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Myocardial infarction and severe thromboembolic complications. As seen in an estrogen-dependent transsexual
Insights
Conjugated estrogen therapy can cause antithrombin III deficiency, leading to blood clots in transgender individuals. Stopping estrogen therapy resolved this deficiency and reduced thrombotic risk.
Area of Science:
- Cardiology
- Endocrinology
- Hematology
Background:
- Estrogen therapy is common in transgender individuals.
- Myocardial infarction and thromboembolic events are serious cardiovascular risks.
Observation:
- A genetic-male transsexual experienced myocardial infarction and thrombosis despite heparin therapy.
- The patient had no other cardiac risk factors but showed antithrombin III deficiency.
Findings:
- Antithrombin III deficiency resolved upon withdrawal of conjugated estrogen therapy.
- Estrogen-induced antithrombin III deficiency is a potential cause of thrombotic diathesis.
Implications:
- Identifies a previously unrecognized population at risk for estrogen-induced thrombosis.
- Highlights the need for prophylactic and therapeutic considerations in transgender patients on estrogen therapy.
Abstract:
An estrogen-dependent genetic-male transsexual had an extensive anterior wall myocardial infarction, despite insignificant coronary artery disease, a subsequent mural thrombosis, and resultant multiple cardioarterial thromboembolic events, despite heparin therapy. With an otherwise lack of cardiac risk factors, the patient was demonstrated to have an antithrombin III deficiency that resolved when conjugated estrogen therapy was withdrawn. Although congenital, plasminogen-activator dysfunction, or heparin-induced etiologies could not be ruled out, we believe this case demonstrated an estrogen-induced-antithrombin III deficiency culminating in thrombotic diathesis. This identifies a previously unrecognized population at risk. Prophylactic and therapeutic considerations are discussed.