Contact Activation Is Alleviated by Testosterone Replacement Therapy in Klinefelter Syndrome: Evidence of Hormonal and Metabolic Modulation

March 27, 2026AndrologyOpen Access

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Key Points

The study aims to examine the dysregulation of the contact activation system in Klinefelter syndrome and the effects of testosterone replacement therapy.
Conducted a longitudinal study with three groups: testosterone-treated Klinefelter syndrome, untreated Klinefelter syndrome, and age-matched controls.
Measured plasma levels of contact activation system proteins using enzyme-linked immunosorbent assays.
Assessed activity of the contact activation system through functional assays measuring endogenous kallikrein potential and thrombin generation.
Analyzed correlations with sex hormones and body composition using mixed-effects models.
Untreated Klinefelter syndrome showed higher levels of coagulation factor XII and C1 esterase inhibitor than controls.
Testosterone replacement therapy significantly reduced levels of coagulation factor XII and C1 esterase inhibitor.
Body fat positively correlated with prekallikrein and endogenous kallikrein potential, suggesting a link to metabolic regulation.
Contact activation system activation leaned toward inflammatory rather than procoagulant pathways.

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Longitudinal study investigates testosterone's effect on thromboinflammatory risk in Klinefelter syndrome, suggesting hormonal and metabolic links.

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Chang et al. (2026) studied this question.

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