Serum Levels of Unconjugated and Total Oestrogens and Dehydroepiandrosterone, Progesterone and Urinary Oestriol Excretion in Pre-Eclampsia

Rosing, Ulf; Carlström, Kjell

doi:10.1159/000299081

Cited by 45 publications

(22 citation statements)

References 19 publications

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“…Women with preeclampsia, notably severe preeclampsia, have been reported to have lower estrogen levels during pregnancy (5,21). Some studies have also reported higher levels of androgens in women with preeclampsia (22), and low levels of androgens have been implicated in the pathogenesis of testicular cancer (23).…”

Section: Discussionmentioning

confidence: 99%

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Pettersson

Richiardi²,

Cnattingius³

et al. 2008

Cancer Research

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Altered levels of pregnancy hormones have been suggested to initiate testicular cancer prenatally in the male fetus. The placenta is the main source of pregnancy hormones, and pregnancy hypertension and preeclampsia are associated with placental malfunction, including altered levels of hormones such as estrogen and human chorionic gonadotropin. We therefore evaluated fetal exposure to pregnancy hypertension and preeclampsia in relation to risk of testicular cancer in adolescent and adult life. We identified 293 cases of germ cell testicular cancer in the Swedish Cancer Register, and 861 controls in the Swedish Medical Birth Register. The standardized antenatal and delivery charts of the cases and controls were traced in the archives of the delivery units, and information about maternal and pregnancy characteristics such as gestational hypertension, proteinuria, anemia, and glucosuria were extracted. Odds ratios (OR) with 95% confidence intervals (CI) were calculated using conditional logistic regression. We found a strongly decreased risk of testicular cancer among subjects exposed to severe gestational hypertension (OR, 0.29; 95% CI, 0.12-0.74, compared with no hypertension), whereas the risk was increased among those exposed to mild gestational hypertension (OR, 1.62; 95% CI, 0.98-2.69) during the fetal period. The mechanism behind the association between pregnancy hypertension and testicular cancer is unclear, but our findings may reflect a potentially protective effect of the altered pregnancy hormones such as human chorionic gonadotropin that occur in severe gestational hypertension and preeclampsia. [Cancer Res 2008;68(21):8832-6]

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Section: Discussionmentioning

confidence: 99%

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Pettersson

Richiardi²,

Cnattingius³

et al. 2008

Cancer Research

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“…Although the study subjects themselves measured some end point variables (weight, height, and waist and hip circumferences), it is highly unlikely that any possible measurement error differs by exposure status. Altered placental function is described in preeclampsia, and several hormonal factors that may relate preeclampsia to decreased risk of breast cancer have been reported: reduced levels of estrogens (19) and IGF-1 (20), and increased levels of progesterone (21) and androgens (19,22). These factors may influence the offspring through programming, which hypothetically would alter age at menarche or final height.…”

Section: Discussionmentioning

confidence: 99%

Tall or Short? Twenty Years after Preeclampsia Exposure In Utero: Comparisons of Final Height, Body Mass Index, Waist-to-Hip Ratio, and Age at Menarche among Women, Exposed and Unexposed to Preeclampsia during Fetal Life

et al. 2001

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Women exposed to preeclampsia during fetal life have lower risk of breast cancer, compared with unexposed women, possibly through fetal programming. Hypothetically, preeclampsia exposure could affect well-known risk factors for breast cancer, such as pubertal development or adult anthropometry. Women born in a defined geographic area of Sweden from 1973 through 1978, with verified preeclampsia exposure (n ϭ 230) and nonexposure (n ϭ 359) during fetal life, answered questions about anthropometric measures, smoking, parity, and age at menarche in a telephone interview in early adulthood. Compared with unexposed offspring, female offspring of women who had preeclampsia were lighter and shorter for gestational age, but in young adulthood there were no differences in height, body mass index, waist-to-hip ratio, or age at menarche. When analyzing the effects of other maternal and fetal characteristics, the results indicate that approximately 50% of the variance in final height was explained by parental heights and birth length for gestational age. Young-adult body mass index was weakly associated with maternal body mass index, maternal smoking, and birth weight for gestational age, which together explained 12% of the variance. Neither of the assessed maternal or fetal characteristics were significantly associated with age at menarche or waist-tohip ratio. These data indicate that neither adult anthropometry nor age at menarche is in the causal pathway between intrauterine preeclampsia exposure and the reduced risk of breast cancer. Women exposed to preeclampsia during their fetal life are reported to have decreased risk of breast cancer (1, 2). Other well-known risk factors for breast cancer are early menarche and tall stature (3, 4). Both the association between preeclampsia and breast cancer and the association between early menarche or tall stature and breast cancer have been hypothesized to be caused by intrauterine estrogen exposure (5-7). Therefore, one reasonable hypothesis is that preeclampsia exposure could affect well-known risk factors for breast cancer, such as pubertal development or adult anthropometry, which in turn are important for breast cancer development.Birth characteristics and adult central obesity are also reported to be associated with breast cancer, coronary heart disease, insulin resistance, and hypertension (8 -13), but whether intrauterine exposure to preeclampsia influences the adult fat distribution of growth-restricted individuals is presently not known.To better understand the biologic pathway for how the intrauterine environment might influence adult morbidity, we assessed the effects of preeclampsia exposure and birth characteristics on known risk factors for breast cancer, such as final height, difference from target height, BMI, waist-to-hip ratio, and age at menarche. METHODS

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“…However, circulating maternal estrogens near delivery do not seem to be lower in preeclampsia compared with uncomplicated pregnancy (33,34). Alterations in estrogen conjugation in preeclampsia may explain why concentrations are reduced in urine (the conjugated form), but not in maternal serum (33,35). In addition, the limited data are not consistent with lower umbilical cord blood (from here on referred to as ''cord'') estriol, estradiol, and estrone concentrations in preeclampsia (36).…”

Section: Prominent Hypotheses To Explain Prenatal Risk Factorsmentioning

confidence: 99%

Exploring the Underlying Hormonal Mechanisms of Prenatal Risk Factors for Breast Cancer: A Review and Commentary

Troisi

Potischman

Hoover

2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Prenatal factors have been hypothesized to influence subsequent breast cancer development. Directly evaluating the associations of in utero exposures with risk, however, presents several methodologic and theoretical challenges, including the long induction period between exposure and disease and the lack of certainty regarding the critical timing of exposure. Indirect evaluation of these associations has been achieved by use of proxies such as gestational and neonatal characteristics. Evidence suggests that preeclampsia is associated with a reduced breast cancer risk, whereas high birth weight and dizygotic twinning seem associated with an increased risk. Asians born in Asia have substantially lower breast cancer risks than women born in the West. Although data thus far are few, what exists is not consistent with a unifying hypothesis for a particular biological exposure (such as estrogens or androgens) during pregnancy as mediating the observed associations between pregnancy factors and breast cancer risk. This suggests that additional studies of prenatal factors should seek to broaden the range of hormones, growth, and other endocrine factors that are evaluated in utero. Once candidate biomarkers are identified, assessing them with respect to breast cancer and with intermediate end points in carcinogenesis should be a priority. In addition, investigations should explore the possibility that in utero exposures may not act directly on the breast, but may alter other physiologic pathways such as hormone metabolism that have their effect on risk later in life. (Cancer Epidemiol Biomarkers Prev 2007;16(9):1700 -12)

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Serum Levels of Unconjugated and Total Oestrogens and Dehydroepiandrosterone, Progesterone and Urinary Oestriol Excretion in Pre-Eclampsia

Cited by 45 publications

References 19 publications

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Gestational Hypertension, Preeclampsia, and Risk of Testicular Cancer

Tall or Short? Twenty Years after Preeclampsia Exposure In Utero: Comparisons of Final Height, Body Mass Index, Waist-to-Hip Ratio, and Age at Menarche among Women, Exposed and Unexposed to Preeclampsia during Fetal Life

Exploring the Underlying Hormonal Mechanisms of Prenatal Risk Factors for Breast Cancer: A Review and Commentary

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