Drug Diethylstilbestrol Research Articles

Induction and characterization of a rat model of endometriosis

Endometriosis is a common condition that affects 5% to 10% of women during their reproductive years, although the aetiology and pathophysiology are still unknown. This study aimed to create an endometriosis model in rats to investigate the efficacy of natural and synthetic medications in treating endometriosis. An in vivo endometriotic model was established using a surgical induction method and the endocrine-disrupting drug diethylstilbestrol (DES). In brief, the experiment is categorised into three different groups. Each group contains five rats. The first group had no surgery, while in the in the second group of rats (n = 5), two small tissue grafts were fixed at the right and left walls of the abdomen. But in the in the third group of rats (n = 5), two small pieces of tissue have been grafted on the right and left abdomen walls by surgically along with DES treatments. Noninvasive photoacoustic imaging (PAI) was employed in the study to measure factors such as haemoglobin levels, oxygen saturation, and the size of endometriotic lesions. Histopathological analysis was carried out utilising staining techniques such as Hematoxylin and Eosin, Masson's Trichrome, and Periodic Acid Schiff, as well as immunohistochemistry with marker antibodies. Molecular markers in uterine tissue were examined using Western blots and real-time PCR. The developed endometriosis rat model showed a significant increase in the expression of anti-apoptotic Bcl-2, angiogenic marker VEGF and pro-inflammatory (COX-2 and IL-6) protein markers. In contrast to the control group, the treatment group had considerably lower Caspase-3 expression levels. Photoacoustic imaging (PAI) data demonstrated a constant increase in lesion size, as well as a decrease in oxygen saturation levels. The findings suggest that the in vivo endometriosis rat model may accurately assess the efficacy of natural or synthetic endometriosis treatments. This model may help in the improvement of disease understanding and the development of targeted therapeutic drugs.

The heritable legacy of diethylstilbestrol: a bellwether for endocrine disruption in humans.

Millions of women and their fetuses were exposed to the toxic pregnancy drug diethylstilbestrol (DES) from the 1940s into the 1970s, a time when the medical profession had little knowledge about potential developmental consequences of fetal drug exposures. Pathological consequences of DES exposure to the pregnant mothers and their offspring are well documented, but now generational research is finding that the grandchildren of women given DES in pregnancy are also at risk. This commentary summarizes presentations on this subject from the Beyond Genes panel "Heritable Impacts of Diethylstilbestrol (DES)."

The electrochemical oxidation of diethylstilbestrol (DES) in acetonitrile

The electro-oxidation of the former drug diethylstilbestrol (DES) was examined in detail by means of cyclic voltammetry (CV) and controlled potential electrolysis (CPE) techniques. Analogous to the electrochemistry of the structurally-related compound bisphenol A (BPA), DES undergoes two successive oxidation processes at ca. 0.64 and 0.81 vs. (Fc/Fc+)/V at glassy carbon electrodes in acetonitrile. The former anodic process was determined to involve up to four moles of electrons, whereas the latter anodic peak was assigned as the oxidation of a secondary product formed after the initial oxidation of DES. Results from variable voltammetric scan rate experiments showed that the secondary process can be outrun at high scan rates, while simultaneously detecting a new reduction wave (at ca. 0.50 vs. (Fc/Fc+)/V). Additionally, at fast scan rates, this reduction process was found to be chemically reversible; whereby a corresponding anodic peak was recorded at ca. 0.53 vs. (Fc/Fc+)/V on the second cycle. Following a similar mechanistic pathway as BPA, under prolonged periods of time (e.g. slow scan rates), DES is proposed to undergo an overall four-electron oxidation, whereas at fast scan rates the oxidation of DES was found to only involve two electrons. The CV data were modeled using digital simulations that allowed an estimation of the electrochemical and kinetic parameters associated with the electrode reactions.

Editors' Note: Contesting the Structures of Power and Exclusion

Editors' NoteContesting the Structures of Power and Exclusion Guisela Latorre, Mytheli Sreenivas, and Judy Tzu-Chun Wu Feminist critiques of transformations, movements, and hierarchies in different social contexts have truly enhanced many aspects of humanities and social science research over the past forty years. Gender scholars have offered both nuanced and complex insights into the mechanisms that maintain and police social stratification. We anticipate that the writings featured in this issue will further allow us to ascertain how these mechanisms affect the individual lives of women and gender others. The intersectional, decolonial, and interdisciplinary lenses that our authors use signal exciting new developments in the field of women's, gender, and sexuality studies. Deconstructing the social and scientific technologies of modernity designed to regulate physical and discursive bodies in patriarchal settings is an important intellectual mission for a number of our contributors to this issue. Nicole Sanders in "Gender and Consumption in Porfirian Mexico" explores how new consumer technologies in turn-of-the-century Mexico encouraged middle-and upper-class women to uphold traditional gender roles and racial exclusions. Also interested in how technologies inform body politics, Emily Johnston in "Poisoned Subjects" documents the life narratives of the women who used the fertility drug diethylstilbestrol (des) and developed vaginal and cervical cancer as a result. The technologies of war and women's bodies are the center of the short story "Soldier Girl" by Marjorie Maddox, which provides a semi-fictionalized account of Lynndie England, the woman at the center of the Abu Ghraib prisoner abuse scandal. While addressing the critical role that technologies of modernity play on the physical body, our contributors were also attentive to constructions of discursive bodies through the technologies of language and culture. The article "Fleshing Out the Ambiguous Body" by Sara Cohen Shabot rummages through the writings of South African novelist J. M. Coetzee, who in his various narratives proposes non-binary ways to regard bodies within the culturally hybrid geographies of Africa. [End Page vii] Technology not only informs our physical and figurative embodiments; it also affects our capacity for knowledge production and for literacy acquisition. The gendered discourses of science and progress that it generates, ones that privilege male whiteness, are challenged by some of our authors in this issue. Engineering scholar Kacey Beddoes writes in her essay titled "Institutional Influences that Promote Studying Down in Engineering Diversity Research" that the underrepresentation of women and minorities in that field persist because attempts at diversification ignore structural inequalities within the discipline. Sara Giordano in "Feminists Increasing Public Understandings of Science" urges scholars and students in the sciences to challenge assumptions of objectivity and absolute truth in order to make way for feminist and critical thinking skills in those areas of study. Both of these texts call for a profound transformation of educational institutions, a struggle that feminist educators have been waging for over a century. Some of the origins of the present-day struggles that both Beddoes and Giordano address can be appreciated in Patricia Carter's essay "Guiding the Working-Class Girl," where the author discusses the important work educator Henrietta Rodman carried out on behalf of working-class women during the early twentieth century in New York City. While the structures of inequality that Beddoes, Giordano, and Carter document in their articles are firmly situated within the United States, those addressed in the contributions by Sandra Mizumoto Posey, Sirpa Salenius, Gregory D. Smithers, and Janey Lew in this issue are transnational in nature. The personal narrative "Made in Occupied Japan" by Mizumoto Posey tells of the author's experiences with her transnational family whose history spanned the territories of the United States, Japan, and other parts of Asia, having been subject to gender oppression in all those locales. But empowerment and feminist resistance too are transnational. Salenius in "Transatlantic Interracial Sisterhoods" tells us about the U.S.–European transatlantic dialogues among women that animated social justice causes during the nineteenth century. Likewise, the artwork by Trinh Mai also featured here underscores the strength the artist gains by establishing connections between herself in the United States and her ancestors in Vietnam. By contrast though, Smithers's essay does not look beyond the...

Cyanine-based colorimetric and fluorescent probe for the selective detection of diethylstilbestrol in seawater, shrimp and fish samples

The synthetic estrogen drug diethylstilbestrol (DES) plays important roles in the treatment of estrogen deficiency disorders for human beings. The excessive intakes of DES can lead to physiological dysfunction and raise the risk of ovarian cancer, breast cancer and other diseases. However, it is still abused for improving the fat deposition or sex reversal procedure in aquatic economic creatures for pursuit of huge interests. DES can exist in aquatic products or polluted aquacultural seawater, which seriously threatens human health. Therefore, it is desirable to establish simple and sensitive methods for the detection of DES. In this work, we have developed a new colorimetric and fluorescent probe Cy-DES for the detection of DES with high sensitivity and selectivity. As a near-infrared probe, Cy-DES is able to avoid autofluorescence of dissolved organic compounds and maximize signal-to-background contrast. Taking advantage of the strong electrostatic interaction between the probe Cy-DES and DES, the spectroscopic properties of probe Cy-DES can be obviously changed in presence of DES. Under testing conditions, there is an excellent linearity within the range of 1–8μM (r=0.9997) and the detection limit is 0.2μM. The probe Cy-DES is successfully applied for the detection of DES in spiked seawater, shrimp and fish samples. Additionally, the detection of DES can be directly achieved by naked eyes with the utilizing of probe Cy-DES. The developed method is of great potential for application in the on-site detection of DES.

Shared models and mechanisms? The examples of DES and phthalate syndrome

Background: Historically, major environmental toxicants could be linked to human health outcomes because these early exposures were large and visible and risks to individuals were dramatic. The challenge we are now facing is that of detecting human health risks from invisible, low-level exposures that impact health predominantly at the population level. Endocrine disruption is, I suggest, the primary means by which such exposures impact health. To identify the impacts of these chronic low-levels exposures on human populations, animal toxicology studies can be invaluable as they can provide data that can then be assessed in epidemiology studies. Epidemiology studies can also inform animal toxicology as to possible links between exposures and effects. Aims: 1) To use the example of the drug diethylstilbestrol (DES) to examine how human studies can inform animal toxicology; and 2) to use the example of the phthalate syndrome to discuss how animal toxicology can inform epidemiology. Methods: I will review the historical interplay of animal and human studies in these two examples. Many outcomes of prenatal DES exposure in humans are seen in rodent studies, but not all. Similarly, not all aspects of the phthalate syndrome described first in rodents have been observed in humans. Examining the similarities and differences between outcomes of these exposures in humans and animals demonstrates the value (and challenges) of these cross-species comparisons. Conclusions: When animal and human data are available on an exposure-outcome relationship, and scientists in both areas are willing to learn from each other both the epidemiology and the toxicology benefit. Ultimately the conclusions of both are strengthened, with the result that public health is better protected.

Choice of animal feed can alter fetal steroid levels and mask developmental effects of endocrine disrupting chemicals

Exposure of fetuses to endocrine disrupting chemicals (EDCs), such as the estrogenic drug diethylstilbestrol (DES), disrupts development of the reproductive system and affects other aspects of adult phenotype including diseases, consistent with the developmental origins of health and disease hypothesis. To determine whether diet could influence the effects of DES, we compared mice fed a commonly used combination of soy-based Purina 5008 (breeding and lactation) and 5001 (post-weaning) with mice fed soy-based Purina 5002 throughout life. We exposed fetal CD-1 mice (F1) in utero on different feeds to a 0 (controls), low (0.1 μg/kg/day) or high (50 μg/kg/day) dose of DES via feeding the dam (F0) on gestation days 11–17. Compared to 5008, 5002 feed significantly increased serum estradiol in control fetuses. On 5008 (but not 5002) feed, DES significantly increased fetal serum estradiol at a low dose and reduced it at a high dose. Diet influenced the effects of in utero DES on F1 female onset of puberty and the uterine response to estradiol (an inverted-U dose–response relationship seen for DES on uterine weight with 5008/5001 feed was not observed with 5002). Both low- and high-dose DES reduced daily sperm production (DSP) in adult F1 males on 5008/5001 feed, whereas males fed 5002 showed no DES-induced reduction in DSP. Thus, we observed a number of low-dose effects of in utero DES exposure on Purina 5008/5001 feed that were not observed using Purina 5002, a feed commonly used in industry-funded toxicological studies conducted for regulatory purposes.

Center for Disease Control’s Diethylstilbestrol Update: A Case for Effective Operationalization of Messaging in Social Marketing Practice

The Center for Disease Control's (CDC) Diethylstilbestrol (DES) Update, a campaign to educate people who may have been exposed to the drug DES, is framed on the premises of the social marketing model, namely formative research, audience segmentation, product, price, placement, promotion, and campaign evaluation. More than that, the campaign takes a critical step in extending the social marketing paradigm by highlighting the need to situate the messaging process at the heart of any health communication campaign. This article uses CDC's DES Update as a case study to illustrate an application of a message development tool within social marketing. This tool promotes the operationalization of messaging within health campaigns. Ultimately, the goal of this project is to extend the social marketing model and provide useful theoretical guidance to health campaign practitioners on how to accomplish stellar communication within a social marketing campaign.

Evaluation of estrogenic activity of alcoholic extract of rhizomes of Curculigo orchioides

The rhizomes of Curculigo orchioides Gaertn. (Amaryllidacea) is an important Ayurvedic as well as Unani drug. It is present in several drug formulations used in the treatment of menorrhagia and other gynecological problems. In this study, we conducted a comparative study of estrogenic activity of alcoholic extract of Curculigo orchioides with diethylstilbestrol in bilaterally ovariectomized young albino rats. Bilaterally ovariectomized albino rats were divided into five groups ( n = 9) receiving different treatments, consisting of vehicle (0.6% w/v sodium carboxy methyl cellulose), ethanolic extract of rhizomes of Curculigo orchioides at three different doses (viz., 300, 600, 1200 mg/kg body weight) and standard drug diethylstilbestrol (DES) at a dose of 2 mg/kg body weight. All these were administered orally daily for 7 days. Estrogenic activity was assessed by taking percentage vaginal cornification, uterine wet weight, uterine glycogen content and uterine histology as parameters of assessment. Alcoholic extract of Curculigo orchioides showed a significant increase in percentage vaginal cornification, uterine wet weight ( P < 0.001), uterine glycogen content ( P < 0.001) and a proliferative changes in uterine endometrium compared to the control.

Could hormone residues be involved?

In this issue, Swan et al. report finding a relationship between the amount of beef consumed by women during pregnancy and subsequent sperm concentration in their sons in adulthood. There is extensive evidence that maternal nutrition and maternal consumption of specific nutrients, drugs and chemicals present in food during pregnancy and lactation can have consequences for subsequent pathophysiology of offspring. This has been demonstrated experimentally in animals, and the developmental origins of human health and disease (DoHAD) hypothesis also has considerable support from the epidemiological literature (Fowden et al., 2006; Gluckman et al., 2007). Only recently have researchers interested in fetal nutrition and metabolic diseases become aware of findings relating developmental exposure to the class of environmental chemicals known as endocrine disruptors to metabolic and reproductive disorders in males. Specifically, Skakkebaek et al. (2001) have identified that a cluster of reproductive abnormalities in males (sperm quality and testicular cancer) is associated with conditions identifiable at or shortly after birth (cryptorchidism, hypospadias), which they have named the ‘testicular dysgenesis syndrome (TDS)’. This cluster of abnormalities of male reproductive development is proposed to be due, at least in part, to fetal/neonatal exposure to environmental estrogens (EE) [one example of such an EE is bisphenol A, the chemical used to make polycarbonate plastic and the resin lining of metal cans (vom Saal and Hughes, 2005)] and chemicals with antiandrogenic activity [one example would be phthalates used in PVC plastic and many other products (Swan et al., 2005)]. Skakkebaek’s hypothesis is thus that developmental disorders identifiable at birth are predictive of subsequent male reproductive system pathologies, such as reduced fertility due to low sperm count as well as testicular cancer. Although there are a number of potential factors that could account for the association reported in the current study by Swan et al., these authors suggest based on the Skakkebaek TDS hypothesis that the association between the number of beef meals eaten per week during pregnancy and sperm concentration in male offspring might be due to exposure to hormonal residues in beef. This hypothesis is plausible because during the years this cohort of fertile men were in utero (median year of birth was 1970), beef cattle in North America (where the majority of study participants were born) were routinely treated with the growth-promoting anabolic steroids. For example, the drug diethylstilbestrol (DES) was widely administered to beef cattle in the USA between 1954 and 1979 (Raun and Preston, 2002). Although the use of hormones to promote an increase in lean muscle mass in beef cattle has not been legal in Europe since 1989, and while DES was banned in 1979, administration of combinations of other hormonally active drugs to beef cattle has continued to be a common practice in the USA and Canada. The International Joint Food and Agricultural Organization’s World Health Organization Expert Committee on Food Additives (JECFA) published acceptable (tolerable) daily intake ADIs (TDIs) for all hormones in current use as growth promoters in beef cattle, although the assumptions used by JECFA to determine ‘safe’ daily human exposure levels in their 1988 report have been challenged (Andersson and Skakkebaek, 1999). There has been a trade dispute over the safety of hormone residues in beef going on for many years, with the European Union opposing importing hormonetreated beef from the USA and Canada. The position of the USA and Canada is that hormone residues in beef pose no threat to human health; this position is based primarily on research concerning the mutagenic activity of estradiol. Over the past decade, there has been a shift in the focus of research in endocrinology, cancer and developmental biology based on findings that hormones, hormonally active drugs and *In autumn 2006, the author served on the science advisory committee of the European Union regarding low-dose effects of xenobiotic estrogenic chemicals in food.

Anogenital Distance and Phthalate Exposure: Swan et al. Respond

Anogenital Distance and Phthalate Exposure: Swan et al. Respond

Side‐effects of treatments for locally advanced prostate cancer

Sir,O’Connor and Fitzpatrick [1] neglected androgen deprivation by the generic drug diethylstilbestrol (DES, 1 mg), which was the first chemotherapy for any cancer (1941) and the basis for the Nobel Prize (1966); DES is a non-steroid oestrogen. Cox and Crawford’s 1995 review (96 references) of DES concluded: “A 1 mg dose of diethylstilbestrol remains a medical alternative to bilateral orchidectomy . . .” [2]. The 1986 National Cancer Institute (NCI) summary monograph of the 30-year study of DES, involving > 4000 men (VACUG III) concluded [3] that:(i) DES 1 mg was better than orchidectomy in slowing the progression of prostate cancer as measured by skeletal survey, acid phosphatase and cancer-specific deaths.(ii) DES 1 mg plus orchidectomy was no more effective than DES 1 mg alone, i.e. castrate levels of testosterone were not required and DES has nonsteroidal effects on prostate cancer.Scherr

Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra

Exposure of human fetuses to man-made estrogenic chemicals can occur through several sources. For example, fetal exposure to ethinylestradiol occurs because each year approximately 3% of women taking oral contraceptives become pregnant. Exposure to the estrogenic chemical bisphenol A occurs through food and beverages because of significant leaching from polycarbonate plastic products and the lining of cans. We fed pregnant CD-1 mice ethinylestradiol (0.1 microg/kg per day) and bisphenol A (10 microg/kg per day), which are doses below the range of exposure by pregnant women. In male mouse fetuses, both ethinylestradiol and bisphenol A produced an increase in the number and size of dorsolateral prostate ducts and an overall increase in prostate duct volume. Histochemical staining of sections with antibodies to proliferating cell nuclear antigen and mouse keratin 5 indicated that these increases were due to a marked increase in proliferation of basal epithelial cells located in the primary ducts. The urethra was malformed in the colliculus region and was significantly constricted where it enters the bladder, which could contribute to urine flow disorders. These effects were identical to those caused by a similar dose (0.1 microg/kg per day) of the estrogenic drug diethylstilbestrol (DES), a known human developmental teratogen and carcinogen. In contrast, a 2,000-fold higher DES dose completely inhibited dorsolateral prostate duct formation, revealing opposite effects of high and low doses of estrogen. Acceleration in the rate of proliferation of prostate epithelium during fetal life by small amounts of estrogenic chemicals could permanently disrupt cellular control systems and predispose the prostate to disease in adulthood.

Uterine Responsiveness to Estradiol and DNA Methylation Are Altered by Fetal Exposure to Diethylstilbestrol and Methoxychlor in CD-1 Mice: Effects of Low versus High Doses

We examined the effects on female CD-1 mice of fetal exposure to low doses of the drug diethylstilbestrol (DES) (0.1 μg/kg/day) and the insecticide methoxychlor (MXC) (10 μg/kg/day) as well as 1000-fold higher doses: 100 μg/kg/day DES and 10,000 μg/kg/day MXC. Pregnant females were administered these chemicals on gestation days 12–18. At 7–8 months of age, female offspring were ovariectomized and implanted for 7 days with a Silastic capsule containing estradiol. Relative to controls, females exposed to the 0.1 μg DES dose showed significantly heavier uteri, while females exposed to the 100 μg DES dose showed significantly lighter uteri. Females exposed prenatally to the 10 μg/kg dose of MXC had significantly heavier uteri relative to females exposed to the 10,000 μg/kg dose of MXC, but neither group differed significantly from controls. Liver weight for females exposed to both doses of DES was significantly greater than controls. Using a microarray approach to analyze DNA methylation, an increase in ribosomal DNA (rDNA) methylation was observed. Sequence data and Southern analysis indicate an increase in 18S rDNA and 45S pre-rDNA methylation in uterine samples exposed prenatally to low and high doses of DES. We thus found opposite effects of fetal exposure to a low and a high dose of DES on the uterine response to estradiol (inverted-U dose–response relationship). In contrast, there was a monotonic dose–response relationship found for prenatal DES exposure on both liver weight and ribosomal DNA hypermethylation.

Differential Effects of Diethylstilbestrol and 2,3,7,8-Tetrachlorodibenzo-p-dioxin on Thymocyte Differentiation, Proliferation, and Apoptosis in bcl-2 Transgenic Mouse Fetal Thymus Organ Culture

Both the estrogenic drug diethylstilbestrol (DES) and the pervasive environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibit thymocyte development. The mechanisms by which either agent induces thymic atrophy are still undetermined. We previously found that TCDD and DES inhibited C57BL/6 murine fetal thymocyte organ cultures (FTOC) at different stages of development. Now, using bcl-2 transgenic (TG) mice, we have further investigated their effects on FTOC proliferation, differentiation, maturation, and apoptosis. As with C57BL/6 mice, thymocyte development in C3H/bcl-2 FTOCs was inhibited by either TCDD (10 nM) or DES (20 μM) in both bcl-2 TG− and TG+ littermates. However, the percentage reduction of cell number induced by DES in bcl-2 TG+ FTOCs was significantly less than the level of inhibition in TG− FTOCs. There was no difference in the level of reduction from TCDD-exposed TG+ or TG− FTOC. Whereas TCDD increased production of mature CD8 cells in either strain, DES mainly yielded cells in the CD4−CD8− (DN) stage in TG− mice. The anti-apoptotic bcl-2 transgene overcame some DES blocking of DN thymocyte development, allowing more cells to differentiate into CD4 single-positive cells. Analysis of cell cycle showed that TCDD inhibited entry into S phase, whereas DES blocked cell cycling in the G2/M phase. TCDD did not induce detectable apoptosis in FTOC. However, unlike the effects of 17β-estradiol (E2) in vivo, DES induced apoptosis in the TG− FTOC, and these apoptotic cells were mainly in the DN subpopulation. This apoptosis could be prevented by the overexpression of bcl-2 in the TG+ mice. Our results demonstrate that, in addition to inhibition of fetal thymocytes at different stages of development by TCDD and DES, DES also induces thymic atrophy by both bcl-2-inhibitable apoptosis and by inducing cell cycle arrest in G2/M in the latest stage in the stem cell compartment. TCDD, on the other hand, does not induce apoptosis, but inhibits entry into cell cycle in the earliest stage in the stem cell compartment.

Normal development of the human female reproductive tract and alterations resulting from experimental exposure to diethylstilbestrol

An in vivo model is described for the study of human uterovaginal development in the presence and absence of the teratogenic drug diethylstilbestrol (DES). Intact reproductive tracts from fragments of 29 human embryos and fetuses 5.0 to 17.7 weeks of age obtained after dilatation and curettage were grown for four weeks in vivo in athymic (nude) mice that were either untreated (control) or implanted subcutaneously with a DES pellet. Control specimens grown in vivo continued their anticipated morphogenesis for equivalent in-utero ages; the normal processes observed included fusion of the paired embryonic müllerian ducts into a single uterovaginal canal, stratification of endometrial and tubal mesenchyma into inner (presumptive endometrial stroma) and outer (presumptive myometrium) layers; plication of tubal and endometrial mucosa; uterine gland formation; and stratification (transformation) of the simple columnar epithelium of the vagina and cervix into a stratified squamous plate. Specimens exposed in vivo to DES exhibited anomalies, many of which mimicked those observed clinically in young women exposed prenatally to DES. Glandular epithelium (adenosis) was found in the vagina. The upper genital tract was malformed; its growth was stunted, and the inner and outer stromal layers of the uterine corpus and fallopian tubes failed to segregate. The authors conclude that the in vivo model that they describe, with its built-in controls, provides a valid approach for examining the dynamics of morphogenesis and cytodifferentiation in developing human genital tracts under experimentally regulated conditions.

Consequences of Prenatal Exposure to Diethylstilbestrol

Exposure to the drug diethylstilbestrol (DES) during the first 18 weeks of prenatal life can have many results ranging from benign misconfigurations of the reproductive organs to adenocarcinoma. Since the drug was routinely administered to pregnant American women from 1940 to 1970, a large population of Americans are involved. The key factor is early awareness to the exposure and careful follow-up. Since many of those exposed are unaware that they received DES, the health care profession must be attuned to the signs and symptoms predisposed by the exposure and be able to provide adequate follow-up and education concerning this medical problem.