Endometriosis (endometriosis) is a frequent and common disease among women of reproductive age, with a markedly increasing incidence of up to 10-15% and accounting for more than 30% of general gynecological procedures. Dysmenorrhea, lower abdominal pain and painful intercourse caused by endometriosis seriously affect women’s health and quality of life, and is one of the main causes of infertility. The pathogenesis of endoheterosis is unclear, and the lesions are extensive and diverse in form, and have malignant biological behaviors of infiltration, metastasis and recurrence, making it a difficult disease to treat. The diagnosis and treatment of endoheterosis has become a hot issue in contemporary gynecology, and its basic and clinical research has entered a new stage at the beginning of the new century.
I. Understanding of the pathogenesis of endoheterosis
There are many different theories on the pathogenesis of endometriosis, but the dominant theory is that endometrial cells are implanted with menstrual blood, and the key lies in scientific explanation, model building and clinical evidence. Retrograde flow of menstrual blood into the pelvis is a common, if not physiological, phenomenon, but most people do not suffer from endo. The modern definition of endometriosis is the growth, development, and bleeding of endometrial cells in an ectopic location that causes symptoms. Four basic conditions are required for endothelial cell retrograde implantation.
1, the endocytes must pass through the fallopian tube into the abdominal cavity.
2. the cells in the menstrual blood fragments must be viable
3. the endometrial cells must have the capacity to be transplanted onto pelvic organ tissue
4, the anatomic distribution of endometriosis in the pelvis must be consistent with the implantation principle of the shed endocytes.
If so, the endometrial cells will have to break through 3 ” lines of defense”, namely
1, ascites.
2, peritoneal cells, mainly macrophages, natural killer cells, etc.
3, the peritoneal extracellular matrix.
Thus, the endothelial cells must then complete a “trilogy” of adhesions to invade the blood vessel formation. In this process, estrogen, various enzymes of the local environment, cytokines, etc. play a considerable role. Studies to date have revealed that the molecular and biological characteristics of the in situ endothelium differ between endo- and non-endo-heterozygous patients, and that the source of these differences is genetic. Therefore, genetic differences are the fundamental differences between the in situ endothelium of patients with endo and non-endo; they are a difference between ectopic and in situ endothelium; they are the key to menstrual reflux and the ability of menstrual endothelial fragments to adhere, invade, and grow in “ectopic” places in different individuals (i.e., patients and non-patients); they explain the familial predisposition or heredity of endo; and they are the reason for the familial predisposition or heredity of endo. It is the basis of the theory of gene therapy for endometriosis.
The study of endometrium in situ will be a new target for pathogenesis exploration. The histopathological, biochemical, molecular biological, and genetic characteristics of the in situ endometrium will determine the “fate” of the endometrium that has been retrograded to a different location, the so-called “in situ endometrium determinism”. At the very least, it suggests a new way of thinking for us to fully understand, interpret, and even revise sampson’s theory. It is possible that sampson’s theory has been unable to explain some sites of endometriosis, and the hypothesis of epithelial metaplasia of the corpora cavernosa or paramedian duct (Mullerian duct) could explain the occurrence of endometriosis in sites such as uterine adenomyosis, vaginal rectal endometriosis, and thoracic cavity.
II. Clinical diagnosis of endometriosis
Laparoscopy is currently recognized as the gold standard for the diagnosis of endometriosis, but it is not foolproof to perform laparoscopy in all patients with suspected endometriosis. The search for markers with good specificity and sensitivity is the way forward. In Canada, a new diagnostic test (metrio test) has been introduced with a positive predictive value of 95% and a negative predictive value of 75%, based on a comprehensive analysis of multiple factors in the serum and endometrium of the patient. According to our situation, it can also be a new diagnostic model if the following 5 clinical and test indicators can be analyzed, namely
1, symptoms (dysmenorrhea, lower abdominal pain, painful intercourse or collectively chronic pelvic pain).
2. infertility (primary or secondary infertility, especially secondary infertility).
3. pelvic examination (adnexal masses, rectal fossa nodules, tenderness, etc.).
4, 2 ultrasound scan (anechoic areas in the adnexal region, internal punctate fine enhancing echogenicity, thick walls, poorly defined and images of other areas).
5. serum ca125 level greater than 35mlu/ml, usually 50-80mlu/ml.
Third, the principles of treatment and individualization of endoheterosis
The principles of treatment of endoheterosis are to reduce and eliminate the lesions, alleviate and eliminate pain, improve and promote fertility, and reduce and avoid recurrence. To achieve this goal, laparoscopic surgery is the best treatment, ovarian suppression is the best treatment, and pregnancy-assisting techniques and pregnancy are the best treatment. In addition, different treatment responses, known as individualization of treatment, should be selected according to the patient’s age, marital status, severity of symptoms, degree of lesions, and previous treatment experience.
Surgery, especially laparoscopic surgery, should be emphasized as the first choice. This is because it can clarify the diagnosis, the degree and type of lesion, and perform excision, destruction and reduction of the lesion, separation of adhesions, restoration of anatomy, and help pregnancy; it can reduce symptoms and reduce and prevent recurrence. Also, pharmacological treatment is necessary because deep lesions and hidden lesions may be left behind, besides there are microscopic or neoplastic lesions. Both classical pseudopregnancy therapy and pseudomenopausal therapy are based on the theory of establishing a low estrogen, high progesterone or high androgen environment. In recent years, the most popular drugs used are gonadotropin-releasing hormone analogs.
IV. Endometriosis and infertility and chronic pelvic pain
Infertility is the main problem of endometriosis, which is one of the main causes of infertility and is responsible for more than 30% of infertility. Seriously, the causes of infertility due to endometriosis are multiple and overlapping mechanisms, anatomical and functional, endocrine, immunological, biological, biochemical, and local environmental, and even painful intercourse. As a result, some scholars have scored the combination of all factors as the endo-fertility index (EFI) to estimate the fertility of patients and countermeasures. Surgery can increase the chances of conception. medication alone is difficult to improve the patient’s fertility status, has a high recurrence rate, and only relieves symptoms. gnRHa is an important option for the treatment of severe endoheterosis and preparation for pregnancy assistance. Surgery plus pharmacological treatment can reduce recurrence and can be used as a pre-emptive treatment for assisted conception. Therefore, artificially assisted reproductive technology is an important treatment for those with endoheterozygous infertility. It may be hesitant to compare or choose between ovulation promotion – artificial insemination or in vitro fertilization – embryo transfer, but this is a multifactorial consideration depending on each patient’s age, degree of lesion, treatment, or using EFI as a reference. Collaboration between gynecologists and specialists in reproductive endocrinology and fertility techniques is very important, because about 1/3 of those who seek help with in vitro fertilization A embryo transfer (IVF-ET) have endo. Nowadays, we have developed a preliminary model of consultation and treatment in which
1. first, laparoscopy is performed to clarify the diagnosis, remove the lesion and release the anatomical factors.
2. endocrine examination to remove other factors of infertility.
3, for mild and moderate endo, expect guidance for six months; then perform selective ovulation promotion – artificial insemination if unsuccessful, then IVF-ET.
In short, it is necessary to seize the “golden opportunity” of six months after the operation, and to “make a quick decision”.