Abstract #1403021: HIV Status in a Patient on Testosterone Therapy: Confounder or Modifier to Venous Thromboembolism?

Abstract

The association between venous thromboembolic events (VTE) and testosterone therapy has been controversial. Some studies showed an increased risk of VTE with testosterone use, while few studies showed none. Furthermore, some data suggest HIV can also predispose patients to a hypercoagulable state due to immune dysregulation. A 60-year-old male presented with right leg pain and dyspnea. He was on an aromatase inhibitor and testosterone replacement therapy (TRT) for aromatase excess syndrome, and on bictegravir, emtricitabine and tenofovir alafenamide for HIV infection with normal CD4 count and undetectable viral load. Hospital course revealed right mid-femoral deep vein thrombosis and right-sided pulmonary embolism. He was managed conservatively with IV heparin and eventually discharged on a direct oral anticoagulant. Existing literature on the correlation between VTE and TRT is inconclusive. A case-control study in the USA showed no increased risk of VTE in those on TRT. However, another population-based case-control study in the UK showed that TRT had an increased incidence of VTE compared to general population, with peak risk noted at 6 months. Possible reasons for the higher risk of VTE in patients requiring TRT included increased hematocrit, platelet aggregation, and blood viscosity. A recent case-crossover study that included more VTE-exposed cases showed that TRT patients had greater short-term risk of VTE, especially in the immediate period after initiation of therapy. Another important factor to consider in this patient’s predisposition to VTE is his HIV status which promotes a prothrombotic state and predisposes patients to venous and arterial thromboembolism. Likely due to immune dysregulation secondary to chronic inflammation and immune activation. It usually happens in patients with low CD4 counts and high viral loads. But, in HIV patients with well-controlled viral load and CD4 counts, data suggests that VTE incidence is close to that of general population. In our patient, who was on TRT chronically with no previous VTE, it is hard to assess if his current HIV status was a confounder to his hypercoagulable state or a modifier to an existing risk. With subgroups of TRT-using patients like the transgender population having an increased incidence of HIV, concurrent infection may heighten clinical risk. It is essential to further explore the confounding versus modifying effect that HIV may have on VTE incidence. Currently, there are no large-scale clinical trial data available to identify the true association of VTE with TRT.