目的:观察良性前列腺增生(BPH)合并前列腺炎患者国际前列腺症状评分(IPSS)与前列腺按摩液(EPS)和前列腺组织中炎症因子白介素-8(IL-8)、环氧化酶-2(COX-2)水平的相关性。方法:将80例拟行经尿道前列腺电切术(TURP)BPH患者,根据术后病理...目的:观察良性前列腺增生(BPH)合并前列腺炎患者国际前列腺症状评分(IPSS)与前列腺按摩液(EPS)和前列腺组织中炎症因子白介素-8(IL-8)、环氧化酶-2(COX-2)水平的相关性。方法:将80例拟行经尿道前列腺电切术(TURP)BPH患者,根据术后病理学诊断分为单纯性增生组(30例)和增生伴炎症组(50例),两组均于术前行IPSS评分、EPS中IL-8、COX-2含量测定,术后前列腺组织中IL-8、COX-2的水平测定,进行统计学分析。结果:增生伴炎症组EPS中IL-8和COX-2水平显著高于单纯性增生组[IL-8:(15.31±1.22)ng/ml vs(5.89±0.91)ng/ml,COX-2:(371.09±14.99)ng/ml vs(156.96±29.47)ng/ml,P均<0.01],前列腺组织中两组IL-8和COX-2水平差异也显著(0.15±0.00 vs 0.05±0.02,0.13±0.01 vs 0.07±0.01,P均<0.01),IPSS两组差异也有显著性[(25.60±5.03)分vs(18.47±4.97)分,P<0.01];单纯增生组中IPSS与EPS和组织中IL-8及COX-2的表达呈中度相关(r=0.712、0.699、0.623、0.731,P均<0.05);增生伴炎症组中IPSS与IL-8、COX-2的表达呈高度相关(r=0.819、0.879、0.798、0.855,P均<0.05)。结论:EPS中IL-8、COX-2水平能间接反映前列腺组织中IL-8、COX-2水平,通过检测患者EPS中IL-8、COX-2水平并结合临床症状可以初步判定BPH患者是否合并前列腺组织学炎症。展开更多
The characterization of animal models has indicated that the genetic,dietary and environmental factors and hormonal imbalance may influence the risk to develop prostate inflammatory lesions and prostate cancer(PC)conf...The characterization of animal models has indicated that the genetic,dietary and environmental factors and hormonal imbalance may influence the risk to develop prostate inflammatory lesions and prostate cancer(PC)confirming human epidemiologic data.It is now established that the prostate inflammatory response typically results in major changes in the local microenvironment of epithelial cells of the prostate gland,including an intense stromal remodeling,activation of fibroblasts,infiltration of immune cells such as mast cells,macrophages and B and T lymphocytes and collagen deposition.The immune cells recruited at prostate inflammatory lesions and myofibroblasts may contribute to the release of numerous pro-inflammatory cytokines and chemokines that in turn can promote the oxidative stress,genomic instability and proliferation of epithelial cells.The accumulation of additional genetic and/or epigenetic alterations in prostatic stem/progenitor cells may subsequently culminate to their malignant transformation and PC initiation and progression and more particularly with advancing age.The potential mechanistic relationships between the molecular events associated with the persistent inflammatory response and prostate carcinogenesis have important implications for optimizing the current therapies against different prostatic disorders and PCs.展开更多
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
高迁移率族蛋白1(High mobility group protein,HMGB1)作为炎症反应的关键调节分子,能够通过其下游受体晚期糖基化终末产物受体(RAGE)、Toll样受体(TLR)等来发挥促炎等作用。大量研究表明前列腺炎症为前列腺早期疾病发展提供了免疫微环...高迁移率族蛋白1(High mobility group protein,HMGB1)作为炎症反应的关键调节分子,能够通过其下游受体晚期糖基化终末产物受体(RAGE)、Toll样受体(TLR)等来发挥促炎等作用。大量研究表明前列腺炎症为前列腺早期疾病发展提供了免疫微环境,促进前列腺上皮细胞增生,作用于前列腺间质内的免疫细胞,促进免疫细胞分泌促炎因子白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)等。本文全面综述了高迁移率族蛋白1及其下游受体在前列腺相关疾病中的作用关系,为前列腺炎和前列腺癌相关免疫疾病的转化治疗提供一种参考。展开更多
文摘目的:观察良性前列腺增生(BPH)合并前列腺炎患者国际前列腺症状评分(IPSS)与前列腺按摩液(EPS)和前列腺组织中炎症因子白介素-8(IL-8)、环氧化酶-2(COX-2)水平的相关性。方法:将80例拟行经尿道前列腺电切术(TURP)BPH患者,根据术后病理学诊断分为单纯性增生组(30例)和增生伴炎症组(50例),两组均于术前行IPSS评分、EPS中IL-8、COX-2含量测定,术后前列腺组织中IL-8、COX-2的水平测定,进行统计学分析。结果:增生伴炎症组EPS中IL-8和COX-2水平显著高于单纯性增生组[IL-8:(15.31±1.22)ng/ml vs(5.89±0.91)ng/ml,COX-2:(371.09±14.99)ng/ml vs(156.96±29.47)ng/ml,P均<0.01],前列腺组织中两组IL-8和COX-2水平差异也显著(0.15±0.00 vs 0.05±0.02,0.13±0.01 vs 0.07±0.01,P均<0.01),IPSS两组差异也有显著性[(25.60±5.03)分vs(18.47±4.97)分,P<0.01];单纯增生组中IPSS与EPS和组织中IL-8及COX-2的表达呈中度相关(r=0.712、0.699、0.623、0.731,P均<0.05);增生伴炎症组中IPSS与IL-8、COX-2的表达呈高度相关(r=0.819、0.879、0.798、0.855,P均<0.05)。结论:EPS中IL-8、COX-2水平能间接反映前列腺组织中IL-8、COX-2水平,通过检测患者EPS中IL-8、COX-2水平并结合临床症状可以初步判定BPH患者是否合并前列腺组织学炎症。
基金Supported by In Part by the National Institutes of Health National Cancer Institute,R01CA138791
文摘The characterization of animal models has indicated that the genetic,dietary and environmental factors and hormonal imbalance may influence the risk to develop prostate inflammatory lesions and prostate cancer(PC)confirming human epidemiologic data.It is now established that the prostate inflammatory response typically results in major changes in the local microenvironment of epithelial cells of the prostate gland,including an intense stromal remodeling,activation of fibroblasts,infiltration of immune cells such as mast cells,macrophages and B and T lymphocytes and collagen deposition.The immune cells recruited at prostate inflammatory lesions and myofibroblasts may contribute to the release of numerous pro-inflammatory cytokines and chemokines that in turn can promote the oxidative stress,genomic instability and proliferation of epithelial cells.The accumulation of additional genetic and/or epigenetic alterations in prostatic stem/progenitor cells may subsequently culminate to their malignant transformation and PC initiation and progression and more particularly with advancing age.The potential mechanistic relationships between the molecular events associated with the persistent inflammatory response and prostate carcinogenesis have important implications for optimizing the current therapies against different prostatic disorders and PCs.
基金the ‘Kwaliteitsfonds Jessa ZH’ for the financial support
文摘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.
文摘高迁移率族蛋白1(High mobility group protein,HMGB1)作为炎症反应的关键调节分子,能够通过其下游受体晚期糖基化终末产物受体(RAGE)、Toll样受体(TLR)等来发挥促炎等作用。大量研究表明前列腺炎症为前列腺早期疾病发展提供了免疫微环境,促进前列腺上皮细胞增生,作用于前列腺间质内的免疫细胞,促进免疫细胞分泌促炎因子白细胞介素-6(IL-6)、肿瘤坏死因子α(TNF-α)等。本文全面综述了高迁移率族蛋白1及其下游受体在前列腺相关疾病中的作用关系,为前列腺炎和前列腺癌相关免疫疾病的转化治疗提供一种参考。
