FRI428 VTE And Testosterone Therapy: What Is The Risk?

Abstract

Abstract Disclosure: C. Cheatham: None. J. Colburn: None. M. Kemm: None. Testosterone replacement therapy (TRT) to treat hypogonadism from a variety of underlying etiologies remains increasingly prevalent within the United States. While VTE is a known potential risk, the prevalence, underlying mechanism, and associated risk factors remain incompletely understood. Men initiating TRT for hypogonadism often do not receive adequate pre-treatment evaluation or have therapy initiated despite normal testosterone levels. While a 2021 meta-analysis 1 did not demonstrate significantly increased VTE risk associated with TRT, the wide confidence interval, reported low quality of evidence, and lack of studies examining VTE as a primary outcome with data obtained via adverse event reporting demonstrates the importance of further investigation. Case 1: 55-year-old male with unilateral orchiectomy and associated primary hypogonadism started on TRT 10years prior presented to the hospital with acute onset chest pain and shortness of breath. CT angiography demonstrated right lower lobe segmental pulmonary emboli with parenchymal infarction. At the time of presentation, he was on IM testosterone cypionate 200mg weekly and anastrozole with total testosterone970 ng/dL, free testosterone 298 pg/mL, undetectable estradiol, and hematocrit 41.5%. His testosterone and anastrozole were discontinued at discharge, and he had a negative hypercoagulability workup by a hematologist. Case 2: 61-year-old male with history of OSA, obesity, and TRT initiated 8 months prior for erectile dysfunction presented to the hospital with dyspnea. CT angiography demonstrated large bilateral pulmonary artery emboli with right heart strain consistent with submassive PE. Review of clinical records preceding TRT initiation indicate normal testosterone values of 533 ng/dL with free testosterone 60.6 pg/dL. At the timeof presentation, his total testosterone was 685 ng/dL, free testosterone 139 pg/mL, and hematocrit of 54%with history of polycythemia since TRT initiation and no documented intervention. He was treated withIR thrombectomy and anticoagulation, and TRT was discontinued at discharge. His hematocrit normalized at follow-up and, after negative hypercoagulability evaluation by a hematologist, TRT was felt to be the most likely etiology of his VTE. These reported cases of VTE in men of different ages, underlying pathology, testosterone levels at time of event, presence of polycythemia, and time since testosterone initiation highlights the importance of further investigation on the true risk of thrombotic events in TRT patients and necessity of increased patient counseling of potential adverse outcomes. 1. Ayele HT, Brunetti VC, Renoux C, Tagalakis V, Filion KB. Testosterone replacement therapy and the risk of venous thromboembolism: A systematic review and meta-analysis of randomized controlled trials. Thromb Res. 2021;199:123-131. doi:10.1016/j.thromres.2020.12.029 Presentation: Friday, June 16, 2023