Objective

The pathophysiological process behind the increased risk of cardiovascular disease (CVD) in transgender women remains to be elucidated. The objective of this study was to investigate the effect of feminizing gender-affirming hormone therapy (GAHT) on platelet activation and inflammation as a possible explanation for this phenomenon.

Design

Longitudinal cohort study.

Methods

Venous blood was collected from 17 transgender women at 0, 12 and 52 weeks after GAHT initiation, consisting of estradiol and testosterone suppression. Platelet activation markers plasma thromboxane B2, Closure Time, CD63, CD62p, platelet-leukocyte complexes and immature platelet fraction were measured. CRP and 11 cytokines were measured as inflammation markers.

Results

CD63, CD62p and platelet-leukocyte complexes tended to increase after 12 weeks of GAHT. After 52 weeks, all platelet activation markers showed anti-aggregatory changes, of which Closure Time (measured using an adenosine diphosphate cartridge) (+21%, 6;39) and immature platelet fraction (-19%, -30;-7) were statistically significant. Eight out twelve inflammation markers exhibited a decreasing tendency at week 12, while inflammation marker granulocyte colony-stimulating factor significantly increased (+40%, 9;79). Equivalently, after 52 weeks, eight inflammation markers tended to decrease, only significantly so for IL-12p70 (-82%, -95;-35), while IL-5 was significantly higher (+153%, 4;516).

Conclusions

Our collective findings imply that platelet activation fluctuates during feminizing GAHT, exhibiting an initial increase followed by a decrease. Additionally, inflammation markers tend to decrease. Within the scope of this study, we could not identify GAHT induced platelet activation as a definite contributing factor in the increased risk of CVD in transgender women.