Platelet activation and inflammation in transgender women using hormone therapy

Objective

The pathophysiological process behind the increased risk of cardiovascular disease (CVD) in transgender women remains to be elucidated. This exploratory study aimed to investigate whether changes in platelet activation and inflammation after the start of feminizing gender-affirming hormone therapy (GAHT) could be a contributing mechanism.

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. Eight out twelve inflammation markers exhibited a decreasing tendency at week 12. Equivalently, after 52 weeks, eight inflammation markers tended to decrease, seven of which had also exhibited a decrease at week 12.

Conclusions

The collective findings suggest 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. Studies with larger numbers of participants and longer follow-up duration are needed to further investigate the effect of feminizing gender-affirming hormone therapy on platelet activation and inflammation.

Trial registration

EudraCT #2017-003072-31.