血清TSGF和PSA联合检测对前列腺肿瘤诊断的意义

目的 探讨特异性肿瘤生长因子(TSGF)和前列腺特异性抗原(PSA)联合检测在前列腺痛诊断中的意义.方法 对26例前列腺癌,76例前列腺良性增生,28例急性细菌性前列腺炎,45例慢性前列腺炎,30例正常对照,进行TSGF和PSA联合测定.结果 TSGF测定值存前列腺癌组与良性增生、慢性炎症、健康对照组比较差异具有统计学意义(P<0.01),与急性炎症组比较差异无统计学意义(P>0.05).前列腺癌组PSA测定值与急、慢性炎症组,正常对照组比较差异具有统计学意义(P<0.01),与良性增生组比较差异无统计学意义(P>0.05);前列腺癌组TSGF单独测定敏感性和特异性分别为84.6%、88.4%,PSA单独测定敏感性和特异性分别为88.4%38.4%,二者测定敏感性和特异性分别为92.3%,92.3%.结论 TSGF和PSA联合检测对早期前列腺癌的诊断有一定的临床价值.     

经直肠超声结合前列腺特异性抗原密度检测对前列腺癌的诊断意义

目的 探究经直肠超声(TRUS)结合前列腺特异性抗原密度(PASD)检测对前列腺癌(PCa)的诊断意义.方法 选取PCa患者100例作为观察组,同期良性前列腺增生(BPH)的患者100例作为对照组.2组患者均进行TRUS和实验室指标检验,比较2组患者超声图像和实验室指标水平,并分析TRUS和实验室指标对PCa的诊断价值...     

前列腺特异性抗原的检测对前列腺癌及前列腺增生的诊断意义

目的　探讨血清总前列腺特异性抗原 (t PSA)、游离PSA (f PSA)、PSA密度 (PSAD )及其f PSA/t PSA比值对前列腺癌 (PCa)及前列腺增生 (BPH )的诊断价值。方法　采用酶联免疫分析方法 (ELISA )检测未经治疗的 62例BPH患者和 2 4例PCa患者血清f PSA、t PSA水平 ,并计算f PSA/t PSA值和PSAD ,对检测结果进行统计学处理。结果　BPH组与PCa组的f PSA、t PSA水平均明显高于对照组 (P <0 .0 1) ;前列腺癌组的f PSA /t PSA值明显小于对照组及前列腺癌增生组 (P <0 .0 1) ;PCa组PSAD明显大于对照组和BPH组 (P <0 .0 1)。结论　检测f PSA/t PSA和PSAD比单一检测f PSA、t PSA可显著提高对PCa诊断的特异性及符合率 ,对前列腺体积较大的BPH和PCa患者 ,检测PSAD更有意义     

血清铁蛋白联合前列腺特异性抗原检测对前列腺癌的诊断价值

目的探讨血清铁蛋白(Ferr)、总前列腺特异性抗原(tPSA)、游离前列腺特异性抗原(f PSA)、fPSA/tPSA联合检测对前列腺癌(PCa)的诊断价值。方法选择90例PCa患者、84例前列腺良性病变患者和50例健康男性体检者分别作为PCa组、良性组和对照组,检测3组研究对象的血清Ferr、tPSA、fPSA水平并计算fPSA/tPSA,分析Ferr、tPSA、fPSA、fPSA/tPSA联合检测对PCa的诊断价值。结果PCa组患者的血清Ferr、tPSA、fPSA水平均高于良性组和对照组,fPSA/tPSA低于良性组和对照组,差异均有统计学意义(P﹤0.05)。良性组患者的血清Ferr、tPSA、fPSA水平均高于对照组,fPSA/tPSA低于对照组,差异均有统计学意义(P﹤0.05)。PCa患者的血清Ferr与tPSA、fPSA均呈正相关,tPSA与f PSA呈正相关,tPSA与fPSA/tPSA呈负相关(P﹤0.05)。血清Ferr、tPSA、fPSA、fPSA/tPSA联合检测诊断PCa的灵敏度、特异度、曲线下面积均高于四个指标的三联、两联、单独检测。结论PCa患者的血清Ferr、t PSA、fPSA水平均高于前列腺良性病变患者,fPSA/tPSA低于前列腺良性病变患者。血清Ferr、tPSA、f PSA、f PSA/tPSA联合检测对PCa具有较高的诊断价值,值得在临床中推广应用。     

血清PSA、PSAD、ALP联合检测对前列腺癌骨转移的临床诊断价值

目的 探讨血清前列腺特异性抗原(PSA)、前列腺特异性抗原密度(PSAD)、碱性磷酸酶(ALP)联合检测对前列腺癌(PCa)骨转移的诊断价值.方法 回顾性分析98例PCa患者的临床资料,根据是否发生骨转移分为骨转移组(n=56)和非骨转移组(n=42).检测患者的血清PSA、PSAD、ALP水平,分析3项指标单独及联合检测对PCa骨转移的诊断价值.结果 98例PCa患者中,56例患者发生骨转移,骨转移率为57.1％.骨转移组患者的PSA和PSAD值均高于非骨转移组,差异均有统计学意义(P<0.05).ALP+PSA+PSAD联合诊断PCa骨转移的灵敏度(98.34％)、阳性预测值(90.53％)、阴性预测值(92.33％)及约登指数(73.84)均高于PSA、PSAD、ALP单独诊断的结果.结论 血清PSA、PSAD、ALP联合检测对于PCa骨转移具有较高的诊断价值,值得临床推广应用.     

血清PSA联合PSAD检测对前列腺癌的诊断价值

目的:探讨血清前列腺特异抗原（PSA）、前列腺特异抗原密度（PSAD）对前列腺癌的诊断价值。方法:检测经病理确诊的57例前列腺癌、125例前列腺增生患者的血清PSA。经直肠超声测定其前列腺的体积（PV）并计算PSAD。结果:前列腺癌组患者的PSA、PSAD明显高于前列腺增生组(P<0.05)。PSA值在4.1-10.0,10.1-20.0,>20.0ng/ml区间时PCa诊断率分别为8.8%,36.8%,54.4%。前列腺癌组的ROC曲线图中PSAD的AUC值（0.682）高于PSA的AUC值（0.601）,当取PSAD≥0.18ng/（ml·cm3）时,敏感性为84.5%,特异性为78.6%。比较58例重复穿刺患者的PSA、PSAD,只有PSAD差异有统计学意义(P<0.05)。结论:PSA动态监测结合PSAD是重复穿刺的重要参考指标,PSAD是PSA对前列腺癌诊断的有益补充。     

PSMA和PSA在前列腺癌早期诊断中的价值

目的 探讨前列腺特异性膜抗原(PSMA)、前列腺特异性抗原(PSA)对前列腺癌的诊断价值.方法 将76例前列腺癌患者、31例前列腺炎分别作为前列腺癌组和前列腺炎组,同时将35例健康体检者作为对照组.采用酶联免疫吸附测定(ELISA)检测3组受试者血清PSMA和PSA水平;采用蛋白质印迹法(Western blot)检测...     

尿液前列腺癌基因-3在前列腺癌诊断中的临床价值

[目的]探讨尿液中前列腺癌基因-3(prostate cell antigen 3,PCA3)对前列腺癌的诊断价值.[方法]收集119例前列腺癌(prostate cancer,PCa)患者和207例前列腺增生(benign prostatic hyperplasia,BPH)患者前列腺按摩后尿液,采用反转录聚合酶链反应技术,分析PCA3基因在PCa和BPH患者尿液中的表达情况,并与血中前列腺特异性抗原(prostate specific of antigen,PSA)进行应用价值的比较.[结果]尿PCA3 mRNA阳性104例,其中PCa100例、BPH 4例.尿PCA3 mRNA诊断PCa的敏感度、特异性、准确率、阳性预测值(PPV)、阴性预测值(NPV)、阳性似然比(+LR)、阴性似然比(-LR)分别为84.03％、98.07％、92.94％、96.15％、91.44％、43.49、0.16;血PSA诊断PCa的检出率为48.92％(113/231),明显低于尿PCA3 mRNA诊断PCa的检出率96.15％(100/104),差异有统计学意义(P＜0.01).此外,PSA位于灰色区域4～10ng/ml77例,病理结果显示PCa 8例,BPH 69例,PCa检出率10.39％;尿PCA3 mRNA阳性7例,其中PCa 6例、BPH 1例,PCa检出率85.71％;尿PCA3 mRNA诊断PCa的敏感度和特异性分别为75.00％和98.55％.[结论]与血PSA相比,尿PCA3 mRNA诊断PCa敏感度稍低,但具有很好的特异性和阳性预测值,对于首次活检阴性而尿PCA3 mRNA阳性的患者意义重大,提示可能需要重复穿刺活检.在PSA介于灰色区域4～10ng/ml时,穿刺结果阳性率较低(10.39％),尿PCA3 mRNA诊断PCa的特异性达98.55％,可协助判断是否需要穿刺活检.     

hK2、Ki-67在前列腺癌组织中的表达及其临床意义

目的探讨hK2、Ki-67基因在前列腺癌组织中的表达和临床意义。方法应用免疫组织化学sP法检测40例前列腺癌和30例前列腺增生组织中hK2和Ki-67基因的表达情况。结果前列腺癌组织中hK2、Ki-67的阳性表达率明显高于前列腺增生组织（P〈0．05）。hK2阳性表达与前列腺癌的Gleason分级有关（P〈0．05）,与临床分期无关（P〉0．05）;Ki-67的阳性表达与Gleason分级无关（P〉0．05）,与临床分期有关（P〈0．05）。hK2和Ki-67在前列腺癌组织中的表达呈正相关（P〈0．05）。结论hK2、Ki-67异常表达与前列腺癌的诊断及预后密切相关,联合检测二者的表达有可能作为前列腺癌诊断和预后评估的指标。     

Appearance of angiotensin II expression in non-basal epithelial cells is an early feature of malignant change in human prostate

Background: Despite increasing interest in the renin-angiotensin system in cancer, little is known about angiotensin II (Ang II) expression in human prostate tumors. Methods: Using immunohistochemistry, we examined Ang II expression in prostate cancer (Gleason grades 2–5), benign prostatic hyperplasia (BPH), and high-grade prostatic intraepithelial neoplasia (HGPIN). Results: Ang II was present in proliferating neoplastic cells in HGPIN, in malignant cells in all grades of prostate cancer examined, in basal but not luminal epithelial cells in BPH, and in the cytoplasm of LNCaP, DU145, and PC3 prostate cancer cells. Conclusions: The data establishes the presence of Ang II in pre-malignant and malignant prostate cells, suggests Ang II staining in non-basal epithelial cells is an early sign of malignant change, and supports suggestions that HGPIN and malignant prostate cells both arise from transformed basal cells. Using immunohistochemistry we examined Ang II expression in proliferative disorders of the prostate and concluded that Ang II staining in non-basal epithelial cells is evidence of early malignant change.     

血管内皮生长因子与前列腺癌的相关性研究

目的检测血管内皮生长因子(vascular endothelial growth factor,VEGF)在前列腺癌(human prostate cancer,PCa)和前列腺增生(benign of prostatic hyperplasia,BPH)中的表达,探讨VEGF与前列腺癌的相关性及其临床分期、病理分级的关系。方法收集整理我院1997至2004年收治的23例前列腺癌患者和10例前列腺增生患者的临床资料和病理蜡块标本,其中前列腺癌组为实验组,前列腺增生作对照组。采用原位杂交方法检测VEGF在前列腺癌和前列腺增生中的表达,用计算机图像分析系统分析其表达情况,并应用二步法免疫组化技术进一步验证其试验结果。结果VEGF在前列腺增生组织中呈低表达,前列腺癌组织中呈高表达。在前列腺癌组织的各临床分期和病理分级中,VEGF表达情况亦有差异性。结论VEGF与前列腺肿瘤的发病年龄、前列腺体积、血清前列腺特异抗原(prostatic special antigen,PSA)和组织类型无相关性;与前列腺增生亦无明显相关;与前列腺癌的生长、浸润和转移呈正相关,是检测前列腺癌的较好的分子标志物。     

TPSA、F／T及PSAD在前列腺癌诊断中的意义

目的探讨血清中总前列腺特异性抗原（TPSA）、血清游离PSA（FPSA）与TPSA比值（F／T）及PSA密度（PSAD）在前列腺癌诊断中的意义。方法对50例健康体检男性、467例良性前列腺增生症（BPH）及116例前列腺癌患者TPSA、F／T及PSAD值的差异进行分析、比较。结果血清TPSA值前列腺癌组（53．26±33．10）高于BPH组（8．12±9．70）及对照组（1．51±1．17）;PSAD值前列腺癌组[（1．59±1．46）ng·ml^-1·cm^-3]高于BPH组[（0．14±0．17）ng·ml^-1·cm^-3]及对照组[（0．08±O．07）ng·ml^-1·cm^-3];而F／T值前列腺癌组（0．22±0．16）低于BPH组（0．27±0．15）及对照组（0．36±0．14）,差异均有统计学意义（P值均〈0．01）。PSA处于4～10ng／ml时,前列腺癌组F／T（0．18±0．13）显著低于BPH组（0．27±0．14）（P〈0．05）;前列腺癌组PSAD[（0．21±0．07）ng·ml^-1·cm^-3]显著高于BPH组[（0．11±0．06）ng·ml^-1·cm^-3]（P〈0．001）。取F／T值0．16、PSAD值0．15ng·ml^-1·cm^-3为临界值时,F／T、PSAD值灵敏度、特异度及阳性预测值分别为81．6％、78．2％、96．1％和53．8％、76．9％、97．9％,诊断效率最高。结论F／T、PSAD是诊断前列腺癌的良好指标,当PSA为4-10ng／ml诊断灰区时,F／T与PSAD对诊断前列腺癌有较好的价值。     

Relation of Free PSA/Total PSA in Serum for Differentiating Between Patients with Prostatic Cancer and Benign Hyperplasia of the Prostate: Which Cutoff Should Be Used?

A review on literature data is given concerning free prostate-specific antigen (f-PSA) and the corresponding cutoffs off-PSA/t-PSA for differentiating patients with cancer of the prostate from those with benign prostatic hyperplasia. The special importance of the diagnostic criterion (sensitivity, specificity, efficiency) for establishing the cutoff is demonstrated. On the basis of our own data, the application of the f-PSA% is recommended as an additional decision criterion for biopsy.     

Serum PSA evaluations during salvage radiotherapy for post-prostatectomy biochemical failures as prognosticators for treatment outcomes

Serum prostate specific antigen (PSA) levels have proved to be sensitive markers for the diagnosis of prostate cancer. In addition, PSA levels are useful for detecting and monitoring prostate cancer progression after radiotherapy. Serum PSA evaluations during radiotherapy, however, have not been well documented. In this study, we investigate the prognostic value of PSA evaluations during salvage radiotherapy for prostatectomy failures.

Forty-one patients with biochemical failures after prostatectomy treated with salvage radiotherapy consented to have their serum PSA levels evaluated at 30 Gy and 45 Gy of irradiation. All 41 patients had negative metastatic workup and pathologically uninvolved pelvic lymph nodes at the time of referral for salvage radiotherapy. Radiation therapy was delivered with 10–25 MV photons, with doses of 59.4–66.6 Gy. No patients received hormonal ablation therapy before irradiation.

The mean follow-up for all patients was 30.9 months. At last follow-up, 28/41 patients (68.3%) were free from biochemical failure, with 20 of 41 patients (48.8%) expressing undetectable PSA levels. Serum PSA evaluations at 30 Gy did not significantly predict for either biochemical (p = 0.0917) or clinical (p = 0.106) disease-free outcome. However, serum PSA evaluations at 45 Gy significantly predicted for both biochemical (p = 0.0043) and clinical (p = 0.0244) disease-free outcomes, with PSA elevations at 45 Gy significantly associated with poor outcomes. On univariate analysis of prognosticators for biochemical failures, the following were significant: an elevation in serum PSA levels at 45 Gy, detectable serum PSA immediately after prostatectomy, Gleason score 7–10, and serum PSA level >1 ng/ml before salvage radiotherapy.

Evaluation of serum PSA level at 45 Gy of salvage radiotherapy for biochemical relapses after prostatectomy may serve as a significant prognosticator for both biochemical and clinical disease-free outcomes.     

Hyperinsulinaemia: a prospective risk factor for lethal clinical prostate cancer

Previous studies have suggested that hyperinsulinaemia and other components of metabolic syndrome are risk factors for clinical prostate cancer. This prospective study tested the hypothesis that hyperinsulinaemia and other components of metabolic syndrome are risk factors for lethal clinical prostate cancer. The clinical, haemodynamic, anthropometric, metabolic and insulin profile at baseline in men who had died from clinical prostate cancer during follow-up was compared with the profile of men who were still alive at follow-up. If the hypothesis is true, men with an unfavourable prognosis would have a higher profile at baseline than those with a favourable prognosis. A total of 320 patients in whom clinical prostate cancer, stages T2–3, had been diagnosed were consecutively included in the study during 1995–2003. Height, body weight, waist measurement, hip measurement and blood pressure were determined. Body mass index and waist/hip ratio (WHR) were calculated. Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level. The prostate gland volume was measured using transrectal ultrasound. The annual benign prostatic hyperplasia (BPH) growth rate was calculated. The diagnosis of prostate cancer was established using transrectal ultrasound-guided automatic needle biopsy of the prostate gland. All patients with clinical prostate cancer were followed up until their death or until the study was terminated on 31 December 2003. At follow-up, 54 patients had died from prostate cancer and 219 were still alive. The results showed that the men who died of clinical prostate cancer during the follow-up period were older (P < 0.001), had a larger prostate gland volume (P < 0.001), a faster BPH growth rate (P < 0.001), a higher prevalence of type 2 diabetes (P < 0.035) and treated hypertension (P < 0.023), a higher stage (P < 0.001) and grade (P = 0.028) of clinical prostate cancer, a higher prostate-specific antigen (PSA) level (P < 0.001) and a higher PSA density (P < 0.001) at baseline than men still alive with clinical prostate cancer at follow-up. These men also had a lower HDL-cholesterol level (P = 0.027), a higher fasting plasma insulin level (P = 0.004), a higher WHR (P = 0.097) of borderline significance and a higher uric acid level (P = 0.079) of borderline significance. Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065). In conclusion, hyperinsulinaemia and five other previously established components of metabolic syndrome are shown to be prospective risk factors for deaths that can be ascribed to prostate cancer. These findings confirm previous study, which indicate that prostate cancer is a component of metabolic syndrome. Moreover, these data indicate that hyperinsulinaemia and other metabolic disorders precede deaths caused by prostate cancer. Thus, our data support the hypothesis that hyperinsulinaemia is a promoter of clinical prostate cancer. Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient’s prostate cancer stage, cancer grade and PSA level.