Testosterone administration increases leukocyte-endothelium interactions and inflammation in transgender men

Testosterone induces an increase in leukocyte-endothelium interactions, adhesion molecules, and proinflammatory cytokines in transgender men. These effects could be related to cardiovascular risk in these patients.

VOLUME 115, ISSUE 2, P483-489


Francesca Iannantuoni, Ph.D., Juan Diego Salazar, Ph.D., Aranzazu Martinez de Maranon, Ph.D., Celia Banuls, Ph.D., Sandra Lopez-Domenech, Ph.D., Milagros Rocha, Ph.D., Felipe Hurtado-Murillo, M.D., Ph.D., Carlos Morillas, M.D., Ph.D., Marcelino Gomez-Balaguer, M.D., Ph.D., Víctor Manuel Víctor, Ph.D.



To evaluate the effect of testosterone treatment on metabolic and inflammation parameters and leukocyte-endothelium interactions in transgender men (TGM).


Prospective observational study.


University hospital.


One hundred fifty-seven TGM.


Administration of testosterone undecanoate (1,000 mg, intramuscular) every 12 weeks.

Main Outcome Measure(s)

Endocrine parameters, adhesion molecules (vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, and E-selectin), proinflammatory cytokines interleukin-6, and tumor necrosis factor alpha were evaluated in serum before and after treatment using Luminex’s xMAP technology. In addition, interactions between human umbilical vein endothelial cells and polymorphonuclear leukocytes were assessed by flow chamber microscopy.


Testosterone treatment led to an increase in leukocyte-endothelium interactions due to an increase in polymorphonuclear leukocytes rolling and adhesion and decreased rolling velocity. It also boosted levels of vascular cell adhesion molecule-1, E-selectin, interleukin-6, and tumor necrosis factor alpha. As expected, testosterone also produced a significant increase in free androgenic index, androstenedione, total testosterone, and atherogenic index of plasma and a decrease in sex hormone–binding globulin and high-density lipoprotein cholesterol.


Treatment of TGM with testosterone induces an increase in leukocyte-endothelium interactions and adhesion molecules and proinflammatory cytokines. These effects are a reason to monitor cardiovascular risk in these patients.