Anti- Progesterone polyclonal antibody

We have previously reported that transdermal testosterone attenuates drug-induced QT interval lengthening in older men. However, it is unknown whether this is due to modulation of early ventricular repolarization, late repolarization, or both. In a secondary analysis of a prospective, randomized, double-blind, placebo-controlled three-way crossover study, we determined if transdermal testosterone and oral progesterone attenuate drug-induced lengthening of early and late ventricular repolarization, represented by the electrocardiographic measurements J-T(peak)c and T-peak-T-end, respectively, as well as T-peak-T-end/QT, a measure of transmural dispersion of repolarization. Male volunteers >= 65 years of age (n = 14) were randomized to receive transdermal testosterone 100 mg, oral progesterone 400 mg, or matching transdermal/oral placebo daily for 7 days. On the morning following the seventh day, subjects received intravenous ibutilide 0.003 mg/kg, after which electrocardiograms were performed serially. One subject was excluded due to difficulty in T-wave interpretation. Pre-ibutilide J-T(peak)c was lower during the testosterone phase than during progesterone and placebo (216 +/- 23 vs. 227 +/- 28 vs. 227 +/- 21 ms, P = 0.002). Maximum post-ibutilide J-T(peak)c was also lower during the testosterone phase (233 +/- 22 vs. 246 +/- 29 vs. 248 +/- 23 ms, P < 0.0001). Pre-ibutilide T-peak-T-end was not significantly different during the three phases, but maximum post-ibutilide T-peak-T-end was lower during the testosterone phase (80 +/- 12 vs. 89 +/- 18 vs. 86 +/- 15 ms, P = 0.002). Maximum T-peak-T-end/QT was also lower during the testosterone phase (0.199 +/- 0.023 vs. 0.216 +/- 0.035 vs. 0.209 +/- 0.031, P = 0.005). Progesterone exerted minimal effect on drug-induced lengthening of J-T(peak)c, and no effect on T-peak-T-end or T-peak-T-end/QT. Transdermal testosterone attenuates drug-induced lengthening of both early and late ventricular repolarization in older men.

It has been suggested that dysregulation of hormones is associated with schizophrenia (SCZ). This study aimed to measure the serum levels of progesterone and testosterone in 125 SCZ patients at different stages of treatment and 96 healthy control (HC) subjects. Our results showed that first-episode drug-free SCZ patients had significantly increased testosterone levels when compared with HC subjects, and chronic medication, but not short-term medication, further increased the serum testosterone levels in the patients. Further analysis suggested that the sex of the patients did not affect testosterone levels. In contrast, serum progesterone levels did not show significant differences between first-episode, drug-free SCZ patients and controls, and the antipsychotics increased progesterone levels in the male SCZ patients, but not female patients. Interestingly, our analyses demonstrated that the serum progesterone levels were negatively correlated with PANSS total score and PNASS positive score, suggesting a correlation between blood hormone levels and disease severity in SCZ patients. Taken together, our data showed differential changes in serum testosterone and progesterone levels in SCZ patients with or without antipsychotics, and our results suggest that increased sex hormone levels may be a defensive response to protect the human body under stress.