Pregnancy is normally supposed to occur in the uterus where the fertilized egg is deposited. Unfortunately, the DES Fallopian tube is structurally mutated and abnormal tissue growth can block the passage of the fertilized egg as it makes its way to the uterus in a DES daughter trying to become pregnant. As a result, the pregnancy starts to develop in the Fallopian tube. Ectopic pregnancy can be painful, can cause life threatening bleeding and must always be terminated to protect the health of the mother.
According to the Kaufman report highlighted above, the risk of an ectopic pregnancy in DES-exposed women was 4.2% and for unexposed women, 0.77% with a relative risk of 3.84 (14). In addition, Swan reported that a DES daughter is "8.6 times more likely to experience an ectopic pregnancy" compared to a control group (4). Ankum, in a meta-analysis of risk factors for ectopic pregnancy, determined that in utero exposure to DES was strongly associated with ectopic pregnancy later in life. This degree of risk was similar to other known risk factors for this event, including prior ectopic pregnancy, fallopian tube surgery and documented tubal pathology from sexually transmitted diseases (17).
Decherney et al examined the issue of Fallopian tube abnormalities in a 1981 paper (18). In it, they described 16 women of child-bearing age who had a history of intrauterine DES exposure and infertility. Laparoscopic findings in these women demonstrated DES "withered tubes" characterized by foreshortened, sacculated (with outpouchings) and convoluted with a pinpoint os (opening) at the uterine junction and constricted fimbriae near the ovaries. These departures of internal Fallopian tube architecture from normal clearly underlie the approximately 5-6% risk of ectopic pregnancy cited by Kaufman and other authors in these patients.
Newbold et al. described a DES developmentally arrested oviduct (DAO) mouse model. Of note is the fact that mice reproductive tracts continue to develop after birth, unlike humans (19). Grossly, the oviduct appears to retain a prenatal appearance and does not develop normally. The oviduct or Fallopian tube has a shortened length, a reduced number of fimbriae and an abnormal anatomical location. Histologically, the lining cells of the oviduct are more irregular, and there is epithelial hyperplasia and stromal (supportive structure) thickening. There are more secretory cells, a thicker muscle wall and more inflammatory changes in the DES-treated animals. Functionally, the oviducts of DES treated mice allow dye to pass through from the uterus to the oviduct much more than control mice.
4. Swan S.H. Intrauterine Exposure to Diethylstilbestrol: Long-term Effects in Humans. APMIS 108:793-804, 2000.
14. Kaufman R.H. et al. Continued Follow-up of Pregnancy Outcomes in Diethylstilbestrol-exposed Offspring. Obstetrics and Gynecology. 96;4: 483-9, October, 2000.
17. Ankum W.M. et al. Risk Factors for Ectopic Pregnancy: A Meta-analysis. Fertility and Sterility. 65; 6: 1093-1099, June 1996.
18. DeCherney A.H. et al. Structure and Function of the Fallopian Tubes Following Exposure to Diethylstilbestrol (DES) During Gestation. Fertility and Sterility. 36; 6: 741-745, December 1981.
19. Newbold R.R. et al. Developmentally Arrested Oviduct: A Structural and Functional Defect in Mice Following Prenatal Exposure to Diethylstilbestrol. Teratology. 27: 417-426, 1983.