前列腺内结构和再生速度对考虑在联合α受体阻滞剂治疗后停用杜他雄胺的意义:一项前瞻性的试点研究。

Korean Journal of Urology Pub Date : 2015-04-01 Epub Date: 2015-03-27 DOI:10.4111/kju.2015.56.4.305
Tetsuya Shindo, Kohei Hashimoto, Takashi Shimizu, Naoki Itoh, Naoya Masumori
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引用次数: 1

摘要

目的:我们进行了一项前瞻性单中心研究,以评估在联合α受体阻滞剂治疗良性前列腺增生(BPH)后停用度他雄胺的可能性。材料和方法:我们前瞻性地使用α受体阻滞剂和杜他雄胺(0.5 mg/d)治疗BPH患者。接受抗BPH α受体阻滞剂治疗超过2个月的患者符合条件,20例患者纳入研究。联合治疗6个月后,停用杜他雄胺。患者在戒烟后随访12个月。每6个月评估一次前列腺体积、经直肠超声检查前列腺内结构、峰值尿流率、空后残余尿量、血清前列腺特异性抗原水平,每3个月评估一次国际前列腺症状评分和膀胱过度活跃症状评分(OABSS)。在随访期间,允许患者根据自己的意愿重新开始使用杜他雄胺。结果:12例(12/ 20,60 %)患者在随访6 ~ 12个月重新开始联合治疗。对于重新使用杜他雄胺的患者,停药后前列腺体积和OABSS分别增加和恶化。基线时经直肠超声可见边界清晰的过渡区以及停药后前列腺再生是重新开始治疗的危险因素(man - whitney U检验:p=0.008, p=0.017)。结论:杜他雄胺停药后前列腺增大在不同患者之间存在差异。前列腺的快速再生导致储存症状的恶化和重新使用杜他雄胺的倾向。基线前列腺内结构可能是患者是否适合停药的预测因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Significance of intraprostatic architecture and regrowth velocity for considering discontinuation of dutasteride after combination therapy with an alpha blocker: a prospective, pilot study.

Purpose: We conducted a prospective single-center study to evaluate the possibility of discontinuation of dutasteride after combination therapy with an alpha blocker for benign prostatic hyperplasia (BPH).

Materials and methods: We prospectively treated BPH patients with an alpha blocker and dutasteride (0.5 mg/d). Patients who had been treated with alpha blockers against BPH for more than 2 months were eligible, and 20 patients were included in the study. After 6 months of combination therapy, dutasteride was discontinued. Patients were followed for 12 months after cessation. Prostate volume, intraprostatic architecture determined by transrectal ultrasound, peak urinary flow rate, postvoid residual urine volume, and the serum prostate-specific antigen level were evaluated every 6 months, and the International Prostate Symptom Score and overactive bladder symptom score (OABSS) every 3 months. Patients were allowed to restart dutasteride during the follow-up period according to their desire.

Results: Twelve patients (12/20, 60%) restarted the combination therapy from 6 to 12 months into the follow-up period. For patients who restarted dutasteride, the prostate volume and OABSS had increased and worsened after discontinuation, respectively. A visible transition zone with a clear border on transrectal ultrasound at baseline and regrowth of the prostate after discontinuation of dutasteride were risk factors for restarting the therapy (Mann-Whitney U test: p=0.008, p=0.017).

Conclusions: Prostatic enlargement after discontinuation of dutasteride differs among patients. Rapid regrowth of the prostate leads to deterioration of storage symptoms and a tendency to restart dutasteride. Baseline intraprostatic architecture may be a predictive factor for whether the patient is a good candidate for discontinuation.

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