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本文引用的文献

1
The QT Interval and Selection of Alpha-Blockers for Benign Prostatic Hyperplasia.QT间期与良性前列腺增生症α受体阻滞剂的选择
Rev Urol. 2008 Spring;10(2):85-91.
2
Alpha1-adrenoceptor subtypes and lower urinary tract symptoms.α1肾上腺素能受体亚型与下尿路症状
Int J Urol. 2008 Mar;15(3):193-9. doi: 10.1111/j.1442-2042.2007.01956.x.
3
The evolution of alpha-blockers for the treatment of benign prostatic hyperplasia.用于治疗良性前列腺增生的α受体阻滞剂的演变
Rev Urol. 2006;8 Suppl 4(Suppl 4):S3-9.
4
[Alpha1-adrenoceptor subtype selectivity and organ specificity of silodosin (KMD-3213)].[西洛多辛(KMD-3213)的α1-肾上腺素能受体亚型选择性和器官特异性]
Yakugaku Zasshi. 2006 Mar;126 Spec no.:209-16. doi: 10.1248/yakushi.126.209.
5
Alpha1-adrenergic receptors and their inhibitors in lower urinary tract symptoms and benign prostatic hyperplasia.α1肾上腺素能受体及其抑制剂在膀胱过度活动症和良性前列腺增生中的作用
J Urol. 2004 Mar;171(3):1029-35. doi: 10.1097/01.ju.0000097026.43866.cc.
6
alpha(1)-Adrenoceptor selectivity and the treatment of benign prostatic hyperplasia and lower urinary tract symptoms.α1-肾上腺素能受体选择性与良性前列腺增生和下尿路症状的治疗
Prostate Cancer Prostatic Dis. 2000 Aug;3(2):76-83. doi: 10.1038/sj.pcan.4500410.
7
Tissue selectivity of KMD-3213, an alpha(1)-adrenoreceptor antagonist, in human prostate and vasculature.α1肾上腺素能受体拮抗剂KMD-3213在人前列腺和血管中的组织选择性
J Urol. 2000 Aug;164(2):578-83.
8
The mechanism of adverse events associated with terazosin: an analysis of the Veterans Affairs cooperative study.与特拉唑嗪相关的不良事件机制:退伍军人事务部合作研究分析
J Urol. 2000 Apr;163(4):1134-7.
9
KMD-3213, a uroselective and long-acting alpha(1a)-adrenoceptor antagonist, tested in a novel rat model.KMD-3213,一种对尿道有选择性的长效α(1a)肾上腺素能受体拮抗剂,在一种新型大鼠模型中进行了测试。
J Pharmacol Exp Ther. 1999 Oct;291(1):81-91.
10
Localization and expression of the alpha1A-1, alpha1B and alpha1D-adrenoceptors in hyperplastic and non-hyperplastic human prostate.α1A-1、α1B和α1D肾上腺素能受体在增生性和非增生性人前列腺中的定位与表达
J Urol. 1999 Feb;161(2):635-40.

良性前列腺增生的病理生理学:该疾病药物治疗的见解

Pathophysiology of benign prostatic hyperplasia: insights from medical therapy for the disease.

作者信息

Lepor Herbert

机构信息

Department of Urology, New York University School of Medicine New York, NY.

出版信息

Rev Urol. 2009 Fall;11(Suppl 1):S9-S13.

PMID:20126609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2812891/
Abstract

The medical treatment of benign prostatic hyperplasia (BPH) has its roots in the early 1970s. During this era, the first clinical trials investigating alpha-blockade and androgen deprivation therapy were reported for men with clinical BPH. The observation that clinical BPH was improved following administration of both alpha-blockers and androgen deprivation therapy supported the evolving paradigm that clinical BPH resulted from dynamic and static pathways. During the past several decades, the evolution of alpha-blockers for the treatment of BPH has been impacted by innovations targeted to simplify the administration and improve tolerability while maintaining their effectiveness.

摘要

良性前列腺增生(BPH)的医学治疗始于20世纪70年代初。在这个时期,首次报道了针对临床BPH男性的α受体阻滞剂和雄激素剥夺疗法的临床试验。服用α受体阻滞剂和雄激素剥夺疗法后临床BPH得到改善这一观察结果支持了不断发展的范式,即临床BPH是由动态和静态途径导致的。在过去几十年中,用于治疗BPH的α受体阻滞剂的发展受到了旨在简化给药并提高耐受性同时保持其有效性的创新的影响。