Abstract

The concentration of microscopically detectable blood vessels was significantly lower in endometrium exposed to progesterone-releasing intrauterine contraceptive devices (IUDs) than in control endometrium (mean vessel density 2.39 and 3.92, respectively). The percentage of vessels with defects was significantly higher in IUD samples (35.0%) than in control samples (13.4%). There was no significant difference in hemostatic response to vessel injury between the IUD and control samples. Although they were more defective than in controls, the blood vessels of progesterone IUD-exposed endometrium were far fewer in number, which may account for significantly less uterine blood loss in the users of these devices. In addition, the progesterone IUDs do not appear to inhibit hemostasis in the endometrium so that blood loss from injured vessels may be minimized.

PIP:

It has been previously demonstrated that increased vascularity, vessel defect formation, and poor hemostasis are prime factors in the increased endometrial bleeding associated with plastic IUDs. This paper presents the results of a morphologic sutdy on progestogen IUD-exposed endometrium to determine the reasons for long-term decreased menstrual blood loss and short-term increased intermenstrual blood loss following insertion of such an IUD. Endometrial biopsies were collected from 8 women wearing a Progestasert at various times in the cycle, and from 9 control women during the middle to late luteal phase of the menstrual cycle. All morphometric and electron microscopic studies were done at the Women's Hospital, Los Angeles County/USC Medical Center. Biopsies from the Progestasert users were taken 54 months after initial insertion. Each progesterone-IUD was replaced approximately every 24 months. Electron microscopy was used to examine the tissue samples. Chi-square test and the Mann-Whitney U Test according to Siegel were used in statistical analysis. Average blood vessel density for the 8 progesterone users was 2.39 (range, 13.0 to 3.71) compared to 3.92 for the controls (range, 3.33 to 4.68); the difference was significant at p0.01, Mann-Whitney test. Vessel concentration ratio of experimental to control endometrium was 3.5. Defective vessels for control cases expressed as a percentage of total vessels ranged from 0% to 24%. For progesterone IUD-endometrium, values per case varied from 7.1% to 64%. Average percentage of defective vessels for controls was 13.4 and for Progestasert users, 35.0%; the difference was significant at p0.001, Chi-square test. Majority of defects in the Progestasert users were associated with degenerative changes in endothelium. The increased concentration of vascular defects in the progesterone IUD-exposed endometria compared to control tissue in this series confirm earlier studies with plastic IUDs and defective vessels. Several factors contribute to decreased endometrial bleeding in women who have worn a progestrone-releasing IUD for at least 6 months. 2 critical factors include: 1) decreasing concentration of blood vessels in the endometrial functionalis (possibly the cause for progressive endometrial atrophy); and 2) no apparent inhibition of platelet hemostasis.