| Induced abortion has a long history as a remedial measurement of contraceptive failure. Surgical abortion which is an invasive procedure impairs women's health. For more than ten years medical abortion has been used in our country. The complete abortion rate of termination of early pregnancy by mifepristerone and misoprostol is above 90%. The advantages of medical abortion are convenience, natural, less pain and greater privacy. It is an alternative method for women who needed abortion. But uterine prolonged bleeding after medical abortion is still unsolved, which influences its security and receptivity.Many studies on the problem of uterine prolonged bleeding after medical abortion have been done. Some suggested that decidual cells produced a great deal of laminins(LM) and fibronectins ( FN) after termination of early pregnancy by mifepristerone and misoprostol, laminins(LM) and fibronectins ( FN) made decidual tissue stick to the endometrium closely, which had an influence on repair of endometrium. It was assumed that fibrinolysis system hyperfunction and significantdecreasing of ER and PR expression in decidual tissues correlated with uterine prolonged bleeding after abortion.The effect of mifepristerone on ovarian function has been proved. In follicular phase of menstrual cycle, mifepristerone inhibited development of follicle and delayed ovulation. In early follicular phase of menstrual cycle, mifepristerone temporarily inhibited the follicular development, estradiol secretion decreased during treatment. Serum FSH, LH levels had no changes. In mid- and late follicular phase of menstrual cycle, with the doses increasing, previous dominant follicle was atrophied, estradiol secretion decreased and maintained at a low level. Once stopping administration of mifepristerone, new follicle began to develop; or dominiant follicle was inhibited to some extent, the dominant follicle recovered to grow after treatment,. With low doses of mifepristerone (1mg/day), it did not inhibit the follicle growth, but inhibited ovulation. when follicular growth was not inhibited, mifepristerone still delayed ovulation for two-five days. The reason was that it inhibited the progesterone secretion before ovulation or delayed the LH surge which resulted from mifepristerone resisting the positive feedback of progesterone in hypothalamus and pituitary levels. In this phase, serum FSH, LH levels decreased. Mifepristerone had influences on luteal function of ovary in luteal phase of menstrual cycle, especially in mid- and late luteal phase. In early luteal phase, mifepristerone did not affect luteal function or length of the cycle. With high doses given, mifepristerone can induce luteolysis in advance, so estradiol and progesterone secretion decreased rapidly and luteal phase of cycle was shorter. When low dose given, mifepristerone can inhibit luteal function of cycle reversibly, estradiol and progesterone secretion recovered after decreased slightly, slight lengthening or no change of luteal phase. So the effect of mifepristerone on the luteal function of cycle is associated with its doses and various stages during menstrual cycle. Physiology and pathology of uterine endometrium is closely correlated with ovarian function. So we presumed thatinhibition of ovarian function after medical abortion influenced the repair of uterine endometrium and results in uterine prolonged bleeding.WHO studied reproductive hormone profiles after pregnancy termination with mifepristerone of two different doses. Serum estradiol and progesterone levels on 1st 4 days ,eighth .fifteenth, and forty-third after abortion were assayed by RIA. Serum estradiol levels increased during the 1st 48 hours after the start of treatment, and their concentrations were still higher than pretreatment values on day 4. In contrast ,the levels of serum progesterone started to decline immediately and were significantly lower on day 4 than on day 1. After prostaglandin, the concentrations of all two hormones rapidly decreased to nonpregnant values. He CH et al assa...
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