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#diethylstilbestrol

2 public questions tagged with this topic.

Teratogens

DES exposure was historically used to prevent:

Diethylstilbestrol history illustrates misuse of synthetic hormone in obstetrics. Between 1940s and early 1970s physicians prescribed DES believing synthetic estrogen would support pregnancy by stimulating placental growth, increasing uterine blood flow and preventing miscarriages especially in women with recurrent abortion history. Randomized trials later showed no preventive benefit and revealed teratogenic sequelae in offspring. Marketed for threatened abortion prophylaxis, DES was not intended for neural tube defects or infection treatment. Its extensive use to prevent miscarriages despite lack of efficacy became notorious example of iatrogenic endocrine disruption causing reproductive tract anomalies and neoplasia.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: DES historically used to prevent miscarriages.

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Teratogens

DES exposure in utero is strongly associated with:

Prenatal exposure to diethylstilbestrol during organogenesis of reproductive tract produces long-term carcinogenic outcome. Daughters exposed in utero develop vaginal adenosis where glandular epithelium persists in vagina, progressing to clear-cell adenocarcinoma rare gynecologic malignancy normally occurring postmenopausally. Risk appears between ages fifteen to twenty-two illustrating fetal origin of adult cancer. DES induces epigenetic alterations in HOXA and WNT genes, persistent changes in estrogen receptor expression, leading to neoplastic transformation decades after exposure. Association established causal link between in utero estrogenic teratogen and adolescent clear-cell adenocarcinoma becoming textbook example of transplacental carcinogenesis.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 20: DES association clear-cell adenocarcinoma.

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