Contraception-Related Venous Thromboembolism in Adolescents

O’Brien, Sarah H.

doi:10.1055/s-0033-1363469

Cited by 11 publications

(13 citation statements)

References 22 publications

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“…A major harmful effect of oral estrogen for menopausal hormone therapy (MHT) or combined oral contraceptive (COC) users is an imbalance in hemostasis leading to a global enhancement of thrombin generation that increases the risk of venous thromboembolism (Canonico 2014, O'Brien 2014, Scarabin 2014). In addition, several studies have linked the use of exogenous estrogen preparations to the risk of initiating breast cancer (Stahlberg et al 2004, Lai et al 2011, Turkoz et al 2013.…”

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confidence: 99%

Estetrol is a weak estrogen antagonizing estradiol-dependent mammary gland proliferation

Gérard¹,

Blacher²,

Communal³

et al. 2014

Journal of Endocrinology

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Estetrol (E 4 ) is a natural estrogen produced exclusively by the human fetal liver during pregnancy. Its physiological activity remains unknown. In contrast to ethinyl estradiol and estradiol (E 2 ), E 4 has a minimal impact on liver cell activity and could provide a better safety profile in contraception or hormone therapy. The aim of this study was to delineate if E 4 exhibits an activity profile distinct from that of E 2 on mammary gland. Compared with E 2 , E 4 acted as a low-affinity estrogen in both human in vitro and murine in vivo models. E 4 was 100 times less potent than E 2 to stimulate the proliferation of human breast epithelial (HBE) cells and murine mammary gland in vitro and in vivo respectively. This effect was prevented by fulvestrant and tamoxifen, supporting the notion that ERa (ESR1) is the main mediator of the estrogenic effect of E 4 on the breast. Interestingly, when E 4 was administered along with E 2 , it significantly antagonized the strong stimulatory effect of E 2 on HBE cell proliferation and on the growth of mammary ducts. This study characterizes for the first time the impact of E 4 on mammary gland. Our results highlight that E 4 is less potent than E 2 and exhibits antagonistic properties toward the proliferative effect of E 2 on breast epithelial cells. These data support E 4 as a potential new estrogen for clinical use with a reduced impact on breast proliferation.

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confidence: 99%

Estetrol is a weak estrogen antagonizing estradiol-dependent mammary gland proliferation

Gérard¹,

Blacher²,

Communal³

et al. 2014

Journal of Endocrinology

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“…A comparison group of controls was established with patients observed for other-than-IBD conditions at our Unit and at the Unit of Gynaecology and Obstetrics (ratio 1:2) [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] . Demographics and physical information of patients were collected from the clinical charts.…”

Section: Methodsmentioning

confidence: 99%

Hormonal contraceptives and venous thromboembolism: Are inflammatory bowel disease patients at increased risk? A retrospective study on a prospective database

Pellino

Sciaudone

Caprio

et al. 2015

Annals of Medicine &Amp; Surgery

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Recent studies showed an increased risk of venous thromboembolism (VTE) in patients receiving oral hormonal contraceptives. Inflammatory bowel diseases (IBD) often affect young patients and represent a pro-coagulant condition. This could result from active inflammation, but a potential role for genetic and molecular factors has been suggested. Hormonal contraceptives have also been associated with increased risk of VTE and the risk may be greater in IBD patients that already are in a pro-coagulant status, but no definitive data are available in this population. The purpose of our study was to seek for differences of the risk of VTE in IBD patients receiving hormonal contraceptives compared with controls.This is a retrospective study. We interrogated a prospectively maintained database of IBD patients observed at our outpatient clinic between 2000 and 2014. All female patients managed conservatively, with no active disease, who were taking oral hormone contraceptives in the study period, were included. Patients observed for other-than-IBD conditions at our Unit and at the Unit of Gynaecology and Obstetrics, receiving contraceptives, served as controls (ratio 1:2). Patients with cancer, those receiving hormonal therapy, and those with known genetic predisposition to VTE were excluded.We included 146 six IBD patients and 290 controls. One patient in each group developed VTE. Overall, the incidence of VTE associated with oral contraceptives was 0.5%. IBD was associated with increased risk of VTE (OR 1.9, 95% CI 0.12–32.12, p > 0.99). Active smokers since 10 years (17.2%) had higher risks of VTE (OR 8.6, 95% CI 1.16–19.25, p = 0.03).Our data show that patients with IBD in remission are not at higher risk of VTE due to oral oestrogen-containing contraceptives compared with non-IBD controls. Smokers are at increased risk, irrespective of the baseline disease.

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“…In this perspective, although we have studied a small cohort of patients with a short period of follow-up, we feel confident that we are presenting the results of an individualised prophylaxis based on clinical outcomes. Winning this award encourages us to keep on improving the quality of patient care, maintaining In a retrospective mood, I decided to review the Young Investigator awardees from previous years as well as the outcome of their subsequent submissions [11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27] to Seminars in Thrombosis & Hemostasis, and as summarized in ►Table 2. Indeed, what I find personally gratifying is that each article [11][12][13][14][15][16][17] from every Young Investigator Award winner from 2009 and 2010 has appeared in the top 100 Table 2 Young investigator awardees from previous years…”

Section: Young Investigator Awardeesmentioning

confidence: 99%