cyclotraxin-B抑制大鼠膀胱过度活动症的实验研究

目的:探讨运用尿动力学方法研究cyclotraxin-B(CTX-B)抑制大鼠膀胱过度活动症(OAB)的可行性。方法:选择30只成年SD雌性大鼠,随机分为对照组、模型组和CTX-B组,腹腔单次注射环磷酰胺(200mg/kg)建立OAB大鼠模型。建模后第2天采用BL-410生物机能实验系统测定膀胱压参数,记录逼尿肌不稳定(DI)收缩频率、最大排尿压(MVP)、最大膀胱容量(MCC)和排尿间隔(ICI)。用光镜观察三组大鼠膀胱组织的病理学改变。结果:模型组和CTX-B组大鼠在充盈期均出现DI,形成锯齿状图型,DI收缩频率和MCC明显升高,MVP和ICI明显降低,其差异有显著统计学意义(P0.01)。CTX-B组的膀胱病理学改变较模型组明显减轻。结论:CTX-B可显著抑制OAB的逼尿肌不稳定收缩。     

膀胱出口部分梗阻对逼尿肌生物力学特性的影响

目的 探讨膀胱出口部分梗阻(P-BOO)对膀胱逼尿肌生物力学特性的影响及机制.方法 采用Wistar雄性大鼠,膀胱颈不全结扎法建立P-BOO动物模型.依据梗阻时间分为假手术组、梗阻6周组(P-B006W)及梗阻12周组(P-B0012W),其中P-B006W组根据充盈性膀胱测压所示逼尿肌是否稳定分为逼尿肌稳定组(DS)和逼尿肌不稳定组(DI).采用灌流肌槽,以拟胆碱药物(氯化氨基甲酰胆碱)作为刺激因素,用拉力传感器测定离体逼尿肌条的主动收缩功能.充盈性膀胱测压检测最大膀胱容量、膀胱漏尿点压及膀胱顺应性的变化.结果P-BOO模型均成功建立,DI组最大膀胱容量、膀胱漏尿点压、膀胱顺应性[(10.8±3.0)ml,(39.4±7.1)cm H20,(0.27±0.08)ml/cm H20]、DS组[(10.3±1.9)ml,(35.9±6.2)cm H2O,(0.29±0.05)ml/cm H2O]及P-B0012W组[(9.5±2.3)ml,(48.6±9.5)cm H20,(0.21±0.05)ml/cm H2O]均明显高于假手术组[(2.1±0.3)ml,(16.2±2.1)cm H2O,(0.13±0.03)ml/cm H2O],差异有统计学意义(P＜0.05).DI组逼尿肌条拟胆碱药物刺激产生的收缩力显著低于假手术组和DS组.P-B0012W组逼尿肌条均未检测到明确的收缩波(波幅＜0.05 g).结论 P-BOO后膀胱逼尿肌生物力学特性发生了改变:DI组逼尿肌收缩功能受损,DS组发生代偿,但如果梗阻未解除,则逼尿肌收缩性损害,最终导致不可逆的收缩功能丧失;梗阻后膀胱顺应性增大与膀胱容积显著增加密切相关,逼尿肌稳定性对其影响不显著.     

膀胱出口梗阻对逼尿肌功能的影响

膀胱出口梗阻 (BOO)常常导致逼尿肌功能改变 ,依膀胱出口梗阻的程度及时间的不同 ,逼尿肌功能变化有所差别 ,但BOO导致副尿肌功能变化的病理生理及最终结果却相对一致 ,包括逼尿肌不稳定 (DI)、逼尿肌收缩功能受损和逼尿肌顺应性改变。本文综合文献 ,对BOO后逼尿肌功能改变及其机制进行综述。     

雄性兔膀胱出口部分梗阻所致逼尿肌功能障碍的研究

目的探讨膀胱出口部分梗阻所致逼尿肌功能改变.方法取新西兰雄性白兔14只,梗阻组和对照组各7只.梗阻组行手术人为造成膀胱出口部分梗阻,饲养5周后解剖膀胱,测定膀胱重量、容量;检测逼尿肌功能;对膀胱逼尿肌细胞超微结构进行观察.结果梗阻组膀胱重量为(12.129±1.627)g,对照组膀胱重量为(3.762±1.067)g(P＜0.05);梗阻组膀胱容量为(64.000±6.272)m1,对照组膀胱容量为(94.432±12.850)ml(P＜0.05);单位重量膀胱逼尿肌对各种刺激反应性均明显下降(P＜0.05或P＜0.01);梗阻膀胱逼尿肌细胞中粗面内质网明显扩张,线粒体水肿.结论通过手术可人为建立膀胱出口部分梗阻动物模型;膀胱出口部分梗阻将导致逼尿肌功能障碍;逼尿肌功能变化与其形态学变化相关.     

大鼠逼尿肌不稳定模型的建立及评估

目的建立大鼠逼尿肌不稳定（detrusor instability,DI）模型并进行效果评估。方法选取雌性Wistar大鼠25只,随机分为实验组15只和对照组10只。实验组大鼠行膀胱出口部分结扎术建立模型,对照组在相同部位行相同操作但不结扎尿道。术后6周对两组大鼠进行经尿道插管充盈性膀胱测压并评估尿动力学检测结果。结果实验组术后死亡2只,余13只大鼠于术后第6周行充盈性膀胱测压,结果9只（69.2%）出现DI表现,2只逼尿肌稳定,2只膀胱测压未见明显收缩波。DI组大鼠的膀胱容量、排尿量、残余尿量及最大逼尿肌压与对照组比较均显著增加（P〈0.05）。结论对大鼠膀胱出口进行部分结扎建立DI模型方法简便,可重复性强;在术后6周左右麻醉下行插管测压评估DI效果最为适宜。     

逼尿肌厚度评估神经源性膀胱患者下尿路功能障碍

目的通过超声检测逼尿肌厚度(DWT)在评估神经源性膀胱(NB)患者下尿路功能障碍的临床价值。方法选取本院2015年7月至2018年7月诊治的78例因脊髓损伤引起的成年NB患者为病例组,以40例正常成年人群为对照组。超声测量DWT、尿动力学检测最大膀胱容量(MCC)、膀胱顺应性(BC)、残余尿量(PVR)及逼尿肌漏尿点压(ALPP)等指标。统计学分析比较DWT与MCC、BC、PVR及ALPP各指标的关系。结果病例组患者膀胱容量分别在50、100、150、200、250、300、400、500 mL时测得的DWT均明显大于对照组人群(P<0.05)。与低DWT组相比,高DWT组BC明显较低,而DLPP明显较高(P<0.05),组间PVR、MCC差异无统计学意义(P>0.05)。Pearson线性相关分析结果表明,DWT与BC呈明显负相关(r=0.635,P=0.001),与DLPP呈明显正相关(r=0.621,P=0.003),而与PVR、MCC无相关性(r=0.422、0.331,P=0.158、0.341)。结论NB患者DWT增加,DWT与膀胱顺应性呈负相关,而与DLPP呈正相关。应用超声评估NB患者DWT有助于反映NB下尿路功能障碍。     

大鼠膀胱出口梗阻致膀胱重构的形态结构研究

目的观察大鼠膀胱出口部分梗阻不同时期的膀胱逼尿肌细胞增生、凋亡及间质中胶原纤维的变化情况。方法 Wistar大鼠40只,采用经会阴途径球部尿道部分结扎的方法建立膀胱出口部分梗阻模型,随机分为假手术组10只,梗阻2周组15只,梗阻4周组15只。采用免疫组化方法分析增殖细胞核抗原(PCNA)表达情况;通过末端转移酶标记(TUNEL)法测逼尿肌细胞凋亡指数;运用VG染色分析胶原纤维占膀胱逼尿肌面积比例变化情况。结果假手术组、梗阻2周组和梗阻4周组PCNA阳性表达率分别为(17.19±1.37)%、(50.74±3.15)%、(33.58±2.80)%,梗阻组之间差异有统计学意义(P0.05),梗阻组与假手术组之间差异有统计学意义(P0.05)。假手术组、梗阻2周组和梗阻4周组逼尿肌细胞凋亡指数分别为(20.22±1.70)%、(33.90±1.86)%、(51.18±3.30)%,梗阻组之间差异有统计学意义(P0.05),梗阻组与假手术组之间差异有统计学意义(P0.05)。假手术组、梗阻2周组和梗阻4周组胶原纤维占膀胱逼尿肌面积比例分别为(7.07±0.67)%、(13.19±1.50)%、(22.98±2.89)%,梗阻组之间差异有统计学意义(P0.01),梗阻组与假手术组之间差异有统计学意义(P0.01)。结论不同时期大鼠膀胱出口梗阻的膀胱逼尿肌形态结构的变化,可能是膀胱逼尿肌细胞增生、凋亡以及间质中胶原纤维占膀胱逼尿肌比例变化的综合作用结果。     

前列腺增生并发恢复期中枢神经疾病的膀胱逼尿肌功能改变

目的:探讨前列腺增生(BPH)并发恢复期中枢神经疾病的膀胱逼尿肌改变.方法:对60例BPH并发恢复期中枢神经疾病患者(研究组)和60例BPH患者(对照组)进行尿动力学检查分析.结果:研究组膀胱顺应性(BC)值(18.61±5.83)ml/cmH2O,逼尿肌不稳定(DI)20例(33.3%),逼尿肌无力15例(25%),低顺应性膀胱33例(55%).对照组BC值(19.20±4.87)ml/cmH2O,DI 17例(28.3%),逼尿肌无力16例(26.7%),低顺应性膀胱29例(48.3%).DI和BC与膀胱流出道梗阻相关(P＜0.05).结论:尿动力学检查有助于了解BPH并发恢复期中枢神经疾病的患者的膀胱逼尿肌功能改变,明确患者排尿困难的原因,指导诊断和选择治疗方法,预测预后和判断疗效.DI和BC与膀胱流出道梗阻相关.     

膀胱出口梗阻对逼尿肌功能的影响

膀胱出口梗阻（BOO）常常导致逼尿肌功能改变,依膀胱出口梗阻的程度及时间的不同,逼尿肌功能变化有所差别,但BOO导致逼尿肌功能变化的病理生理及最终结果却相对一致,包括逼尿肌不稳定（DI）,逼尿肌收缩功能受损和逼尿肌顺应性改变,本文综合文献,对BOO后逼尿肌功能改变及其机制进行综述。     

膀胱出口梗阻后大鼠逼尿肌细胞内质网形态及GRP78表达的研究

目的观察膀胱出口部分梗阻后膀胱重构中,逼尿肌平滑肌细胞内质网形态及内质网应激标志性蛋白——葡萄糖调节蛋白78(GRP78)的表达情况,探讨内质网应激在膀胱重构机制中可能的作用。方法雄性Wistar大鼠40只,随机分为假手术组10只,梗阻2周组15只,梗阻4周组15只,采用经会阴途径球部尿道部分结扎的方法建立膀胱出口部分梗阻模型。采用透射电子显微镜观察逼尿肌平滑肌细胞的超微结构,通过免疫组化和Real-time PCR分别检测逼尿肌中GRP78蛋白及mRNA表达变化。结果假手术组、梗阻2周组和梗阻4周组大鼠膀胱逼尿肌细胞GRP78蛋白阳性表达率分别为(3.37±0.38)%、(51.22±0.27)%、(27.02±1.85)%,梗阻2周组大鼠膀胱逼尿肌中GRP78阳性表达明显增多,与假手术组相比有明显差异(P0.01),梗阻4周组大鼠逼尿肌中GRP78阳性表达增多,与假手术组相比有明显差异(P0.01),但比梗阻2周组表达量减少(P0.01)。各组GRP78mRNA表达量分别为(22.21±1.58)、(30.62±2.49)、(24.52±2.24),梗阻2周组大鼠膀胱逼尿肌细胞GRP78mRNA表达较假手术组明显增加(P0.01);与梗阻2周组相比,梗阻4周组大鼠膀胱逼尿肌细胞GRP78mRNA表达量下降,有显著性统计学意义(P0.01),梗阻4周组与假手术组相比无统计学意义。结论在梗阻后膀胱重构过程中,逼尿肌平滑肌细胞内质网形态有明显损伤性变化,GRP78蛋白及mRNA表达水平明显增加,提示内质网应激参与膀胱重构的进展。     

前列腺增生致膀胱出口梗阻后逼尿肌功能改变对尿动力学参数的影响

目的探讨良性前列腺增生症（BPH）致膀胱出口梗阻（BOO）后逼尿肌功能改变对尿动力学参数的影响。方法109例具有完整尿动力学结果的BPH患者根据有无B00分为梗阻组和非梗阻组;梗阻组根据梗阻级别分Ⅲ、Ⅳ、Ⅴ、Ⅵ级4组;逼尿肌收缩力分为逼尿肌收缩力减弱（DCA）与收缩力正常组;逼尿肌不稳定（DI）分DI与非DI;膀胱顺应性（BC）分高、正常、低顺应性三组;28例患者行经尿道前列腺切除术（TURP）术前及术后尿动力参数对比。结果BOO组的前列腺体积（PV）、国际前列腺症状评分（IPSS）、DI、急性尿潴留（AUR）发生率明显高于非BOO组（P〈O．05）;BOO组的最大尿流率（Qmax）、BC值、DCA发生率明显低于非BOO组（P〈0．05）;逼尿肌收缩力正常组的残余尿（RV）与BC值明显低于减弱组（P〈0．05）,而BOO和DI的发生率明显高于减弱组（P〈0．01）;DI组的年龄、BC值及DCA的发生率明显低于非DI组（P〈0．05）,而B00级别和AUR的发生率明显高于非DI组（P〈0．01）;低BC组IPSS、BOO级别、AUR发生率明显高于正常及高BC组（P〈0．05）,而DCA发生率明显低于正常及高BC组（P〈0．01）;术后Qmax、BC值较术前明显升高（P〈0．05）,RV、IPSS、DI发生率较术前明显减小（P〈0．01）。结论①BOO常与低顺应性膀胱、DI、AUR合并存在;②IPSS评分不能提示是否存在DI,DI的存在不影响IPSS评分;③TURP是治疗前列腺增生的金标准;④尿动力检查能全面了解有无BOO及BOO所致逼尿肌功能改变情况,对BPH的临床鉴别诊断、预后估计及选择恰当治疗方案都具有重要意义。     

前列腺增生患者膀胱出口梗阻程度对尿动力学指标的影响

目的探讨前列腺增生患者膀胱出口梗阻程度对尿动力学指标的影响及临床意义。方法分析113例前列腺增生患者的尿动力学资料,根据膀胱出口有无梗阻分为梗阻组和非梗阻组,梗阻组又根据梗阻级别分Ⅲ、Ⅳ、Ⅴ、Ⅵ级四组。结果梗阻组的最大尿流率、膀胱顺应性值和逼尿肌收缩力减弱发生率明显低于非梗阻组,逼尿肌不稳定和急性尿潴留发生率明显高于非梗阻组。梗阻组内各梗阻级别之间在顺应性值、逼尿肌不稳定和急性尿潴留的发生率上无显著性差异,随梗阻级别增加尿流率和逼尿肌收缩功能受损发生率下降。结论一些反映排尿异常和逼尿肌功能的尿动力学指标受膀胱出口梗阻程度影响,在无法进行压力/流率分析时综合分析这些指标有助于判断出口梗阻及其程度。     

膀胱出口梗阻后逼尿肌肾上腺素β3受体mRNA表达和作用

目的：初步研究前列腺增生患者膀胱出口梗阻后逼尿肌肾上腺素能β3受体亚型mRNA表达和作用.方法：选择前列腺增生膀胱出口无梗阻（对照组）9名和膀胱出口梗阻患者（实验组）21名,根据尿动力学将实验组分为逼尿肌稳定组和不稳定组,半定量RT-PCR方法检测三组逼尿肌β3受体亚型mRNA的表达,离体逼尿肌拉力实验检测β3受体激动剂对三组逼尿肌收缩力的影响.结果：对照组、逼尿肌稳定组和不稳定组β3受体mRNA相对含晕为（18.48±2.84）、（17.28±2.57）和（10.42±1.22）,不稳定组β3受体明显降低（P＜0.05）;β受体激动剂和β3受体激动剂诱导逼尿肌松驰效应呈浓度依赖性,对不稳定组作用小于稳定组和对照组（P＜0.05）,对照组与稳定组没有差别.结论：膀胱出口梗阻逼尿肌不稳定患者β3受体mRNA含量下降,并且对β3激动剂的松驰反应降低,逼尿肌肾上腺素能受体β3亚型可能参与膀胱出口梗阻后逼尿肌收缩力变化.     

Urothelial dysfunction and sensory protein expressions in patients with urological or systemic diseases and hypersensitive bladder

ObjectiveTo investigate the underlying pathophysiology in the urothelium of different lower urinary tract diseases (LUTDs) and in patients with overactive bladder (OAB) or hypersensitive bladder (HSB), including chronic inflammation, barrier proteins, and sensory functional receptors.Materials and MethodsA total of 156 patients, including 14 with idiopathic OAB, 11 with detrusor overactivity and inadequate contractility (DHIC), 19 with end-stage renal disease (ESRD) and HSB, 26 with spinal cord injury (SCI) and detrusor overactivity (DO), 23 with bladder outlet obstruction (BOO) and DO, 19 with diabetes mellitus (DM) and OAB, 20 with interstitial cystitis (IC), and 24 with ketamine cystitis (KC) were investigated for urothelial dysfunction and sensory protein expressions. Twenty control patients without LUTD were invited and separated into two groups for comparative studies. All participants had urodynamically proven DO or increased bladder sensation on video urodynamic studies. Urothelial dysfunction and functional receptor expressions were investigated and compared between patients with LUTD and controls.ResultsAll patient subgroups had significant increases in mast cell activation and apoptotic cell counts and a decrease in E-cadherin expression. P2X3 expression was significantly decreased in DHIC but was increased in BOO/DO. Urothelial M3 expression was significantly increased in patients with OAB, BOO/DO, DM/OAB, and KC. M2 expression was significantly decreased in DHIC but increased in patients with BOO/DO. β3-AR expression was significantly decreased in patients with OAB and increased in patients with DHIC, ESRD/HSB, DM/OAB, and KC. Patients with OAB and BOO/DO had significantly increased M2/β3-AR. Lower M2/β3-AR was associated with lower voiding efficiency and large postvoid residual (PVR) in DHIC, ESRD/HSB, and SCI/neurogenic detrusor overactivity (NDO).ConclusionPatients with OAB or HSB showed increased urothelial inflammation and lower barrier protein expression. Increased M3/β3-AR or M2/β3-AR in the urothelium was associated with OAB, whereas decreased M3/β3-AR or M2/β3-AR was associated with poor voiding efficiency and large PVR in LUTD.     

Comparison of doxazosin with or without tolterodine in men with symptomatic bladder outlet obstruction and an overactive bladder

OBJECTIVE: To assess the efficacy of combined treatment with doxazosin and tolterodine, as although alpha-blockers are commonly used and generally effective in men with symptomatic bladder outlet obstruction (BOO), a subset of men with BOO and overactive bladder (OAB) symptoms often complain of persistent symptoms. PATIENTS AND METHODS: In a prospective study of 144 consecutive men with BOO at one tertiary urology centre, all had a baseline pressure-flow urodynamic study and were then subdivided into those with BOO or BOO + OAB, based on absence or presence of involuntary detrusor contractions. The Abrams-Griffiths nomogram was used to determine obstructive BOO. After the initial evaluation, all patients were treated with doxazosin 4 mg/day for 3 months. In patients with no symptomatic improvement, tolterodine 2 mg twice daily was added for an additional 3 months. RESULTS: Of the 144 patients, 76 (53%) were diagnosed as having BOO and 68 (47%) BOO + OAB. The patients with BOO + OAB were older (P < 0.05) and had a higher International Prostate Symptom Score. After 3 months of treatment with doxazosin, 60 (79%) with BOO and 24 (35%) BOO + OAB reported a symptomatic improvement. In those patients with no improvement, six of 16 with BOO and 32 of 44 (73%) with BOO + OAB improved after adding tolterodine. Acute urinary retention developed in only two of 60 men (3.3%) treated with the combined therapy. CONCLUSION: About half of men with symptomatic BOO had an OAB; while about three-quarters of men with symptomatic BOO and no OAB improved with doxazosin, only a third with BOO + OAB were helped with doxazosin alone. Combining tolterodine with doxazosin was effective in three-quarters of men with BOO + OAB. Overall, most men with BOO with or with no OAB were helped with doxazosin alone or with the addition of tolterodine.     

前列腺增生症所致膀胱出口梗阻患者逼尿肌中神经生长因子mRNA的变化及意义

目的　探讨前列腺增生症 (BPH)所致膀胱出口梗阻 (BOO)患者膀胱逼尿肌中神经生长因子 (NGF)mRNA的表达变化及意义。方法　对同龄对照组 8例膀胱癌患者、BPH梗阻逼尿肌稳定组 2 4例患者和BPH梗阻逼尿肌不稳定组 16例患者的膀胱壁逼尿肌组织 ,采用逆转录聚合酶链反应(RT PCR)检测膀胱逼尿肌细胞中NGFmRNA的表达。结果　NGFmRNA在同龄对照组、BPH梗阻逼尿肌稳定组和梗阻逼尿肌不稳定组患者的膀胱逼尿肌细胞中均有表达 ,三组患者的平均表达水平两两之间差异均有显著性意义 (P <0 0 1) ,而且NGFmRNA在同龄对照组、BPH梗阻逼尿肌稳定组和梗阻逼尿肌不稳定组的平均表达水平逐渐增加。结论　前列腺增生症引起膀胱出口梗阻后 ,膀胱逼尿肌细胞中NGFmRNA表达水平增高 ,并可能与逼尿肌不稳定 (DI)的发生有关。     

肾上腺素α1受体亚型与大鼠膀胱出口梗阻所致逼尿肌不稳定的关系

目的：探讨肾上腺素α1受体亚型与大鼠膀胱出口梗阻（BOO）所致逦尿肌不稳定（DI）的关系。方法：利用雄激素诱导前列腺肥大建立雄性SD大鼠膀胱出口梗阻模型,梗阻6周后行允盈性膀胱测压、离体逼尿肌条收缩实验及Western Blotting蛋白印迹实验。结果：BOO动物模型梗阻6周后逼尿肌不稳定的发生率为90％,DI组与对照组相比．排尿压力升高．（69．30±9．90）vs（49．60±8．36）cmH2O（P〈0．05）。剩残余尿量增加（0．29±0．07）vs（0,10±0．05）ml（P〈0．05）。膀胱容量增加（0．59±0．07）vs（0．23±0．05）ml（P〈0．05）。肌条收缩力升高（O．89±0．07）vs（0．43±0．05）g（P〈0．05）。α1D受体蛋白表达程度高于对照组,α1A受体表达程度未发生变化。结论：肾上腺素α1D受体主要参与到大鼠膀胱出口梗阻后逼尿肌不稳定的发生发展中。     

前列腺增生致膀胱出口梗阻患者逼尿肌神经生长因子表达及超微结构改变

目的通过人前列腺增生（BPH）致膀胱出口梗阻（BOO）后逼尿肌神经生长因子（NGF）表达及超微结构的研究揭示BOO后逼尿肌功能损害,了解BOO后膀胱逼尿肌的病理生理改变。方法免疫组化SABC法分实验组（梗阻组）33例和对照组（非梗阻组）15例,检测神经生长因子（NGF）的表达;超微结构实验组和对照组各5例,用电镜观察两组超微结构并对比。结果免疫组化梗阻组和非梗阻组NGF均表达,梗阻组表达明显高于非梗阻组（P〈0．01）;电镜部分对照组逼尿肌细胞排列整齐,细胞间隙有少量胶原纤维,细胞间以中间连接为主;实验组逼尿肌肥大,扭曲变形,排列不齐,增宽的细胞间隙中有大量的胶原纤维,细胞间中间连接减少,代替缝隙连接及桥粒连接等方式。结论BPH致BOO后膀胱逼尿肌细胞中NGF表达水平增高与逼尿肌不稳定（DI）及逼尿肌去神经改变等病理生理变化有关;BPH致BOO后逼尿肌不稳定及逼尿肌功能减退与逼尿肌形态改变及细胞连接等超微结构改变有关系。     

Correlation of urinary nerve growth factor level with pathogenesis of overactive bladder

AIMS: The origin of overactive bladder (OAB), which is a leading cause of lower urinary tract symptoms, remains unknown. Nerve growth factor (NGF) is one of the neurotrophic factors which are needed for the maintenance of sensory neurons. It is known that too much expression of NGF may induce bladder hyperactivity. In this study, we explored the correlation of the level of urinary NGF with various pathogenic OAB such as idiopathic, neurogenic OAB, and bladder outlet obstruction (BOO). METHODS: The study group included 51 OAB patients. Thirteen patients (7 females and 6 males) had idiopathic detrusor overactivity (DO) without BOO, 6 female idiopathic OAB without DO (sensory urgency), 16 patients with BOO due to BPH, and 16 patients with neurogenic DO (10 due to spinal cord injury (SCI), 6 due to cerebrovascular disease (CVD)). Thirty-two patients who had normal cystometric findings (23 females and 9 males) without OAB symptoms were used as controls. Urinary NGF levels were measured by enzyme-linked immunosorbent assay technique (ELISA) and the results were normalized based on creatinine (Cr) concentration. RESULTS: The urinary NGF levels in patients with neurogenic DO due to SCI, BOO, and sensory urgency were significantly higher compared with those of normal cystometric finding patients. However, the levels of urinary NGF were not statistically significant between patients with idiopathic DO without BOO, neurogenic DO due to CVD and patients with normal cystometric findings. CONCLUSIONS: These data suggest that urinary NGF levels could serve as a basis for adjunct diagnosis of OAB.     

Clinical diagnosis of bladder outlet obstruction in men with lower urinary tract symptoms: reliability of commonly measured parameters and the role of idiopathic detrusor overactivity

AIMS: There is no generally accepted consensus how to evaluate patients with lower urinary tract symptoms (LUTS) suggestive of bladder outlet obstruction (BOO). We have tried to determine whether the most frequently used objective variables as prostate volume, IPS-score, maximum flow rate, residual urine volume, functional bladder capacity, and pressure-flow study are reliable for diagnosis of BOO and we investigated the influence of idiopathic detrusor overactivity (IDO) on this condition. METHODS: A total of 153 men with LUTS and suspected BOO were systematically examined with routine investigation including digital rectal examination, transrectal ultrasound (TRUS), post-void residual urine volume measurement, uroflowmetry, and pressure-flow study. All patients completed IPS-score. Patients were divided into groups based on Sch?fer's grade of obstruction and incidence of IDO and clinical and urodynamical variables were compared. RESULTS: At baseline, 45.8% of the patients were urodynamically moderately obstructed and 37.9% were found to be severely obstructed. The grade of obstruction did not correlate with age. Prostate volume, post-void residual volume (PVR), and maximum flow rate correlated significantly with the degree of obstruction. The mean IPS-score remained almost unchanged throughout all obstruction groups. The incidence of IDO was 40.5% and increased from 16% in the minor obstruction group to 38.6% and 53.4% in the moderate and severe obstruction group, respectively. The patients with IDO were older, had larger prostates and were more obstructed. There was no impact of IDO on symptomatology of BOO. CONCLUSIONS: These data indicate that IPS-score does not achieve sufficient diagnostic accuracy and its role in the assessment of BOO is limited. The grade of obstruction is more related to prostate volume, PVR, and maximum flow rate. BOO and IDO seem to be related and have numerous mutual interactions.