Goh V H
Department of Obstetrics and Gynaecology, National University of Singapore, National University Hospital, Kent Ridge, Singapore.
J Clin Endocrinol Metab. 1999 Sep;84(9):3313-5. doi: 10.1210/jcem.84.9.6006.
The present study made use of the female transsexual model and sought to evaluate the contributions of the ovarian, endometrial, and breast tissues to the androgen up-regulated production of prostate specific antigen (PSA). Serum levels of PSA were significantly raised in female transsexuals before surgery, after long-term androgen therapy (mean +/- SE = 35.3 +/- 6.2 pg/mL) when compared with female transsexuals before surgery, but with no androgen therapy (mean +/- SE = 1.53 +/- 0.25 pg/mL). In addition, in androngenized female transsexuals, after surgery, concentrations of PSA (mean +/- SE = 14.5 +/- 2.8 pg/mL) were significantly lowered compared with androngenized female transsexuals after surgery, but the levels were, nevertheless, significantly higher than in normal females. Monthly i.m. injection of 250 mg Sustanon-250 to female transsexuals had raised serum testosterone levels to within the male range. In five subjects, in whom serial measurements were taken, serum testosterone levels were greatly raised 24 h after the testosterone therapy; the mean level (+/-SE) was 19.5 +/- 2.1 ng/mL. But in spite of these high testosterone levels, serum PSA levels (mean +/- SE = 2.2 +/- 0.9 pg/mL) were not significantly raised. However, after 12 months of androgen therapy, the mean (+/- SE) PSA level in these five subjects was 47 +/- 11.6 pg/mL and was significantly higher than the mean level in nonandrogenized female transsexuals. The present study confirmed that high levels of testosterone were able to up-regulate PSA production in women. This up-regulation of PSA production is both a dose- and time-dependent process. Furthermore, the evidence indicates that breast tissues are possibly a nonprostatic source of androgen up-regulated production of PSA women.
本研究采用女性易性症模型，旨在评估卵巢、子宫内膜和乳腺组织对雄激素上调前列腺特异性抗原（PSA）产生的作用。与未接受雄激素治疗的术前女性易性症患者（平均±标准误=1.53±0.25 pg/mL）相比，术前接受长期雄激素治疗的女性易性症患者血清PSA水平显著升高（平均±标准误=35.3±6.2 pg/mL）。此外，在接受雄激素治疗的女性易性症患者中，术后PSA浓度（平均±标准误=14.5±2.8 pg/mL）与术后接受雄激素治疗的女性易性症患者相比显著降低，但仍显著高于正常女性。每月给女性易性症患者肌肉注射250 mg丙酸睾酮使血清睾酮水平升高至男性范围内。在5名进行连续测量的受试者中，睾酮治疗后24小时血清睾酮水平大幅升高；平均水平（±标准误）为19.5±2.1 ng/mL。尽管睾酮水平很高，但血清PSA水平（平均±标准误=2.2±0.9 pg/mL）并未显著升高。然而，雄激素治疗12个月后，这5名受试者的平均（±标准误）PSA水平为47±11.6 pg/mL，显著高于未接受雄激素治疗的女性易性症患者的平均水平。本研究证实，高水平的睾酮能够上调女性PSA的产生。这种PSA产生的上调是一个剂量和时间依赖性过程。此外，有证据表明乳腺组织可能是女性雄激素上调产生PSA的非前列腺来源。
