyperplasia to endometrial cancer, and progesterone can reduce the endometrial cell Mitosis.
Long-term continuous estrogen stimulation of the endometrium In the long-term continuous stimulation of estrogen without progesterone antagonism, endometrial hyperplasia or cancer can occur. Systematic factors Endometrial cancer tends to occur in women with obesity, hypertension, diabetes, infertility or infertility, and menopause. About 20% of endometrial cancer patients have a family history of genetic factors.
At present, the etiology of endometrial cancer is still not very clear. According to clinical data and epidemiological research results, the mechanism of endometrial cancer can be divided into two types: estrogen-dependent and non-estrogen-dependent.
If there is a functional uterine bleeding with anovulatory type or corpus luteum dysfunction, long-term menstrual disorders will cause the endometrium to continue to be stimulated by estrogen, without progesterone resistance or insufficient progesterone, and the endometrium lacks periodic changes. In a state of proliferation.
Especially the infertility caused by non-ovulation of the ovary, the risk of endometrial cancer is significantly increased. Among patients with endometrial cancer, about 15% to 20% have a history of infertility. These patients lack or insufficient progesterone due to non-ovulation or low ovulation, so that the endometrium is continuously stimulated by estrogen. During pregnancy, the placenta produces estrogen and progesterone, so that the endometrium undergoes corresponding pregnancy changes; during lactation, due to the action of the hypothalamus and pituitary, the ovarian function is temporarily inhibited, and the endometrium is free from estrogen stimulation. Infertility, especially infertility caused by anovulation, keeps the endometrium in a hyperplastic state for a long time.
Especially obesity after menopause significantly increases the risk of endometrial cancer. Ovarian function declines after menopause, and androstenedione secreted by the adrenal gland can be converted into estrone in adipose tissue by aromatase. The more adipose tissue, the stronger the conversion ability, and the higher the level of estrone in plasma.
Estrone is the main estrogen in the body of postmenopausal women. The endometrium is the target organ of estrogen. The endometrium is long-term affected by estrone without progesterone antagonism, which can cause the endometrium to change from hyperplasia to cancer. Certain basic studies have also pointed out that if the conversion of androstenedione to estrone is increased, the incidence of intimal hyperplasia to cancer is also increased.
According to some statistics, according to the standard body weight, the risk of endometrial cancer is increased by 3 times if overweight is 9 to 23 kg. If overweight> 23 kg, the risk is increased by 10 times.
Obesity-hypertension-diabetes is generally called the triad of endometrial cancer. From 1970 to 1991, the Department of Obstetrics and Gynecology of the First Affiliated Hospital of Beijing Medical University admitted 153 cases of endometrial cancer patients whose main treatment was surgery. Among them, 20% were obese, 44.4% had hypertension, and 11.1% had diabetes. In fact, hypertension and diabetes are not directly related to endometrial cancer.
Obesity, high blood pressure, and diabetes may all be the result of hypothalamic-pituitary-adrenal dysfunction or abnormal metabolism. At the same time, the function of pituitary gonadotropin may also be abnormal, resulting in anovulation and no secretion of progesterone, so that the endometrium is continuously stimulated by estrogen for a long time.
Some people believe that premenopausal obesity, especially those obese from a young age, is also a high-risk factor for endometrial cancer, because obese people are often accompanied by relatively insufficient secretion of progesterone during the luteal phase, or accompanied by irregular menstruation or even amenorrhea.
According to related reports, the risk of endometrial cancer in menopausal age> 52 years is 1.5 to 2.5 times that of menopausal patients before 45 years of age. After a few years of late menopause, there is no ovulation, but the effect of estrogen is extended.
Late menarche (delayed menarche) is a protective effect for endometrial cancer, especially for premenopausal women. Late menarche can reduce the risk of endometrial cancer by 50%. Delayed menarche can reduce the continuous stimulation of estrogen on the endometrium.
Among endometrial cancer patients under the age of 40, approximately 19% to 25% suffer from polycystic ovary syndrome. In patients with polycystic ovary syndrome, the ovarian follicles last for a long time, but they cannot mature to achieve ovulation, which makes the endometrium under continuous estrogen stimulation, lack of progesterone regulation and periodic endometrial shedding, leading to endometriosis Hyperplasia changes.
Androgen levels in patients with polycystic ovary syndrome are also increased, about 3 to 4 times higher than the average person, and androgens can be converted into estrone, leading to endometrial hyperplasia or hyperplasia, and then dysplasia and even endometrial cancer. Girls with polycystic ovary syndrome are four times more likely to develop endometrial cancer than girls of the same age with normal menstruation.
Ovarian tumors that produce estrogen, such as granulosa cell tumors and follicular cell tumors. About 25% of pure vesicular cell tumors are complicated by endometrial cancer.
Many studies have pointed out the relationship between the application of estrogen replacement therapy and endometrial cancer. The risk of endometrial cancer for those who use estrogen replacement therapy is 3 to 4 times that of those without replacement therapy. The risk is related to the dose of estrogen, especially the duration of medication.
Those who have used higher doses of estrogen for more than 10 years have a 10-fold increase in the chance of suffering from endometrial cancer. In the absence of progesterone antagonism or insufficient progesterone, long-term estrogen replacement therapy can lead to intimal hyperplasia and even cancer. Endometrial cancer has been reported in young patients with long-term use of estrogen replacement therapy for gonadal dysfunction or Turner syndrome.
In recent years, in the application of estrogen replacement therapy, progesterone is added for at least 10 days in each cycle, which neutralizes the carcinogenic effects of long-term use of estrogen and significantly increases its safety. Therefore, the replacement therapy of estrogen plus progesterone (combined estrogen), if the protective effect of progesterone is sufficient, is safe even for long-term application.
However, some people hold objections that even combined estrogen, such as long-term application, still has an adverse effect on the endometrium. It is also recommended that for long-term replacement therapy, the endometrial condition should be closely followed, and endometrial biopsy should be performed if necessary.
In recent years, the application of tamoxifen as an adjuvant treatment of breast cancer has increased day by day. In a report by FoRNAnder et al., a survey of 1,800 Swedish women with breast cancer was conducted. Those who used tamoxifen for more than 2 years, compared with those who did not receive adjuvant therapy or who only used chemotherapy, endometrial cancer The incidence of the former is twice that of the latter. The incidence of endometrial cancer is 5 times that of those who use tamoxifen for 5 years.
“Kurman” et al. retrospectively analyzed 170 cases of endometrial hyperplasia patients with curettage specimens and followed up for an average of 13.4 years. The results were: 1% of simple hyperplasia developed into cancer, 3% of complex hyperplasia developed into cancer, and 8% of atypical simple hyperplasia It develops into cancer, 29% of atypical hyperplasia develops into cancer, and those with atypical hyperplasia, such as surgical removal of the uterus, 25% are accompanied by well-differentiated endometrial cancer. Therefore, dysplasia has a tendency to become cancerous and belongs to precancerous lesions.
Family history. People with a family history of ovarian cancer, bowel cancer or breast cancer are more likely to develop endometrial cancer than those without family history. Economic conditions are better, especially those with a high-fat diet are also at high risk of endometrial cancer.
In the United States, some people have done a comparative study and found that the incidence of endometrial cancer in women with a high educational level and high economic income is lower than that of women with low economic income. However, some people believe that it may be due to the common application of estrogen replacement therapy in the former, the long time and the obesity.
Generally speaking, the incidence of endometrial cancer in economically developed countries is higher than that in underdeveloped countries, and the incidence in cities is higher than in rural areas.
Whether the pathogenic factors are related to race is still inconclusive. In a retrospective analysis in 1997, Matthews and others pointed out that the incidence of endometrial cancer in white women is higher than that in black women. But black women suffering from endometrial cancer have a low survival rate and a high mortality rate.
Serous papillary carcinoma and clear cell carcinoma of the endometrium are more common in black women than in white women. These two subtypes of endometrial cancer are often poorly differentiated and clinically advanced, so the prognosis is poor. The reason is not clear. The overexpression of the known mutant p53 gene is significantly higher in black women than in white women.
Eating habits, excessive fat, carbohydrate and protein intake can cause obesity, and increasing physical exercise, green vegetables and fruits have obvious protective effects.
(source:internet, reference only)
Disclaimer of medicaltrend.org