I. Pathogenesis of endometriosis
1. Not yet fully understood The leading theories are Sampson’s reflux implantation, somatic epithelial metaplasia, and induction theory.
The role of endometrium The endometrium needs to undergo the process of adhesion, invasion, and angiogenesis outside the uterine cavity to be able to implant, grow, and develop lesions, and the qualities of in situ endometrium may play a decisive role.
3, the role of immune function and hormones, etc. In the completion of the above process, the collective systemic and local immune status and function, hormones, cytokines and enzymes play an important role in ectopic endometrium.
4.Ectopic ectopic disease has family aggregation.
5.The role of external environmental pollution such as dioxin may have some influence.
Second, the clinical manifestations and auxiliary examination methods
1. pain 70%-80% of patients have varying degrees of pelvic pain, not exactly parallel to the degree of lesion. 1) dysmenorrhea: typically secondary and progressively aggravated; 2) non-menstrual abdominal pain: chronic pelvic pain; 3) painful intercourse and painful defecation, etc.; 4) rupture of ovarian endometriosis cysts can cause acute abdominal pain.
2. Infertility About 50% of patients are combined with infertility.
3. Abnormal menstruation.
4. pelvic mass.
5.Specific sites of endoheterosis Various symptoms often have cyclic changes and can be combined with clinical manifestations of pelvic endoheterosis.
1.Endoheterosis of the digestive tract, with symptoms such as increased frequency of stool or constipation, blood in stool, and painful defecation.
2.Urinary tract endoheterosis, frequent urination, painful urination, hematuria and back pain, even causing urinary system obstruction and renal dysfunction.
3) Respiratory tract endoheterosis, menstrual hemoptysis and pneumothorax. 4) Scar endoheterosis: nodules at incision scars after surgery such as abdominal wall caesarean section, which increase in size and pain during menstruation; nodules at perineal incision or wound scars, which increase in size and pain during menstruation.
6. Gynecological examination The uterus is often posterior and poorly mobile in typical cases. Tender nodules in the uterosacral ligament, rectal fossa of the uterus or posterior vault. There may be a cystic inactive adnexal mass at the same time.
7. Blood CA125 test CA125 level is mostly mild to moderately elevated.
8. Imaging examination
Ultrasound scan is mainly meaningful for the diagnosis of ovarian endometriosis cysts. The typical ultrasound image is an anechoic mass in the adnexal region with a strong light spot inside, and MRI is meaningful for the diagnosis and evaluation of ovarian endometriosis cysts, extra-pelvic endometriosis and deep infiltrative lesions.
9. Others Other auxiliary examinations such as IVP, cystoscopy, colonoscopy, etc. are feasible when necessary.
III. Diagnosis of endoheterosis
1. Symptoms: pain (dysmenorrhea, CPP, painful intercourse, etc.), infertility.
2.Gynecological and auxiliary examinations: pelvic examination reveals endoheterosis lesions, imaging reveals endoheterosis lesions, and serum CA125 level is mildly or moderately elevated.
3.Laparoscopic examination: laparoscopy is the common method for diagnosing endoheterosis at present. The basis of diagnosis is mainly based on the morphology of the lesions under laparoscopy, but it is difficult to confirm all of them by pathology.
IV. Clinical staging of endoheterosis
Currently, the commonly used staging method for endoheterosis is the American Fertility Society’s 1985 revised endoheterosis staging (r-AFS) method, which is mainly based on the size and depth of the peritoneal or ovarian lesions, the extent of adhesions between the ovaries and fallopian tubes and the degree of adhesions, and the degree of closure of the utero-rectal recess for scoring. The specific staging table will not be written, read the book.
V. Treatment of endometriosis
The goals of treatment are to reduce and eliminate lesions, relieve and relieve pain, improve and promote fertility, and reduce and avoid recurrence. The main factors to be considered in treatment are age, fertility requirements, severity of symptoms, extent of lesions, previous treatment history, and the patient’s wishes. Treatment measures should be standardized and individualized. The treatment of pelvic pain, infertility and pelvic masses should be treated separately. Treatment methods can be divided into surgical, pharmacological, interventional and assisted reproductive treatment.
(i) Surgical treatment
1. Purpose of surgery: The purpose of surgery is to remove the lesion and restore the anatomy.
2.Surgical classification: Surgery for endometriosis is divided into different procedures according to the following.
(1) conservative surgery: to preserve the patient’s reproductive function, to remove as much as possible the lesions visible to the naked eye and the ovarian endometriosis cysts, and to separate the pelvic adhesions. It is suitable for those who are young or need to preserve their reproductive function.
(2) Semi-radical surgery: Removal of the uterus and lesions but preservation of the ovaries, mainly for those who have no reproductive requirements but wish to preserve the secretory function of the ovaries.
(3) Radical surgery: Removal of the whole uterus + both adnexa and all the lesions visible to the naked eye. It is suitable for those who are older, have no fertility requirements, have severe symptoms or have failed to respond to multiple treatments.
(4) Adjunctive surgery: such as uterine nerve removal and presacral nerve resection, for those with pain in the midline area.
(ii) Pharmacological treatment
The aim of drug therapy is to inhibit ovarian function, stop the progression of endometriosis, reduce the activity of endometriosis lesions as well as reduce the formation of adhesions. The choice of medication should be informed by.
(1) Drug therapy is recommended for cases with a basic diagnosis and long-term “experimental therapy” is not recommended;
(2) There are no standardized protocols for drug therapy;
(3) The efficacy of various regimens is basically the same, but the side effects are different;
(4) The patient’s wishes and financial ability should be considered. The four main types of drugs available for the treatment of endometriosis are oral contraceptives, highly effective progestins, androgen derivatives, and GnRH-a.
Commonly used medication regimens, mechanisms of action and side effects are listed below.
1.Oral contraceptive pills: continuous or cyclic administration for a total of 6 months, which can inhibit ovulation; less side effects, but may have gastrointestinal symptoms or abnormal liver function, etc.
2.High-efficiency progestin: 20-30mg/d of medroxyprogesterone acetate, divided into 2-3 oral doses, for 6 months. Medroxyprogesterone acetate can cause meconium-like changes in endothelial tissue, eventually leading to endothelial atrophy, and at the same time can negatively feedback inhibit hypothalamic-pituitary-ovarian axis. Side effects include breakthrough bleeding, breast pain, weight gain, gastrointestinal symptoms, and abnormal liver function.
3.Androgen derivatives: The androgen derivatives used for the treatment of endometriosis are.
(1) Danazol: 600-800mg/d, divided into 2-3 oral doses for 6 months. Danazol inhibits the mid-menstrual luteinizing hormone (LH) peak, thereby inhibiting ovulation; it also inhibits a variety of enzymes involved in steroid synthesis and increases the level of free testosterone in the blood. The side effects are mainly masculine manifestations, such as increased hair, mood changes, and thickening of the voice; in addition, it may also affect lipoprotein metabolism, cause liver function damage, and weight gain.
(2) Pregnatrienone: 2.5mg orally 2-3 times/week for 6 months. Pregnant trienone can antagonize progesterone and estrogen, reduce the level of sex hormone binding protein, and increase the level of free testosterone in blood. The side effects are mainly anti-estrogen and androgen-like effects, basically the same as Danazol, but less severe.
4.GnRH-a: According to the different dosage forms, it is divided into subcutaneous injection and intramuscular injection, once a month for 3-6 months, GnRH-a can down-regulate the pituitary function, causing temporary de-escalation and low estrogen status in the body. The side effects are mainly menopausal symptoms caused by hypoestrogenemia, such as hot flashes, vaginal dryness, decreased libido, insomnia and depression, etc. Long-term application can cause bone loss.
The theoretical basis of the GnRH-a+Add-back regimen is based on the “estrogen window dose theory”, which states that different tissues have different sensitivities to estrogen, and that the estrogen level in the body should be maintained in a range that does not stimulate the growth of ectopic endometrium without causing menopausal symptoms and bone loss (estradiol levels between 110-146 pmol/l), which does not affect the therapeutic effect and reduces the side effects in order to prolong the treatment time.
Add-back regimens include
(1) Combined estrogen and progestin regimen: combined estrogen 0.3-0.625mg/d (or Tegretol 1-2mg) + medroxyprogesterone acetate 2-4mg/d.
(2) Tibolone: 1.25mg/d. GnRH-a has been applied for more than 3 months, and the Add-back regimen is mostly advocated. Depending on the severity of symptoms, it can also be started in the 2nd month of medication, and the treatment dose should be individualized, and estrogen levels should be monitored when available.