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早期糖尿病大鼠膀胱的动力学及病理组织学 被引量:1
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作者 卫中庆 gommert van koeveringe +6 位作者 严春寅 田成功 易超然 孙则禹 侯建全 温端改 Philip van Kerrebroeck 《苏州大学学报(医学版)》 CAS 北大核心 2008年第3期364-366,382,共4页
目的观察早期糖尿病性膀胱病(DCP)的尿动力学及病理学改变,探讨其发病机制及病理演绎过程。方法建立早期糖尿病大鼠模型(30只),以正常大鼠(30只)作对照,饲养60 d后,进行膀胱静态压、最大膀胱容量、最大膀胱收缩压等尿动力学指标测定。... 目的观察早期糖尿病性膀胱病(DCP)的尿动力学及病理学改变,探讨其发病机制及病理演绎过程。方法建立早期糖尿病大鼠模型(30只),以正常大鼠(30只)作对照,饲养60 d后,进行膀胱静态压、最大膀胱容量、最大膀胱收缩压等尿动力学指标测定。然后行膀胱湿重、膀胱壁厚度及光镜、电镜病理学观察。结果60 d后,糖尿病组膀胱静态压、最大膀胱容量、最大膀胱收缩压、膀胱顺应性、膀胱湿重、膀胱壁厚度分别为(0.95±0.10)kPa、(3.49±0.40)ml、(3.09±0.10)kPa、(1.39±0.11)ml/kPa、(182.0±1.5)mg、(1.41±0.07)mm,而对照组分别为(0.60±0.03)kPa、(1.82±0.12)ml、(4.91±0.30)kPa(0.68±0.07)ml/kPa、(149.0±1.4)mg、(0.93±0.04)mm。两组对应参数相比,差异均有统计学意义(P<0.05或<0.01)。糖尿病组膀胱逼尿肌边缘有空泡样变性、肌细胞固缩、细胞连接纤维化、成纤维细胞变性及胶原纤维排列紊乱。结论DCP大鼠早期就有膀胱的动力学及病理学改变,提示对DCP患者应尽早干预,控制病情的进一步恶化。 展开更多
关键词 糖尿病性膀胱病 动物模型 尿动力学 病理学
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糖尿病膀胱病的临床尿动力学研究 被引量:9
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作者 卫中庆 田成功 +6 位作者 gommert van koeveringe 王昱 孙则禹 于洪波 易超然 陈炜 Philip van Kerrebreck 《医师进修杂志(外科版)》 2005年第10期10-12,共3页
目的观察糖尿病膀胱病(DCP)患者的尿动力学改变,探讨发病机制及病理演绎过程,减少晚期DCP的发生,为早期诊治提供依据。方法按糖尿病患者病程分为:早期DCP患者组(32例),晚期DCP组(28例)及非糖尿病人群对照组(22例)分别进行尿动力学测定,... 目的观察糖尿病膀胱病(DCP)患者的尿动力学改变,探讨发病机制及病理演绎过程,减少晚期DCP的发生,为早期诊治提供依据。方法按糖尿病患者病程分为:早期DCP患者组(32例),晚期DCP组(28例)及非糖尿病人群对照组(22例)分别进行尿动力学测定,获得最大尿流率、排尿量、初始感膀胱容量、最大膀胱压力、最大逼尿肌压、最大膀胱容量、残余尿、膀胱颈压、最大尿道压及括约肌肌电图等参数,对以上数据作相关统计学处理。结果相对于正常对照组,早期DCP患者最大尿流率偏低[(15.97±5.71)ml/s,P<0.05],逼尿肌活动亢进(占59%),逼尿肌/括约肌协同失调(占37.5%);而晚期DCP患者最大尿流率明显下降[(8.75±4.20)ml/s,P<0.01],膀胱容量增加[(472.5±32.9)ml,P<0.01],残余尿量增多[(62.59±19.87)ml,P<0.01],逼尿肌收缩功能减弱。结论糖尿病患者在早期就有膀胱尿道的动力学改变,以逼尿肌活动功能亢进、逼尿肌/括约肌协同失调较常见,晚期以逼尿肌收缩功能减弱为主,建议对DCP患者早期就应给予干预,控制病情的进一步恶化。 展开更多
关键词 糖尿病膀胱病 尿动力学 糖尿病患者 膀胱病 动力学研究 逼尿肌收缩功能 尿动力学改变 最大尿流率 早期诊治 正常对照组
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Alternative mechanisms for prostate-specific antigen elevation:A prospective analysis of 222 transurethral resections of prostate patients
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作者 Koenraad van Renterghem JJMCH de la Rosette +4 位作者 Herbert Thijs Erika Wisanto Ruth Achten Jean-Paul Ory gommert van koeveringe 《World Journal of Clinical Urology》 2014年第2期144-151,共8页
AIM: To investigate the relationship between prostatespecific antigen(PSA) levels and(1) bladder outlet obstruction(BOO) and(2) the severity of prostate inflammation.METHODS: Two hundred and twenty-two consecutive pat... AIM: To investigate the relationship between prostatespecific antigen(PSA) levels and(1) bladder outlet obstruction(BOO) and(2) the severity of prostate inflammation.METHODS: Two hundred and twenty-two consecutive patients undergoing transurethral resection of the prostate(TURP) were prospectively included. Patients with proven urinary tract infection and/or known prostate cancer were excluded. PSA levels, International Prostate Symptoms Score(IPSS), prostate weight, post residual volume and pressure flow parameters were determined. A histopathological assessment of the presence and severity of inflammation was also performed.RESULTS: Patients had a mean age of 69.1 ± 8.6 years(45-90 years), with mean preoperative PSA levels of 4.7 ± 5.4 ng/m L(0.2-32.5 ng/m L) and IPSS of 15.7 ± 6.9(0-32). Mean Pdet Q max was 96.3 ± 34.4 cm H2O(10-220 cm H2O). The mean resected prostate weight was 39.4 ± 27.3 g(3-189 g). Correlations were observed between PSA(logarithmic) and resected prostate weight(r = 0.54; P < 0.001), PSA(logarithmic) and Pdet Q max(r = 0.17; P = 0.032), and resected prostate weight and Pdet Q max(r = 0.39; P < 0.001). Furthermore, low correlations were observed between PSA(logarithmic) and active(r = 0.21; P < 0.0001) and chronic(r = 0.19; P = 0.005) inflammation. CONCLUSION: In this study we showed a correlation between BOO(Pdet Q max) and PSA(logarithmic). Furthermore, we demonstrated a weak correlation between PSA(logarithmic) and active as well as chronic prostatic inflammation. 展开更多
关键词 TRANSURETHRAL resection of the PROSTATE Prostate-specific antigen BLADDER outlet OBSTRUCTION Lower URINARY TRACT symptoms PROSTATE inflammation
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