Hematologists are often asked to weigh-in on the risks and benefits of exogenous hormone administration for non-hematologic indications. Meanwhile, aberrant hormone signaling pathways contribute to common and unusual hematologic conditions. This unique session explores the hematologic significances of exogenous hormone administration to transgender individuals, how estrogen-platelet signaling pathways contribute to sex-differences in platelet function and thrombotic risks, and the role of steroids in erythropoiesis.

Dr. Jean Connors will discuss the impact of exogenous hormones on the individual patient, reviewing both physiologic changes and effects on risk profiles for adverse events important for hematologists to understand. Unique risks and benefits of the use of specific hormones in cisgender and transgender patients will be explored using a case-based presentation format.

Dr. Dale Abel will present on data that demonstrates how OPA1 expression in platelets is increased in females and correlates with increased risk of thrombosis. Platelet OPA1 levels are regulated by estrogen. In female mice, genetic deletion of OPA1 in platelets reduces platelet function and in vivo thrombosis. In contrast, in male mice, genetic deletion of OPA1 in males leads to increased thrombosis and is reversed by increasing circulating levels of estrogen. The mechanism and potential impact of this novel estrogen regulated pathway will be explored in various thrombosis models and clinical contexts.

Dr. Robert Richard will address the role of steroids in erythropoiesis. The important role of steroids in red blood cell development was described over 50 years ago. Recent studies remind us that steroids have a central role in erythropoiesis as well as continuing therapeutic potential. Androgens have been the most studied steroid, but other steroid dependent pathways play an equally important role. Studies using corticosteroids in Diamond-Blackfan Anemia (DBA) point to signaling pathways that synergize with the glucocorticoid receptor. Identification of erythroid progenitors with increased sensitivity to glucocorticoids could lead to improvements in steroid based therapies for DBA and perhaps other underproduction anemias.