https://onlinelibrary.wiley.com/doi/full/10.2164/jandrol.107.002683#b26
There was a small but significant elevation of systolic blood pressure in the MENT group with no change in the testosterone group. A similar finding was reported in a previous study investigating MENT alone (von Eckardstein et al, 2003). Systolic blood pressure may reflect arterial stiffness and is increasingly recognized to be a strong cardiovascular risk factor (Oliver and Webb, 2003). Arterial stiffness is inversely related to testosterone concentrations in older men (Hougaku et al, 2006) and was increased by induced hypogonadism in men with prostate cancer (Smith et al, 2001). During MENT administration both testosterone and estradiol concentrations are low. Recent data suggest that endogenous estradiol may be vasculoprotective (Arnlov et al, 2006). Although MENT is aromatized to an active estrogen (LaMorte et al, 1994), the low serum concentrations both of MENT and therefore of potential active metabolites may contribute to increased arterial stiffness and a rise in systolic blood pressure, which therefore might actually be less affected by administration of a higher, more effective dose.
Anyone see a potential huge flaw in discussion above?
Study Design and Medication
The study was a randomized, open‐label trial investigating MENT implants or testosterone in combination with etonogestrel implants, with both groups scheduled for treatment for 48 weeks. Following 2 screening visits, subjects were randomized using a computer‐generated list and numbered sealed envelopes. Subjects in the MENT group were administered 2 implants each containing 135 mg of MENT acetate formulated as in previous studies to release about 400 μg of MENT Ac per implant per day (Anderson et al, 2003; von Eckardstein et al, 2003) subcutaneously with local anesthesia into the medial aspect of 1 arm, and 2 etonogestrel implants 4 cm long, each containing 68 mg of etonogestrel (Implanon; N.V. Organon, Oss, The Netherlands) into the other upper arm. The testosterone group was administered 600‐mg testosterone pellets (3 × 200 mg, N.V. Organon) subcutaneously into the anterior abdominal wall, repeated at weeks 12, 24, and 36, with 2 etonogestrel implants at first administration of testosterone. The etonogestrel and MENT implants were removed at the end of the treatment period, at which time the subjects entered the recovery phase.
