follicle luteinization

Introduction

Introduction It means that the follicle is mature but not broken, the egg cell is not discharged and is in situ flavin, forming the corpus luteum and secreting progesterone, and the body effect organ undergoes a series of similar ovulation cycle changes. Clinically, the menstrual cycle is often the same, with similar ovulation performance but persistent infertility as the main feature. It is a special type of anovulatory menstruation and one of the important causes of infertility.

Cause

Cause

1. Central endocrine disorders: Ovulation is a complex process that is accomplished by the synergy of multiple hormones. Central endocrine disorders can directly affect the growth and development of follicles and the occurrence of ovulation. Studies have shown that the ovulation process is triggered by the peak secretion of LH/FSH, which is mainly stimulated by LH. When the central endocrine disorder is caused by various reasons, the level of LH peak secretion is not enough, and the secretion of LH does not reach the threshold value, it can not stimulate the biochemical and histological changes leading to the digestion and rupture of the follicular wall, but it can lead to reduction. The re-activation of several divisions and the luteinization of follicular cells, the secretion of progesterone, and the phenomenon of "pseudo-ovulation" in which follicles are not discharged and progesterone is elevated. However, some studies have reported that LUFS has nothing to do with LH levels. It has been reported that the effect of LH on LUFS is due to a decrease in the amount of LH receptor.

2, local disorders: endometriosis; pelvic inflammatory disease can cause pelvic adhesions and cause follicles to not rupture without ovulation, but endogenous LH can promote follicular luteinization. Studies have shown that after ovarian surgery, it is mainly related to the thin film-like adhesion of the ovarian surface. In addition, ovarian inflammation and even subclinical ovarian inflammation are local factors that cause the ovarian skin to thicken and cause LUFS to occur.

3, enzyme or kinase deficiency or defects or prostaglandin deficiency: enzyme production is also the result of LH and FSH, LH deficiency affects the increase of CAMP, so that the activity of fibrin and plasminogen activator in the ovary is low, before ovulation The plasminogen activity on the follicular cells is reduced, affecting the dissolution of fibrin and the self-effect of the follicular wall. Proteolytic enzymes also act on follicular rupture, and when these enzymes are deficient, they inhibit follicular ovulation.

4. High PRL: PRL affects the release of gonadotropin-releasing hormone (GnRH), which causes blood LH to decrease. Floating L can change the positive feedback regulation of E2 to LH. In addition, PRL can also inhibit the secretion of E2 and P from the ovaries and reduce the response of the ovaries to GnRH, so that ovulation cannot occur.

5, the role of external factors such as drugs: drug-induced ovulation or super-promoting ovulation cycle, the incidence of this syndrome is significantly higher than the natural cycle, indicating that the development and maturity of follicles during the process of ovulation induction is not exactly the same as the natural cycle. Such as clomiphene (CC) can significantly increase the syndrome, it is believed that drugs such as CC can cause ovarian stroma and follicular luteinization.

6. Mental and psychological factors: Some people think that it is related to mental and psychological factors. Long-term infertile women are in a state of tension and constant stress, causing repeated peaks in blood prolactin levels and affecting ovulation.

Examine

an examination

Related inspection

Gynecological ultrasound examination of endocrine function test

1, B-ultrasonic continuous detection. From the 8th to 9th day of the ovulation period. Daily observation of follicular development with vaginal B-ultrasound, if there is dominant follicle formation, the standard of mature follicles (the maximum diameter of follicles >18mm clear, clear boundaries, etc.), and no ovulation, that is, follicles do not disappear or no Significantly reduced (follicular retention type), or continue to increase (30 ~ 45mm, follicles continue to grow large), uterine rectal recession without free liquid, can be considered as unruptured follicular luteinization (LUF) cycle. In the B-ultrasound monitoring cycle, it should be checked by a special person to unify the standard and avoid the cystic corpus luteum after ovulation.

2, laparoscopy. Laparoscopy can further confirm the diagnosis of unruptured follicular luteinization. It is generally believed that the ovulation sign remains in the 1.5 days after ovulation, and will gradually close afterwards, complete epithelialization in 4 to 5 days, and the ovulation hole is closed. Therefore, in the early stage of the corpus luteum (before the 20th day of the menstrual cycle, BBT rose 2 to 4 days), the ovarian surface was directly observed by laparoscopy, and there was a corpus luteum but no ovulation hole.

3, after the sputum puncture liquid steroid hormone determination mature follicle contains a large number of female, progesterone, when the follicle rupture released into the pelvic cavity, so that the concentration of estrogen and progesterone in the peritoneal fluid is significantly higher than the blood concentration, usually progesterone can be up to 3 times the above.

Therefore, in the early stage of corpus luteum puncture, the peritoneal fluid was taken, and the concentration of estrogen and progesterone was measured. Compared with the blood concentration, it can be inferred whether the follicle had been ruptured.

4, endocrine examination blood LH peak measurement is lower than normal or premature.

Diagnosis

Differential diagnosis

In addition to infertility (such as long-term or "unexplained" infertility), there are often no other obvious symptoms, so Chinese medicine should focus on the syndrome differentiation of Chinese and Western syndromes. The clinical testimony is mainly caused by kidney deficiency and blood stasis, and each combination of liver qi stagnation, dampness and heat resistance or heart and liver anger.

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