Scherr Douglas, Pitts W Reid, Vaughn E Darracott
Department of Urology, The New York Presbyterian Hospital-Cornell Medical Center, New York, New York, USA.
J Urol. 2002 Feb;167(2 Pt 1):535-8. doi: 10.1016/S0022-5347(01)69080-3.
It is well described in the urological literature that androgen deprivation can result in accelerated bone breakdown and osteoporosis. Therefore, we evaluate the degree of bone breakdown in patients on conventional androgen deprivation with those on diethylstilbesterol alone or in conjunction with luteinizing hormone releasing hormone agonists or orchiectomy.
During an 18-month period a total of 54 patients with clinically localized prostate cancer and 24 with benign prostatic hyperplasia were evaluated. All patients with prostate cancer were either treated with external beam radiotherapy without androgen deprivation or were started on androgen deprivation therapy. All patients were prospectively followed and evaluated for serum testosterone and estradiol along with urinary collagen type I cross-linked N-telopeptides. Three separate morning urine samples on 3 separate months were collected on each patient and analyzed for N-telopeptides. To correct for different levels of renal function, all N-telopeptides were measured as a ratio of urinary N-telopeptides/urine creatinine. All patients with any bone or skeletal abnormalities were excluded from study as were those with osseous metastatic disease.
There was a statistically significant (p < 0.05) higher level of urinary N-telopeptides/creatinine in patients on androgen deprivation therapy who were not treated with diethylstilbesterol. The estrogenic effect of diethylstilbesterol protects one from bone resorption. Patients on diethylstilbesterol did not have any higher levels of bone breakdown than patients with benign prostatic hyperplasia or those who never received any androgen deprivation.
Rapid bone turnover and resorption can be prevented with 1 mg. diethylstilbesterol alone or in conjunction with other modes of androgen deprivation. Therefore, diethylstilbesterol should be considered as monotherpy in men who require long-term antiandrogen therapy.
泌尿学文献中已充分描述,雄激素剥夺会导致骨分解加速和骨质疏松。因此,我们评估接受传统雄激素剥夺治疗的患者与仅接受己烯雌酚治疗或联合促黄体生成素释放激素激动剂或睾丸切除术治疗的患者的骨分解程度。
在18个月期间,共评估了54例临床局限性前列腺癌患者和24例良性前列腺增生患者。所有前列腺癌患者要么接受了无雄激素剥夺的外照射放疗,要么开始接受雄激素剥夺治疗。对所有患者进行前瞻性随访,并评估血清睾酮、雌二醇以及尿I型胶原交联N-末端肽。每位患者在3个不同月份分别采集3份晨尿样本,并分析其中的N-末端肽。为校正不同的肾功能水平,所有N-末端肽均以尿N-末端肽/尿肌酐的比值进行测量。所有有任何骨骼异常的患者以及有骨转移疾病的患者均被排除在研究之外。
未接受己烯雌酚治疗的接受雄激素剥夺治疗的患者,其尿N-末端肽/肌酐水平在统计学上显著更高(p < 0.05)。己烯雌酚的雌激素作用可保护机体免受骨吸收影响。接受己烯雌酚治疗的患者的骨分解水平并不高于良性前列腺增生患者或从未接受过任何雄激素剥夺治疗的患者。
单独使用1毫克己烯雌酚或与其他雄激素剥夺方式联合使用,可预防快速的骨转换和骨吸收。因此,对于需要长期抗雄激素治疗的男性,应考虑将己烯雌酚作为单一疗法。