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An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
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Pulmonary embolism due to exogenous estrogen intoxication
Caner Çelik1, Murat Carus1, Fatih Büyükcam2
1Department of Emergency Medicine, Bağcılar Education & Research Hospital, Bağcılar, İstanbul, Turkey.
The American Journal of Emergency Medicine
|October 18, 2017
Summary
A single high-dose of ethinyl estradiol and cyproterone acetate, commonly found in birth control pills, can trigger pulmonary embolism (a blood clot in the lungs). This risk is important to consider even without prior predisposing factors.
Area of Science:
- Pharmacology
- Cardiology
- Toxicology
Background:
- Pulmonary embolism (PE) is a significant cause of morbidity and mortality, often linked to venous thromboembolism (VTE).
- Exogenous estrogen use is a known risk factor for VTE, typically associated with therapeutic dosages.
Observation:
- A case report details a 29-year-old female presenting with acute pulmonary embolism.
- The embolism was attributed to a single, high-dose ingestion of 17 pills containing ethinyl estradiol (0.035mg) and cyproterone acetate (2mg) in a suicide attempt.
- The patient had no previously identified risk factors for thromboembolism.
Findings:
- Thrombolytic therapy was administered for the acute pulmonary embolism.
- The patient was subsequently discharged on oral warfarin for anticoagulation.
- This case highlights a potential link between acute, high-dose exogenous estrogen exposure and the development of PE.
Implications:
- Clinicians should consider the potential for acute VTE, including pulmonary embolism, following even a single high-dose ingestion of combined oral contraceptives or similar estrogen-containing medications.
- This case underscores the importance of a thorough medication history, including recent ingestions, in patients presenting with unexplained thromboembolic events.
- Further research may be warranted to elucidate the precise mechanisms and dose-response relationship of acute estrogen exposure in inducing VTE.
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