良性前列腺增生诊断治疗

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良性前列腺增生

前列腺正常解剖
前列腺增生时，腺体突向尿道和膀胱颈，后尿道延长
临床表现
良性前列腺增生
最初表现：尿频（刺激期）。最重要的症状：排尿困难（代偿期）。最痛苦的时候：尿潴留（失代偿期）。最终不良后果：感染、结石、出血、肾功能不全。容易导致：疝、痔、脱肛。
良性前列腺增生
诊断
病史：50岁以上男性出现下尿路症状。国际前列腺症状（I-PSS）评分。体检：直肠指检，了解前列腺大小、质地、有无硬结、压痛等。 B超：大小、结节回声、残余尿。尿流动力学：最大尿流率小于15ml/s。 PSA：排除前列腺癌。并发症：急性尿潴留、肾积水及肾功能不全、膀胱结石、反复泌
良性前列腺增生的治疗
等待观察药物治疗
a受体阻滞剂：平滑肌张力，尿道阻力，排尿症状改善 5α还原酶抑制剂：抑制睾酮向双氢睾酮转变→缩小前列腺体积，改善排尿症状；植物制剂等。手术治疗：经尿道前列腺电切术（TURP）、经尿道激光治疗、开放手术其他疗法
Thanks
尿系感染、反复血尿、膀胱憩室、痔、腹股沟疝。
前列腺增生引起的病理改变
国际前列腺症状（I-PSS）评分表
在最近一个月内，您是否有以下症状？
在五次中
症状
无少少大多于几评分
于于约半数乎
一半半
每
次数数
次
1. 是否经常有尿不尽感? 2. 两次排尿间隔是否经常小于两小时? 3. 是否曾经有间断性排尿? 4. 是否有排尿不能等待现象? 5. 是否有尿线变细现象? 6. 是否需要用力及使劲才能开始排尿? 7. 从入睡到早起一般需要起来排尿几次?
第四节
良性前列腺增生
良性前列腺增生
概念
良性前列腺增生（benign prostatic hyperplasia，BPH）简称前列腺增生。病理学表现为细胞增生，是引起老年男性排尿障碍原因中最为常见的一种良性疾病。

2022良性前列腺增生的治疗用药及其区别(全文)

良性前列腺增生的治疗用药及其区别（全文）良性前列腺增生（BPH）是一种常见的以排尿障碍为主的慢性病，是泌尿科的常见疾病，通常在男性40岁以后发生。

BPH是由前列腺移行区和尿道周围区域的上皮和纤维肌组织的增生所致，主要表现为解剖学上的前列腺体积增大（BPE）、组织学上前列腺间质和腺体成分增生、尿动力学上的膀胱出口梗阻（BOO）和以下尿路症状（LUTS）为主的症状。

其中LUTS症状可分为储尿期症状（尿频、尿急、夜尿增多等）、排尿期症状（排尿困难、尿等待、尿流变细等）和排尿后症状（排尿不完全/尿不尽感、尿后滴沥等）。

BPH的治疗药物主要包括：αl受体阻滞剂、M受体拮抗剂、5a-还原酶抑制剂、β3受体激动剂、磷酸二酯酶-5（PDE-5）抑制剂等。

一.al受体阻滞剂包括选择性al受体阻滞剂（包括特拉嘤嗪、多沙嘤嗪、阿夫嘤嗪）和高选择性al 受体阻滞剂（包括坦索罗辛、赛洛多辛、禁哌地尔）。

al受体阻滞剂可松弛前列腺平滑肌、缓解尿路症状与膀胱出口动力性梗阻，并改善储尿期症状（包括尿急、尿频、尿失禁及夜尿增多等）与排尿期症状（包括排尿踌躇、排尿困难及间断排尿等），同时提高尿流率，但不影响前列腺体积和血清前列腺特异性抗原（PSA）水平，较少产生心血管不良反应。

αl受体阻滞剂连续使用4-6周无明显症状改善时，可考虑更改剂型、剂量或换用不同类型药物。

注意事项：常见副作用包括头痛、头晕、困倦、乏力、体位性低血压（易发生于老年人、合并心血管疾病或同用血管活性药物者）、异常射精等。

体位性低血压者慎用。

αl受体阻滞剂使用者接受白内障手术时可能出现虹膜松弛综合征，建议白内障手术前停用。

二.M受体拮抗剂包括非选择性M受体拮抗剂（托特罗定、奥昔布宁等）和选择性M3受体拮抗剂（索利那新）。

M受体拮抗剂可缓解逼尿肌过度兴奋、降低膀胱敏感性，而改善BPH者的储尿期症状（包括尿频、尿急、尿失禁以及夜尿增多等），可用于无明显的梗阻症状、以储尿期症状为主、残余尿量无明显增加的患者。

2022良性前列腺增生诊疗及健康管理指南(最全版)

2022良性前列腺增生诊疗及健康管理指南（最全版）良性前列腺增生（BPH）是中老年男性常见的排尿障碍为主性慢病，是泌尿男科临床诊疗中最为常见的疾病之一。

BPH一般发生在40岁以后，发生率随年龄的增长而逐年增加，51-60岁约20%,61-70岁男性人群中BPH的发生率达50%,81-90岁时高达83%。

随着生活水平的提高，BPH患者对治疗效果的需求也在逐渐变化，规范BPH诊疗及健康管理显得极其重要。

中华医学会男科学分会组织相关临床专家根据现有的临床证据共同研究并制定指南，对BPH患者尤其是对有性功能需求的患者，提供了规范的诊治指导与参考。

医脉通将其中要点整理如下。

诊断与评估强烈推荐的检查包括：病史问询、国际前列腺症状评分（IPSS1体格检查、尿常规检查、血清前列腺特异性抗原（PSA）检测、经直肠或经腹部超声检查。

推荐的可选检查包括：尿流率及残余尿测定、生活质量（QOL）评分、膀胱过度活动症症状评分（OABSS）等。

特殊情况下建议做的检查包括：1.肾功能检测。

对于存在肾功能损害病史及相关危险因素的患者，如尿潴留导致肾积水的患者推荐进行肾功能检测。

2.上尿路超声检查。

对于伴有膀胱残余尿过多、血尿、泌尿系结石病史的患者，推荐行上尿路超声检查。

3.尿道膀胱镜检查。

对于合并有镜下或肉眼血尿史、尿道狭窄史或膀胱癌病史的患者，应行尿道膀胱镜检查，对于需要进行尿道膀胱镜检查的患者有条件的可以使用膀胱软镜以减少患者痛苦。

4.尿流动力学检查。

主要目的是探索患者出现下尿路症状（LUTS）的功能机制，提示患者是否存在导致不利临床结局的危险因素，为制定临床决策提供更多依据。

由于尿流动力学检查是一项侵入性检查，因此，仅在特定患者中推荐行此检查。

对于有神经系统疾病史、盆腔根治性手术史或怀疑有神经源性下尿路功能障碍的患者，强烈建议行尿流动力学评估。

5.影像尿动力学检查。

可提供较常规尿动力学更多的解剖和功能信息，如果临床医生认为需要了解患者的病理生理机制时，可以选择该项检查。

良性前列腺增生诊断治疗指南

如果在您今后的生活中始终伴有现在的排尿症状，您认为如何？
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生活质量评分（QOL）=
• 体格检查： • 1、外生殖器检查：除外尿道口狭窄或其他可能影响排尿的疾病（包茎、阴茎肿瘤） • 2、指肠指检（DRE）：重要检查之一。了解前列腺的大小、形态、质地、有无结节及压痛、中央沟是否变浅或消失以及肛门括约肌张力情况。 • 3、局部神经系统的检查：神经源性膀胱功能障碍。
BPH的临床进展性
• BPH为一种缓慢进展的前列腺良性疾病。 • 症状随年龄增加而进行性加重，并出现相应的并发症。 • 定义：随着病程的延长，BPH患者的主观症状和客观指标进行性加重的趋势。
怀疑BPH 伴或不伴有LUTS
BPH诊断流程图
推荐检查项目（初始评估）问卷调查病史询问尿常规血清PSA 前列腺超声尿流率检查
IPSS评分
QOL评分
一般病史
体格检查 DRE及外生殖器检查可选检查项目
LUTS特点
手术药物史
会阴部神经检查
排尿日记
血肌酐
静脉尿路造影
尿动力学检查
尿道膀胱经检查
上尿路超声检查
不推荐检查项目
CT
MRI
BPH的临床进展性内容
• • • • • • • LUTS加重而导致患者生活质量下降最大尿流率进行性下降反复血尿反复尿路感染膀胱结石急性尿潴留（AUR）肾功能损害
0 0 0
5 5 5
4、是否有排尿不能等待现象？
5、是否有尿线变细现象？ 6、是否需要用力及使劲才能开始排尿？ 7、从入睡到早起一般需要起来排尿几次？症状总评分=

泌尿外科基本诊疗路径

（九）变异及原因分析
1.治疗后出现结石残留，需要进一步诊治，导致住院时间延长、费用增加。 2.结石合并感染控制不佳，需请相关科室会诊并治疗。 3.住院后出现其他内、外科疾病需进一步明确诊断，可进入其他路径。
（十）肾和输尿管结石基本诊疗路径双向转诊流程
一、向上级医院转诊指征具备下列任一指征可转上级医院： 1.肾输尿管结石直径大于0.6cm，估计保守治疗无效者； 2.肾功能差，血钾高，并出现恶心、呕吐、少尿或无尿等症状； 3.肾输尿管结石伴有尿路感染并出现发热症状。
（四）治疗方案——药物治疗
BPH患者药物治疗的短期目标是缓解患者的下尿路症状，长期目标是延缓疾病的临床进展，预防并发症的发生。在减少药物治疗副作用的同时保持患者较高的生活质量是 BPH药物治疗的总体目标。
1. α-受体阻滞剂 2．5-α还原酶抑制剂 3．联合治疗 4．中药和植物制剂
（四）治疗方案——药物治疗—α-受体阻滞剂
类型名称 Ⅰ 急性细菌性前列腺炎（ABP）
特征急性前列腺感染性炎症
Ⅱ 慢性细菌性前列腺炎（CBP）
复发性尿路感染/前列腺慢性感染性炎症
Ⅲ 慢性非细菌性前列腺炎/慢性盆底盆区疼痛和不适/各种排尿
痛综合征（CPPS）
和性功能异常/无明显感染
迹象
ⅢA 炎性盆底痛综合征
EPS/VB3/精液中可见多量的WBC
（六）标准住院日为4-7天
（七）住院期间检查项目
入院后第1-2天 1.必检项目（1）血常规、尿常规、大便常规，肝肾功能，电解质；（2）泌尿系B超，KUB（腹部平片）。 2.选检项目（1）尿培养+药敏，血型、凝血功能等；（2）胸片、心电图。
（八）出院标准
1.一般情况良好，无肾绞痛，血尿症状消失。 2.结石排出或部分排出。

【2019年整理】7-良性前列腺增生诊断治疗指南-年修改版

良性前列腺增生诊断治疗指南主编张祥华北京大学吴阶平泌尿外科医学中心北京大学首钢医院副主编王行环武汉大学中南医院编委（按姓氏拼音排序，排名不分先后）王刚北京大学泌尿外科研究所北京大学第一医院魏强四川大学华西医院许传亮第二军医大学附属长海医院薛蔚上海交通大学医学院附属仁济医院严维刚中国医学科学院北京协和医学院（清华大学医学部）北京协和医院杨家荣广州军区武汉总医院朱刚卫生部北京医院目录第一节概述一、定义二、流行病学三、病因学四、病理五、病理生理改变六、临床表现、诊断及治疗第二节良性前列腺增生诊治指南的制定方法一、世界各国BPH诊治指南的特点二、制定BPH诊治指南的必要性与目的三、BPH 诊治指南的意义四、BPH诊治指南的制定方法五、BPH诊治指南的推广与不断完善第三节良性前列腺增生的临床进展性一、BPH临床进展性的定义二、临床进展性的评价指标三、BPH临床进展的危险因素分析第四节良性前列腺增生的诊断一、初始评估二、根据初始评估结果需要的进一步检查三、不推荐检查项目四、BPH患者初始评估小结第五节良性前列腺增生的治疗第六节良性前列腺增生的随访第一节概述一、定义良性前列腺增生（benign prostatic hyperplasia, BPH）是引起中老年男性排尿障碍原因中最为常见的一种良性疾病[1]。

主要表现为组织学上的前列腺间质和腺体成分的增生、解剖学上的前列腺增大（benign prostatic enlargement, BPE）、下尿路症状（lower urinary tract symptoms, LUTS）为主的临床症状以及尿动力学上的膀胱出口梗阻（bladder outlet obstruction, BOO）。

二、流行病学组织学上BPH 的发病率随年龄的增长而增加，最初通常发生在40岁以后[2]，到60岁时大于50％，80岁时高达83％[3]。

与组织学表现相类似，随着年龄的增长，排尿困难等症状也随之增加。

前列腺增生的诊断与治疗

BPH合并OAB患者的三级分类治疗策略
BPH合并OAB患者
一级分类标准：是否存在BOO
OAB无BOO证据
生活方式干预行为疗法 M受体拮抗剂
OAB有BOO证据
二级分类标准： OAB/BOO何者为主？
OAB和BOO
以BOO为主
三级分类标准：
M受体拮抗剂 +α1受体阻滞剂
前列腺较小 PSA<1.5ng
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膀胱结石
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膀胱憩室
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BPH的治疗
等待观察 (watchful waiting) 药物治疗手术治疗微创治疗
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BPH的药物治疗
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受体阻滞剂
受体分布于膀胱颈及前列腺的平滑肌大部分BPH平滑肌张力增高前列腺平滑肌收缩可引起梗阻症状受体阻滞剂松弛膀胱颈及前列腺的平滑肌而不
先α1受体阻滞剂后M受体拮抗剂
α1受体阻滞剂 α1受体阻滞剂 5α还原酶抑制剂
BPH合并OAB患者的三级分类治疗策略
BPH合并OAB患者
OAB无BOO证据
生活方式干预行为疗法 M受体拮抗剂
OAB有BOO证据
OAB和BOO
以BOO为主
二级分类标准： OAB/BOO何者为主？
M受体拮抗剂 +α1受体阻滞剂
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I-PSS 评分
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BPH的诊断
症状国际前列腺症状评分(IPSS) 直肠指诊 B超 (经腹或经直肠) 尿流率或尿流动力学
V>150ml, MFR>15ml/s, AFR>10ml/s
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膀胱出口梗阻的后果
尿潴留膀胱憩室、结石上尿路积水、肾功能受损尿路感染反复血尿腹股沟疝、脱肛、痔疮

良性前列腺增生诊疗及健康管理指南

结论
ห้องสมุดไป่ตู้
综上所述，良性前列腺增生症中西医结合多学科诊疗指南对提高诊疗水平和改善患者生活质量具有重要意义。通过中西医结合的手段，可以更好地针对病因病机进行治疗，提高治疗效果。良好的饮食和运动管理以及预防保健措施的采取，可以有效地减少BPH的发生和发展。因此，我们应积极推广和应用中西医结合多学科诊疗指南，为广大患者提供更为高效、安全的治疗选择。
（2）运动：适当增加运动量，如快走、游泳、瑜伽等，有助于减轻前列腺增生的症状。
（3）心理：保持良好的心理状态，可通过心理咨询、冥想、瑜伽等方式进行放松和减压。
2、预防和康复建议
（1）保持前列腺健康：可通过按摩、热水坐浴等方式促进前列腺血液循环，预防前列腺增生。
（2）避免久坐：长时间久坐会加重前列腺负担，应定时起身活动。（3）戒烟限酒：戒烟限酒有助于预防前列腺增生的发生和发展。
总之，良性前列腺增生中西医结合诊疗具有重要意义和可行性。通过综合运用中医和西医手段，可以更好地缓解患者的症状和提高生活质量。但同时也需要注意安全问题、药物使用和饮食调理等方面，以确保诊疗效果最佳。希望本次演示能为临床医生提供有益的参考，也为BPH患者带来更好的治疗体验。
引言
良性前列腺增生症（BPH）是一种常见的泌尿系统疾病，多发于中老年男性。该病的发生与发展严重影响了患者的生存质量和社会负担。为了提高BPH的诊断和治疗水平，本次演示将详细介绍中西医结合多学科诊疗指南在BPH诊疗中的重要性和应用。
谢谢观看
诊断与分类
BPH的诊断主要依靠临床表现和相关检查。中医通过望闻问切四诊合参进行诊断，而西医则采用国际前列腺症状评分（IPSS）和生活质量指数（QOL）进行评估。根据病情严重程度，BPH可分为轻、中、重三度。

良性前列腺增生症及治疗ppt课件

医生通过手指触摸前列腺，了解前列腺的大小、质地、有无硬结等，是初步诊断良性前列腺增生的方法。
通过超声波显示前列腺形态，了解前列腺大小、内部结构及是否存在结节。
血清前列腺特异抗原（PSA）检测
尿流率测定
通过检测血液中PSA水平，有助于鉴别良性前列腺增生和前列腺癌。
通过测量排尿时的尿流速率，评估排尿困难程度，辅助诊断良性前列腺增生。
尿道狭窄
尿道狭窄也可能引起排尿困难症状，需要通过尿道造影等检查进行鉴别。
神经源性膀胱
神经源性膀胱是由于神经系统病变引起的膀胱功能障碍，需要通过神经系统的相关检查进行鉴别。
03 良性前列腺增生症的治疗
药物治疗
雄激素拮抗剂
植物药
通过拮抗雄激素的作用，缩小前列腺体积，缓解症状。
如普适泰等，具有抗炎、抗水肿、改善排尿症状的作用。
生活方式调整
根据病情调整生活方式，如适当运动、合理饮食等。
05 良性前列腺增生症的最新研究进展
药物治疗研究进展
药物治疗是良性前列腺增生症的主要治疗方法之一，近年来在药物研发方面取得了重要进展。
新型药物如5α-还原酶抑制剂和抗雄激素药物等，在改善症状和延缓疾病进展方面表现出良好的效果。
此外，一些中药和植物药也被证实具有一定的治疗作用，为药物治疗提供了更多的选择。
THANKS FOR WATCHING
感谢您的观看
诊断标准
01
症状：尿频、尿急、尿不尽、夜尿增多等排尿障碍症状。
02
直肠指诊阳性：医生手指触摸前列腺增大。
03
超声检查阳性：前列腺体积增大，形态饱满。
04
血清PSA正常或轻度增高：排除前列腺癌的可能性。

EAU-良性前列腺增生指南2004 2009

Guidelines onBenignProstaticHyperplasia J. de la Rosette, G. Alivizatos, S. Madersbacher,C. Rioja Sanz, J. Nordling, M. Emberton,S. Gravas, M.C. Michel, M. Oelke © European Association of Urology 2009TABLE OF CONTENTS pAgE 1. Background 51.1 Prevalence 51.2 Is BPH a progressive disorder? 51.2.1 Indicators of progression 61.2.2 conclusions 71.2.3 references 72. rISk FacTorS 92.1 For developing the disease 92.2 For surgical treatment 92.3 references 103. aSSESSMEnT 103.1 Symptom scores 113.1.1 International Prostate Symptom Score (I-PPS) 113.1.2 Quality-of-life assessment 113.1.3 Symptom score as decision tool for treatment 113.1.4 Symptom score as outcome predictor 113.1.5 conclusions 123.1.6 recommendations 123.1.7 references 123.2 Prostate specific antigen (PSa) measurement 123.2.1 Factors influencing the serum levels of PSa 123.2.2 PSa and prediction of prostatic volume 123.2.3 PSa and probability of having prostate cancer 123.2.4 PSa and prediction of BPH-related outcomes 123.2.5 conclusions 123.2.6 recommendation 133.2.7 references 133.3 creatinine measurement 143.3.1 conclusions 143.3.2 references 143.4 urinalysis 153.4.1 recommendation 153.5 digital rectal examination (drE) 153.5.1 drE and cancer detection 153.5.2 drE and prostate size evaluation 163.5.3 conclusions and recommendations 163.5.4 references 163.6 Imaging of the urinary tract 173.6.1 upper urinary tract 173.6.2 Lower urinary tract 183.6.3 urethra 183.6.4 Prostate 183.6.5 references 183.7 Voiding charts (diaries) 203.7.1 conclusions 203.7.2 references 203.8 uroflowmetry 203.8.1 references 213.9 Post-void residual volume (PVr) 213.10 urodynamic studies 213.10.1 outcome 213.10.2 conclusions 223.10.3 references 223.11 Endoscopy 233.11.1 LuTS caused by bladder outlet obstruction 233.11.2 Morbidity of urethrocystoscopy 23 2 uPdaTE MarcH 20043.11.3 relationship between trabeculation and peak flow rate 233.11.4 relationship between trabeculation and symptoms 233.11.5 relationship between trabeculation and prostate size 233.11.6 relationship between trabeculation and obstruction 233.11.7 Bladder diverticula and obstruction 243.11.8 Bladder stones and obstruction 243.11.9 Intravesical pathology 243.11.10 conclusions 243.11.11 references 243.12 recommendations for assessment 254. TrEaTMEnT 264.1 Watchful waiting (WW) 264.1.1 Patient selection 264.1.2 Education, reassurance and periodic monitoring 264.1.3 Lifestyle advice 274.1.4 conclusions 274.1.5 references 274.2 Medical treatment 284.2.1 5-alpha reductase inhibitors 284.2.1.1 Finasteride (type 2, 5-alpha reductase inhibitor) 284.2.1.1.1 Efficacy and clinical endpoints 284.2.1.1.2 Haematuria and finasteride 284.2.1.1.3 Side-effects 284.2.1.1.4 Effect on PSa 294.2.1.2 dutasteride 294.2.1.3 combination therapy 294.2.1.4 conclusions 294.2.1.5 references 304.2.2 alpha-blockers 324.2.2.1 uroselectivity 324.2.2.2 Mechanism of action 324.2.2.3 Pharmacokinetics 334.2.2.4 assessment 334.2.2.5 clinical efficacy 334.2.2.6 durability 334.2.2.7 adverse effects 334.2.2.8 acute urinary retention 334.2.2.9 conclusions 334.2.2.10 references 344.2.3 Phytotherapeutic agents 344.2.3.1 conclusions 344.2.3.2 references 354.3 Surgical management 354.3.1 Indications for surgery 354.3.2 choice of surgical technique 354.3.3 Perioperative antibiotics 364.3.4 Treatment outcome 364.3.5 complications 364.3.6 Long-term outcome 364.3.7 conclusions and recommendations 374.3.8 references 374.4 Lasers 384.4.1 Laser types 384.4.2 right-angle fibres 384.4.3 Interstitial Laser coagulation (ILc) 394.4.4 Holmium laser resection of the prostate (HoLrP) 404.4.5 conclusions 414.4.6 references 41 uPdaTE MarcH 2004 34.5 Transrectal high-intensity focused ultrasound (HIFu) 434.5.1 assessment 434.5.2 Procedure 434.5.3 Morbidity/complications 434.5.4 outcome 444.5.5 urodynamics 444.5.6 Quality of life and sexual function 444.5.7 durability 444.5.8 Patient selection 444.5.9 conclusions 454.5.10 references 454.6 Transurethral needle ablation (Tuna®) 464.6.1 assessment 464.6.2 Procedure 464.6.3 Morbidity/complications 464.6.4 outcome 464.6.5 randomized clinical trials 464.6.6 Impact on bladder outflow obstruction 464.6.7 durability 464.6.8 Patient selection 464.6.9 conclusions 464.6.10 references 474.7 Transurethral microwave therapy (TuMT) 474.7.1 assessment 474.7.2 Procedure 474.7.3 The microwave thermotherapy principle 484.7.4 Morbidity 484.7.5 High-intensity-dose-protocol 494.7.6 Prostatic temperature feedback treatment 494.7.7 durability 494.7.8 Patient selection 494.7.9 conclusions 494.7.10 references 494.8 recommendations for treatment 505. FoLLoW-uP 525.1 Watchful waiting 525.2 alpha-blocker therapy 525.3 5-alpha-reductase inhibitors 525.4 Surgical management 525.5 alternative therapies 526. aBBrEVIaTIonS uSEd In THE TEXT 53 4 uPdaTE MarcH 20041. BACKgROUNDBenign prostatic hyperplasia (BPH) is a condition intimately related to ageing (1). although it is not life-threatening, its clinical manifestation as lower urinary tract symptoms (LuTS) reduces the patient’s quality of life (2). Troublesome LuTS can occur in up to 30% of men older than 65 years (3).1.1 prevalencealthough many epidemiological clinical studies have been conducted worldwide over the last 20 years, the prevalence of clinical BPH remains difficult to determine. a standardized clinical definition of BPH is lacking, which makes it intrinsically difficult to perform adequate epidemiological studies. among the published epidemiological studies, some include probability samples from an entire country, while others represent age-stratified random samples or enroll participants from general practice, hospital populations or responders to selective screening programmes. There is also a lack of homogeneity among these studies in the way in which BPH is assessed, with different questionnaires and methods of administration.Barry et al. have provided the histological prevalence of BPH, based on a review of five studies relating age to histological findings in human male prostate glands (4). Histological BPH was not found in men under the age of 30 years but its incidence rose with age, reaching a peak in the ninth decade. at that age, BPH was found in 88% of histological samples (4). a palpable enlargement of the prostate has been foundin up to 20% of males in their 60s and in 43% in their 80s (5); however, prostate enlargement is not always related to clinical symptoms (2).clinical BPH is a highly prevalent disease. By the age of 60 years, nearly 60% of the cohort of the Baltimore Longitudinal Study of aging had some degree of clinical BPH (6). In the uSa, results of the olmstead county survey, in a sample of unselected caucasian men aged 40-79 years, showed that moderate-to-severe symptoms can occur among 13% of men aged 40-49 years and among 28% of those older than 70 years (1). In canada, 23% of the cohort studied presented with moderate-to-severe symptoms (7). The findings for prevalence of LuTS in Europe are similar to those in the uSa. In Scotland and in the area of Maastricht, the netherlands, the prevalence of symptoms increased from 14% of men in their 40s to 43% in their 60s (8,9). depending on the sample, the prevalence of moderate-to-severe symptoms varies from 14% in France to 30% in the netherlands (10,11). The proportion of men with moderate-to-severe symptoms doubles with each decade of life (10). Preliminary results of one of the most recent European epidemiological studies on the prevalence of LuTS show that approximately 30% of german males aged 50-80 years present with moderate-to-severe symptoms according to the International Prostate Symptom Score (i.e. I-PSS > 7) (12).a multicentre study performed in different countries in asia showed that the age-specific percentages of men with moderate-to-severe symptoms were higher than those in america (13,14). The prevalence increases from 18% for men in their 40s to 56% for those in their 70s (13). curiously, the average weight of Japanese glands seemed to be smaller than those of their american counterparts (15). despite methodological differences, some conclusions can be drawn from the studies mentioned above:• Mild urinary symptoms are very common among men aged 50 years and older• Mild symptoms are associated with little bother, while moderate and severe symptoms are associated with increasingly higher levels of inconvenience and interference with living activities (16)• The same symptoms can cause different troublesome and daily living interference (17)• The correlation between symptoms, prostate size and urinary flow rate is relatively low (18).It must be stressed that there is still a need for an epidemiological definition of BPH and its true incidence has yet to be determined (19).1.2 Is BpH a progressive disorder?as it is almost impossible to obtain agreement on what it is that defines a man with LuTS/BPH, it seems logical to say that progression cannot be defined in terms of a transition from non-cases to cases. Instead, progression must be measured by documenting deterioration in any number of physiological variables that we associate with the LuTS/BPH syndrome. Traditionally these have included the following:• decrease in maximum flow rate• increase in residual volume• increase in prostate size• deterioration (increase) in symptom score.In addition, definable events, such as the occurrence of acute urinary retention or prostate surgery, have been used. Less commonly, changes in urodynamic variables and deterioration in disease-specific quality of life have been advocated. considerable interest currently rests with PSa. It appears to be as good a predictor of progression as any of the variables mentioned above.uPdaTE MarcH 2004 51.2.1 Indicators of progressionThe strongest evidence to support progression comes from the olmsted county (20) community-based study and the PLESS placebo group (21).The strength of evidence for individual parameters as indicators of progression is summarised in Table 1 and is categorised as strong, weak, or none. The actual rates of progression of the individual parametersas determined from the papers reviewed is shown in Table 2. These parameters could potentially be used in decisions about treatment management. Patients who show signs of more pronounced disease progression could be targeted for preventative strategies. The same strategy could be applied to patients who are at increased risk of progression based on recognised risk factors.risk factors for progression were found to be age (olmsted county), PSa (PLESS) and prostate volume (combined 2-year placebo analysis). other baseline risk factors can be identified, such as symptom severity and decreased urinary flow rate, but current data are not as convincing as those for age, PSa level and prostate volume.Several other complications, such as renal impairment and bladder dysfunction, have been associated with progression of BPH. although these are important, they are very rare and therefore could not be evaluated accurately in community-based and clinical studies. The evidence for the progression of BPH has been summarised previously (22).Table 1: Strength of evidence for specific parameters as indicators of progression of benign prostatic hyperplasia (BpH)parameter Community- based studies Clinical trials LuTS I-PSS S n/W*BII S n/nQoL n W/S*BPE drE n nTruS S SMrI n S/S*Boo Qmax S W/S*BPH Histology n/a n/a Miscellaneous aur S S/S*Surgery S W/S*crossover/treatment S n*Conditional risk factors: age and prostate-specific antigen (PSA); S = strong; W = weak; N = no evidence;N/A = not available.AUR = acute urinary retention; BOO = bladder outlet obstruction; BPE = benign prostatic enlargement;BII = BPH Impact Index; DRE = digital rectal examination; I-PSS = International Prostate Symptom Score; LUTS = lower urinary tract symptoms; MRI = magnetic resonance imaging; Qmax = maximum flow rate;QoL = quality of life; TRUS = transrectal ultrasonography.Table 2: Rates of progression of individual parameters in BpHStudy Rate of progressionLUTS Flow rate prostate Acute urinary retention a Surgery a(points) size (Incidence/1000 (Incidence/1000person years) person years)40-49 > 70 40-49 > 70years years years years olmsted 0.18 -2% 1.9% 3.0 34.7 0.3 10.9 (20, 23-26) per year per year per yearHealth Pro- nr nr nr 3.3 11.3 nr nr fessional (27)PLESS (28) -1.3 in +0.2 mL/s +14% 7% over 4 years 10% over 4 years4 years b in 4 years b in 4 years2-year studies nr nr nr 1.6-4.2%c nr(22, 29-32) 0.5-3.9%dnorth ame- nr nr nr nr 10-39%erican (33)a Men with moderate to severe symptoms.b F low rate and LUTS responded to placebo treatment by showing an initial improvement, which deteriorated6 uPdaTE MarcH 2004baseline during the course of the placebo-controlled trial.c According to baseline prostate volume.d According to baseline prostate-specific antigen (PSA) level.LUTS = lower urinary tract symptoms; NR = not reported.1.2.2 ConclusionsBased on published data on consequences and complications of the disease, BPH can be considered a progressive disease. There are limited published data on longitudinal studies and the key pieces of evidence that support this notion are the olmsted county and PLESS studies. a group of patients at increased risk of progression can be identified based on specific risk factors, i.e. age, PSa level and prostate volume. It might be appropriate to identify these patients at risk of progression and initiate early preventative treatment.1.2.3 References1. chute cg, Panser La, girman cJ, oesterling JE, guess Ha, Jacobsen SJ, Lieber MM. The prevalenceof prostatism: a population based survey of urinary symptoms. J urol 1993;150(1):85-9./pubmed/76854272. donovan JL, kay HE, Peters TJ, abrama P, coast J, Matos-Ferreira a, rentzhog L, Bosch JL,nordling J, gajewski JB, Barbalias g, Schick E, Silva MM, nissenkorn I, de la rosette JJ. usingthe IcSQoL to measure the impact of lower urinary tract symptoms on quality of life: evidence fromthe IcS-‘BPH’ study. International continence Society - Benign Prostatic Hyperplasia. Br J urol1997;80(5):712-21./pubmed/93932913. chapple cr. BPH disease management. Eur urol 1999; 36(Suppl 3):1-6./ProduktedB/produkte.asp?aktion=Showabstract&artikelnr=52342&ausgab e=227835&Produktnr=2240834. Berry SJ, coffey dS, Walsh Pc, Ewing LL. The development of human benign prostatic hyperplasiawith age. J urol 1984;132(3):474-9./pubmed/62062405. Lytton B, Emery JM, Harvard BM. The incidence of benign prostatic obstruction. J urol1968;99(5):639-45./pubmed/41719506. arrighi HM, Metter EJ, guess Ha, Fozzard JL. natural history of benign prostatic hyperplasia and riskof prostatectomy, the Baltimore Longitudinal Study of aging. urology 1991;35(Suppl):4-8./pubmed/17146577. norman rW, nickel Jc, Fish d, Pickett Sn. Prostate-related symptoms in canadian men 50 years ofage or older: prevalence and relationships among symptoms. Br J urol 1994;74(5):542-50./pubmed/75301158. garraway WM, collins gn, Lee rJ. High prevalence of benign prostatic hypertrophy in the community.Lancet 1991;338(8765):469-71./pubmed/17145299. Wolfs gg, knottnerus Ja, Janknegt ra. Prevalence and detection of micturition problems among2,734 elderly men. J urol 1994;152(5 Pt 1):1467-70./pubmed/793318510. Sagnier PP, McFarlane g, Teillac P, Botto H, richard F, Boyle P. Impact of symptoms of prostatismon level of bother and quality of life of men in the French community. J urol 1995;153(3 Pt 1):669-73./pubmed/753223011. Bosch JL, Hop Wc, kirkels WJ, Schröder FH. The international prostate symptom score in acommunity-based sample of men between fifty-five and seventy-four years of age. Prevalence andcorrelation of symptoms with age, prostate volume, flow rate and residual urine volume. Br J urol1995;75(5):622-30./pubmed/754213212. Berges rr, Pientka L. Management of the BPH syndrome in germany: who is treated and how? Eururol 1999; 36(Suppl 3):21-7./pubmed/1055962713. Homma Y, kawabe k, Tsukamoto T, Yamanaka H, okada k, okajima E, Yoshida o, kumazawa J,gu FL, Lee c, Hsu Tc, dela cruz rc, Tantiwang a, Lim PH, Sheikh Ma, Bapat Sd, Marshall Vr,Tajima k, aso Y. Epidemiologic survey of lower urinary tract symptoms in asia and australia using the International Prostate Symptom Score. Int urol 1997;4(4):40-6./pubmed/9179665uPdaTE MarcH 2004 714. Tsukamoto T, kumamoto Y, Masumori n, Miyakr H, rhodes T, girman gJ, guess Ha, Jacobsen SJ,Lieber MM. Prevalence of prostatism in Japanese men in a community-based study with comparison to a similar american study. J urol 1995;154(2 Pt 1):391-5./pubmed/754185215. Masumori n, Tsukamoto T, kumamoto Y, Miyake H, rhodes T, girman cJ, guess Ha, Jacobsen SJ,Lieber MM. Japanese men have smaller prostate volumes but comparable urinary flow rates relative to american men: results of community based studies in 2 countries. J urol 1996;155(4):1324-7./pubmed/863256416. guess Ha. Population-based studies of benign prostatic hyperplasia. In: kirby r et al. eds. Textbookof Benign Prostatic Hyperplasia. oxford: Isis Medical Media,1996, pp. 117-124./17. guess Ha, chute cg, garraway WM, girman cJ, Panser La, Lee rJ, Jacobsen SJ, Mckelvie gB,oesterling JE, Lieber MM. Similar levels of urological symptoms have similar impact on Scottish andamerican men although Scots report less symptoms. J urol 1993;150(5 Pt 2):1701-5./pubmed/769210518. girman cJ, Jacobsen SJ, guess Ha, oesterling JE, chute cg, Panser La, Lieber MM. naturalhistory of prostatism: relationship among symptoms, prostate volume and peak urinary flow. J urol1995;153(5):1510-5./pubmed/753625819. oishi k, Boyle P, Barry JM, et al. Epidemiology and natural history of benign prostatic hyperplasia. In:denis L, griffiths k, khoury S et al, eds. Fourth International Consultation on BPH, Paris, July 1997.Plymouth: Health Publications, 1998, pp. 25-59./20. Jacobsen SJ, girman cJ, guess Ha, rhodes T, oesterling JE, Lieber MM. natural historyof prostatism: longitudinal changes in voiding symptoms in community dwelling men. J urol1996;155(2):595-600./pubmed/855866821. Mcconnell Jd, Bruskewitz r, Walsh P, andriole g, Lieber M, Holtgrewe HL, albertsen P, roehrborncg, nickel Jc, Wang dZ, Taylor aM, Waldstreicher J. The effect of finasteride on the risk of acuteurinary retention and the need for surgical treatment among men with benign prostatic hyperplasia.new Engl J Med 1998;338(9):557-63./pubmed/947576222. anderson JB, roehrborn cg, Schalken Ja, Emberton M. The progression of benign prostatichyperplasia: examining the evidence and determining the risk. Eur urol 2001; 39(4):390-9./pubmed/1130687623. Jacobsen SJ, Jacobson dJ, girman cJ, roberts ro, rhodes T, guess Ha, Lieber MM. natural historyof prostatism: risk factors for acute urinary retention. J urol 1997;158(2):481-7./pubmed/922432924. Jacobsen SJ, Jacobson dJ, girman cJ, roberts ro, rhodes T, guess Ha, Lieber MM. Treatment forbenign prostatic hyperplasia among community dwelling men: the olmsted county Study of urinarysymptoms and health status. J urol 1999;162(4):1301-6./pubmed/1049218425. rhodes T, girman cJ, Jacobsen dJ, roberts ro, Lieber MM, Jacobsen SJ. Longitudinal prostatevolume in a community-based sample: 7 year followup in the olmsted county Study of urinarysymptoms and health status among men. J urol 2000;163(Suppl 4):249 abstr 1105.26. roberts ro, Jacobsen SJ, Jacobson dJ, rhodes T, girman cJ, Lieber MM. Longitudinal changes inpeak urinary flow rates in a community-based cohort. J urol 2000;163(1):107-13./pubmed/1060432627. Meigs JB, Barry MJ, giovannucci E, rimm EB, Stampfer MJ, kawachi I. Incidence rates and riskfactors for acute urinary retention: the Health Professional Followup Study. J urol 1999;162(2):376-82./pubmed/1041104228. Mcconnell Jd, Bruskewitz r, Walsh P, andriole g, Lieber M, Holtgrewe HL, albertsen P, roehrborncg, nickel Jc, Wang dZ, Taylor aM, Waldstreicher J. The effect of finasteride on the risk of acuteurinary retention and the need for surgical treatment among men with benign prostatic hyperplasia.Finasteride Long-Term Efficacy and Safety Study group. new Engl J Med 1998;338(9):557-63./pubmed/947576229. arrighi HM, guess Ha, Metter EJ, Fozard JL. Symptoms and signs of prostatism as risk factors forprostatectomy. Prostate 1990;16(3):253-61./pubmed/16918438 uPdaTE MarcH 200430. roehrborn cg, Boyle P, Bergner d, gray T, gittelman M, Shown T, Melman a, Bracken rB, deVereWhite r, Taylor a, Wang d, Waldstreicher J. PLESS Study group. Serum prostate-specific antigenand prostate volume predict long-term changes in symptoms and flow rate: results of a fouryear,randomized trial comparing finasteride versus placebo. PLESS Study group. urology 1999;54(4):662-9./pubmed/1051092531. roehrborn cg, Mcconnell Jd, Lieber M, kaplan S, geller J, Malek gH, castellanos r, coffield S,Saltzman B, resnick M, cook TJ, Waldstreicher J. PLESS Study group. Serum prostate-specificantigen is a powerful predictor of acute urinary retention and the need for surgery in men with clinical benign prostatic hyperplasia. PLESS Study group. urology 1999;53(3):473-80./pubmed/1009636932. roehrborn cg, Mcconnell Jd, Bonilla J rosenblatt S, Hudson PB, Malek gH, Schellhammer PF,Bruskewitz r, Matsumoto aM, Harrison LH, Fuselier Ha, Walsh P, roy J, andriole g, resnick M,Waldstreicher J. ProScar long term efficacy and safety group. Serum prostate-specific antigenis a strong predictor of future prostate growth in men with benign prostatic hyperplasia. ProScarlongterm efficacy and safety study. J urol 2000;163(1):13-20./pubmed/1060430433. gormley gJ, Stoner E, Bruskowitz rc, Imperato-Mckinley J, Walsh Pc, Mcconnell Jd, adriolegL, geller J, Bracken Br, Tenover JS et al. The effect of finasteride in men with benign prostatichyperplasia. The Finasteride Study group. new Engl J Med 1992 oct 22;327(17):1185-91./pubmed/13838162. RISK FACTORS2.1 For developing the diseaseThe aetiology of BPH is multifactorial. currently, there is no strong evidence that smoking, vasectomy, obesity or high alcohol intake are risk factors in the development of clinical BPH. results of the different epidemiolo-gical studies are controversial, probably because of differences in sampling and methods of analysis. In most cases only insufficient marginal differences can be established (1).chronic conditions, such as hypertension or diabetes, have been related to clinical BPH, but given the frequent occurrence of these conditions in ageing men a large proportion of patients can be expected to suffer from such an association (2,3).recently, it has been stated that diabetes and clinical BPH are associated more frequently than would be expected based on chance alone. although more severe BPH symptoms (increased I-PSS and post-void residual) seem to be found in diabetic males even after age adjustment, the fact that both conditions increase with age and can cause partially similar voiding symptoms, produces a considerable bias (3).The only true factors related to the development of the disease are age and hormonal status (4).The crucial role of the testis has been recognized for more than a century and current research has extended into the field of molecular biology (5). Both of these risk factors are currently beyond prevention.2.2 For surgical treatmentalthough the number of surgical procedures for BPH has declined in the uSa and Europe over the last decade (6), they still represent the second most common major operation in aged men (7). ultimately, three in 10 men may undergo surgery for this condition (2).Surgical risk depends on age and the presence of clinical symptoms. In the absence of clinical symptoms, the likelihood of being treated surgically is about 3% (8,9). The need for surgery increases with symptoms and is twice as high in men with a high baseline-symptom score than for those with a low score (10). For men presenting with urinary retention, the cumulative incidence for prostatectomy is 60% at 1 year and 80% at 7 years (11). Multivariate analysis carried out on a sample of 16,219 men, aged at least 40 years, with a mean follow-up of 12 years, showed a positive association with surgery for age, low body mass index, non-smokers, urine pH greater than 5, and a history of kidney X-ray and/or tuberculosis, for each of the five clinical urinary symptoms studied (12).In the Veterans normative aging Study, in a cohort of 2,280 men, the main predictor for surgery was the presence of urinary symptoms. The risk of requiring subsequent surgery also varied with age, the odds ratio being 1.8 for nocturia and 4.3 for hesitancy in young men (aged < 65 years). among older men, only nocturia (odds ratio 2.4) was predictive of surgery (13). In the Baltimore study, the three predictive symptoms for surgery were change in size and force of the urinary stream, sensation of incomplete voiding and digital rectal uPdaTE MarcH 2004 9enlargement of the prostate. Men with one factor had a cumulative incidence of surgery of 9%, those with two factors of 16%, and those with three factors of 37%. nevertheless, the same study showed that increasing age was the predominant risk factor for surgery (8).From the above, it can be concluded that the risk of needing surgery for BPH increases with age and with the degree of clinical symptoms at baseline. nocturia and changes in urinary stream seem to be the most important predictive symptoms.2.3 REFERENCES1. oishi k, Boyle P, Barry JM et al. Epidemiology and natural history of benign prostatic hyperplasia. In:Denis L, Griffiths K, Khoury S et al. eds. Fourth International Consultation on BPH, Paris, July 1997.Plymouth: Health Publications, 1998, pp. 25-59./2. Boyle P. Epidemiology of benign prostatic hyperplasia: risk factors and concomitance withhypertension. Br J clin Pract Suppl 1994;74:18-22./pubmed/75194373. Michel Mc, Mehlburger L, Schumacher H, Bressel Hu, goepel M. Effect of diabetes on lower urinarytract symptoms in patients with benign prostatic hyperplasia. J urol 2000;163(6):1725-9./pubmed/107991694. Isaacs JT, coffey dS. Etiology and disease process of benign prostatic hyperplasia. Prostate1989;(Suppl 2):33-50./pubmed/24827725. Voller Mc, Schalken Ja. Molecular genetics of benign prostatic hyperplasia. In: kirby r et al, eds.Textbook of Benign Prostatic Hyperplasia. oxford: Isis Medical Media, 1996, pp. 109-113./6. Holtgrewe HL, ackermann r, Bay-nielsen H et al. report from the committee on the Economics ofBPH. In: cockett aTk et al, eds. Third international consultation on benign prostatic hyperplasia (BPH).Jersey: Scientific communication International, 1996, pp. 51-70./7. Meigs JB, Barry MJ. natural history of benign prostatic hyperplasia. In: kirby r et al, eds. Textbook ofbenign prostatic hyperplasia. oxford: Isis Medical Media, 1996, pp. 125-135./8. arrighi HM, Metter EJ, guess Ha, Fozzard JL. natural history of benign prostatic hyperplasia and riskof prostatectomy, the Baltimore Longitudinal Study of aging. urology 1991;38(1 Suppl):4-8./pubmed/17146579. diokno ac, Brown MB, goldstein n, Herzog ar. Epidemiology of bladder emptying symptoms inelderly men. J urol 1992;148(6):1817-21./pubmed/127922310. Wasson JH, reda dJ, Bruskewitz rc, Elinson J, keller aM, Henderson Wg. a comparison oftransurethral surgery with watchful waiting for moderate symptoms of benign prostatic hyperplasia.The Veterans affairs cooperative Study group on Transurethral resection of the Prostate. n Engl JMed 1995;332(2):75-9./pubmed/752749311. craigen aa, Hickling Jd, Saunders cr, carpenter rS. natural history of prostatic obstruction: aprospective survey. J r coll gen Pract 1969;18(87):226-32./pubmed/418654512. Sidney S, Quesenberry c Jr, Sadler Mc, Lydick Eg, guess Ha, cattolica EV. risk factors for surgicallytreated benign prostatic hyperplasia in a prepaid health care plan. urology 1991;38(Suppl 1):13-9./pubmed/171465313. Epstein rS, Lydick E, deLabry L, Vokonas PS. age-related differences in risk factors forprostatectomy for benign prostatic hyperplasia: the Va normative aging Study. urology 1991;38(Suppl 1):9-12./pubmed/17146593. ASSESSMENTdiagnostic investigations have been classified as:• recommended: there is evidence to support the use of this test10 uPdaTE MarcH 2004。

良性前列腺增生临床路径标准住院流程

良性前列腺增生临床路径标准住院流程（一）适用对象。

第一诊断为良性前列腺增生（ICD-10：N40）行经尿道前列腺电切术（TURP）（ICD-9-CM-3：60.2901）（二）诊断依据。

根据《中国泌尿外科疾病诊断治疗指南》（中华医学会泌尿外科学分会编著，人民卫生出版社，2007年）1.病史：IPSS、QOL评分。

2.体格检查。

3.实验室检查及影像学检查。

（三）选择治疗方案的依据。

根据《中国泌尿外科疾病诊断治疗指南》（中华医学会泌尿外科学分会编著，人民卫生出版社，2007年）1.适合经尿道前列腺电切术（TURP）。

2.能够耐受手术。

（四）标准住院日为≤10天。

（五）进入路径标准。

1.第一诊断必须符合ICD-10：N40良性前列腺增生疾病编码。

2.当患者同时具有其他疾病诊断，但在住院期间不需要特殊处理也不影响第一诊断的临床路径流程实施时，可以进入路径。

（六）术前准备（术前评估）≤3天。

必需的检查项目：1.血常规、尿常规；2.电解质、肝肾功能、血型、凝血功能；3.感染性疾病筛查（乙肝、丙肝、艾滋病、梅毒等）；4.胸片、心电图。

（七）预防性抗菌药物选择与使用时机。

按照《抗菌药物临床应用指导原则》（卫医发〔2004〕285号）执行，并结合患者的病情决定抗菌药物的选择与使用时间。

（八）手术日为入院第≤3天。

1.麻醉方式：腰麻、硬膜外麻醉或全麻。

2.手术方式：经尿道前列腺电切术（TURP）。

3.术中用药：麻醉用药，必要时用抗菌药物。

4.输血：必要时。

（九）术后住院恢复≤7天。

1.必须复查的检查项目：血常规、尿常规；根据患者病情变化可选择相应的检查项目。

2.术后抗菌药物应用：按照《抗菌药物临床应用指导原则》（卫医发〔2004〕285号）执行。

（十）出院标准。

1.一般情况良好。

2.拔除尿管后，排尿通畅。

3.耻骨上造瘘口无漏尿。

（十一）变异及原因分析。

1.术中、术后出现并发症，需要进一步诊治，导致住院时间延长、费用增加。

《2024版中国良性前列腺增生症防治指南》

《2024版中国良性前列腺增生症防治指南》《2024版中国良性前列腺增生症防治指南》主要介绍了良性前列腺增生症的定义、流行病学、病因、临床表现以及诊断和治疗等方面的内容。

以下是对该指南的详细介绍，共计1200余字。

良性前列腺增生症（BPH）是男性常见的一种疾病，该疾病具有高发性与年龄增长相关性，且临床表现明显。

据流行病学调查数据显示，BPH在50岁男性中的患病率为50%，60岁男性中为60%，70岁男性中为70%。

指南中指出，BPH的病因尚不十分明确，但研究认为与雄激素、雌激素、生活方式、遗传因素以及各种疾病相关。

在病因方面，指南重点强调了BPH与激素的关系。

男性患有BPH的一个主要原因是其体内的雄激素（睾酮）水平升高。

这种升高同时还begint导致了雌激素与睾酮的比例失衡，使得前列腺细胞生长加速。

此外，BPH与生活方式、饮食习惯以及个人习惯也有一定关系，如长时间坐位、久坐不动、较少运动等都可能增加BPH的风险。

在临床表现方面，指南提到了BPH病人常见的症状与体征，如频尿、尿急、尿失禁等。

并强调了BPH相关并发症的发生，如急性尿潴留、慢性尿潴留等。

指南认为，BPH的确诊应包括详细病史采集、体格检查、尿流率、前列腺特异性抗原（PSA）测定等内容。

在治疗方面，指南提出了一系列的治疗原则与方法。

对于非症状性的BPH，指南建议医生采取观察、定期随访的方式进行处理；对于症状性的患者，可使用状态评分系统进行分级治疗，并采用药物治疗、手术治疗以及其他非手术治疗方法治疗。

根据患者的具体情况，医生可以采取药物治疗的方式来减轻症状，如使用α1受体阻滞剂、5α还原酶抑制剂等；对于一些症状严重且药物治疗效果不佳的患者可以考虑手术治疗。

指南提到了多种手术方法，如经尿道前列腺切除术、经尿道膀胱颈部悬吊术等，并对手术的适应症和禁忌症进行了详细说明。

总结起来，《2024版中国良性前列腺增生症防治指南》全面介绍了BPH的定义、病因、临床表现、诊断与治疗，对于临床医生在处理和治疗BPH患者时具有重要的参考价值。

219408649_良性前列腺增生的诊疗

良性前列腺增生的诊疗胡传义蔡志康（上海市浦东新区公利医院泌尿男科学部，上海 200135）摘要良性前列腺增生（BPH）是中老年男性的常见疾病，雄激素和年龄是主要致病因素，代谢综合征亦与BPH 的发生密切相关。

对初次就诊的BPH患者，需进行初次评估，特别强调患者的主观感受。

大多数早期患者通过药物治疗可以改善症状；外科干预治疗以腔内手术为主，需严格遵守手术指征以确保手术疗效。

本文就BPH病因、评估、手术指征、药物治疗、微创治疗进展进行介绍。

关键词良性前列腺增生；病因；药物治疗；腔内手术中图分类号：R697.32 文献标志码：A 文章编号：1006-1533（2023）12-0003-04引用本文胡传义, 蔡志康. 良性前列腺增生的诊疗[J]. 上海医药, 2023, 44(12): 3-6.Diagnosis and treatment of benign prostatic hyperplasiaHU Chuanyi, CAI Zhikang(Department of Urology and Andrology of Gongli Hospital of Pudong New District, Shanghai 200135, China) ABSTRACT Benign prostatic hyperplasia(BPH) is a common disease in the elderly men, androgen and age are the main pathogenic factors, and metabolic syndrome is also closely related to the occurrence of BPH. For BPH patients who visit the clinic for the first time, an initial evaluation is required, with special emphasis on the patients’ subjective feelings. The symptoms of the most patients can be improved through drug treatment; surgical treatment is mainly endovascular surgery, and strict surgical indications are required to ensure the efficacy of surgery. This article introduces the etiology, evaluation, surgical indications, drug therapy, and progress of minimally invasive treatment of BPH.KEY WORDS benign prostatic hyperplasia; etiology; drug therapy; endovascular surgery良性前列腺增生（Benign prostatic hyperplasia，BPH）是世界范围内老年男性最常见的疾病，近年来，随着我国人类的寿命延长、人口老龄化的到来，BPH的发病率较前明显上升。

良性前列腺增生50例诊断及治疗

第31卷第4期吉林医药学院学报V01．31N o．42010年08月Jour nal of Ji li n M e di cal C ol l eg e A ug．2010—203一能，扩张血管、降低血压、促进纤维蛋白溶解的作用旧1。

②活血化瘀。

作为一种血小板活化因子(PA F)抑制剂，它能降低血小板聚集性，增强红细胞变形能力，缓解高凝状态，使血流加快，血流量增加，改善微循环"J。

本组治疗的患者中，自发肢痛、麻木改善率明显比对照组显著，感觉减退和发冷症状亦较对照组改善，深部神经反射改善不明显。

治疗组治疗前后肢体疼痛、麻木改善明显；对照组治疗前后改善不明显。

本研究表明，川芎嗪确有较好的治疗作用，且明显优于常规维生素B族治疗组，且无明显毒副作用。

参考文献：[1]刘新民．实用内分泌学[M]．2版．北京：人民军医出版社，1998：316．[2]许建平，马庭亢，闻良珍．川芎嗪治疗胎儿宫内生长迟缓中氧自由基与血栓素B：、6酮-前列腺索1a的相关性研究[J]．中国中西医结合杂志，1998，18(5)：265-268．[3]黄德弘，叶绍伟，庆方．激光加川芎嗪治疗糖尿病性周围神经病变的临床观察[J]．中国中西医结合杂志，2000，20(8)：620-621．(收稿日期：20104)7—12)文章编号：1673-2995(2010)04-0203-02良性前列腺增生50例诊断及治疗黄伟，王多军(牡丹江医学院第二附属医院泌尿外科，黑龙江牡丹江157009)关键词：良性前列腺增生；诊断；治疗中图分类号：R697+．32文献标识码：B良性前列腺增生简称前列腺增生，亦称前列腺良性肥大，是老年男性常见疾病。

前列腺的病变组织表现为腺管的增生和平滑肌的增生，可能造成尿道压迫症状，引起排尿困难及尿路刺激症状等。

男性自35岁开始前列腺可有不同程度的增生，50岁以上男性出现前列腺增生l临床症状较高。

因良性前列腺增生住院患者比例逐年递增，故对于良性前列腺增生的病因、诊断、治疗及预防已受到了广泛的重视。

良性前列腺增生讲课

诊断：病史、体检、尿动力学检查、影方式调整等
发病原因
01 02 03 04
01
年龄因素：随着年龄增长，前列腺增生发病率逐渐增加
02
激素水平：雄性激素水平失衡，导致前列腺增生
03
生活习惯：长期久坐、缺乏运动、饮食不当等不良生活习惯
04
遗传因素：家族中有前列腺增生病史，发病风险增加
2 尿急、夜尿增多
3 诊断：良性前列腺增生
治疗方案：药
4 物治疗、手术治疗、生活方式调整
预后：经过治
5 疗，症状得到缓解，生活质量得到提高
治疗过程
01 诊断：通过症状、体征、实验室检查等方法确诊前列腺增生
02 药物治疗：使用 α 受体阻滞剂、5α还原酶抑制剂等药物进行治疗
03 手术治疗：根据病情选择合适的手术方式，如经尿道前列腺电切术、激光手术等
04 康复治疗：术后进行康复训练，预防并发症，提高生活质量
康复效果
排尿顺畅：排尿困难、尿潴留等症状
得到缓解
预防并发症：降低感染、结石等
风险
症状减轻：尿频、尿急、夜尿次数减少
改善生活质量：提高睡眠质量，减少对日常生活的影响
良性前列腺增生讲课
目录
01. 前列腺增生概述 02. 前列腺增生诊断与治疗 03. 前列腺增生预防与保健 04. 前列腺增生案例分析
基本概念
良性前列腺增生（BPH）：前列腺组织增生，导致尿道受压，引起排尿困难等症状
病因：年龄、遗传、激素水平、生活方式等因素
症状：尿频、尿急、夜尿增多、排尿困难等
心理支持：增强患者信心，提高治疗