血清PSA含量与前列腺癌临床分期、病理分级的相关性

目的:探讨血清前列腺特异性抗原(PSA)与前列腺癌(PCa)临床分期、病理分级的相关性.方法:对自2004年7月～2009年12月南京市13692例50岁以上的男性在健康体检时行血清PSA检测.以PSA≥4.0ng/ml定为前列腺癌可疑病例.建议行前列腺穿刺活检以确诊.共筛查出PCa患者140例,比较不同PSA值PCa患者的Gleason评分及临床分期.结果:随着PSA值的升高,前列腺癌筛查阳性率亦随之升高,低分化前列腺癌患者血清PSA含量明显高于高分化前列腺癌和中分化前列腺癌患者(P＜0.05),晚期前列腺癌患者血清PSA含量明显高于早期PCa患者(P＜0.01).血清PSA含量≥20ng/ml的前列腺癌人群中低分化前列腺癌及晚期前列腺癌的比例高于血清PSA含量＜20ng/ml的前列腺癌人群(P＜0.01).结论:血清PSA可以为前列腺癌患者的诊断、治疗及预后判断提供重要依据.     

PSA及其相关检测指标在早期前列腺癌诊断中的临床价值

前列腺癌(PCa)是影响老年男性的恶性肿瘤之一,具有较高的发病率和死亡率,我国PCa患者人数逐年升高,因此进行早期的诊断和治疗具有重要意义。前列腺特异性抗原(PSA)对于早期PCa的诊断、治疗和预后具有重要作用,本文分别对PSA相关指标(F/TPSA、CPSA、PSAV、PSAD、PSATZ)应用于早期PCa诊断中的价值进行综述,旨在为临床诊断PCa提供理论依据。     

uPCA3mRNA、tPSA、fPSA/tPSA、PSAD对PSA灰区前列腺癌诊断的临床意义

目的：探讨uPCA3mRNA、tPSA、fPSA/tPSA、PSAD对PSA 灰区前列腺癌的诊断价值。方法：经前列腺穿刺活检诊断为前列 腺增生(BPH) 111 例和前列腺癌(PCa) 89 例,测定血清tPSA、fPSA 与前列腺体积,所有病例均计算fPSA／tPSA、PSAD。用 RT-PCR 的方法检测PSA mRNA、PCA3 mRNA 的含量,以PCA3 mRNA/PSA mRNA 表示PCA3 mRNA 的含量。比较两组间 tPSA、fPSA/tPSA、PSAD 及PCA3mRNA各指标的差异,分析各指标在ROC 曲线下的面积、各指标的诊断敏感性和特异性。结果： PCa 组的fPSA／tPSA较BPH 组降低（P<0.01）,PCa 组的tPSA、PSAD及PCA3 mRNA较BPH 组均升高（P<0.01）。tPSA、fPSA／ tPSA、PSAD及PCA3 mRNA在ROC 曲线下的面积从大到小依次是PCA3 mRNA>PSAD > fPSA ／tPSA>tPSA。当PCA3 mRNA 和PSAD 临界值分别为0.27 和0.15 时,诊断PCa 的敏感性和特异性分别是86.5%和77.5%,80.9%和55.9%。结论：uPCA3 mRNA、fPSA／tPSA、PSAD 的测定能显著提高灰区PCa 诊断的敏感性和特异性,且uPCA3 mRNA 诊断效能最高。     

PSA在前列腺增生和前列腺癌中的诊断价值

目的：探讨临床上检测前列腺特异性抗原（PSA）的变化情况对前列腺增生和前列腺癌等疾病的诊断价值。方法：采用回顾性分析的方法,选取2010年6月至2012年4月在我院泌尿科接受治疗的前列腺增生患者64例定义为前列腺增生组（BPH）,前列腺癌患者83例定义为前列腺癌组（PCa）,另选取同期接受体检的健康人群137例作为对照组。分别检测三组患者入院时的游离前列腺特异性抗原和总前列腺特异性抗原的水平变化情况。对比并分析三组检测结果。结果：经检测,前列腺增生患者的血清总PSA明显高于对照组健康人群的正常值,而前列腺癌患者的血清总PSA比前列腺增生患者增高的更为明显。对照组游离PSA为（2．78±0．94）ng／mL,总PSA（1．05±0．57）ng／mL,游离PSA与总PSA的比值为,（0．38±0．61）;前列腺增生患者游离PSA为（6．36＋3．24）ng／mL,总PSA为（1．64±0．76）ng／mL,游离PSA与总PSA的比值为（0．26±0．23）;前列腺癌患者游离PSA为（12．42±4．97）ng／mL,总PSA为（1．44±0．78）ng／mL,游离PSA与总PSA的比值为（0．12±0．16）。组间比较差异明显,具有统计学意义（P〈0．05）。结论：对患者的PSA进行检测,对前列腺增生和前列腺癌的诊断具有良好的辅助作用和,临床价值。     

PSA相关指标对前列腺癌诊断价值的评价及比较研究

目的:探讨血清总PSA(TPSA)、F/TPSA和PSA密度(PSAD)在前列腺癌(PCa)诊断中的价值,寻找更准确的前列腺癌诊断指标。方法:采用化学发光免疫分析法检测前列腺癌患者(60例)和前列腺增生患者(240例)的血清PSA水平,通过B超测定患者前列腺的体积,计算PSAD,运用ROC曲线评价和比较血清总PSA(TPSA)、F/TPSA和PSAD诊断前列腺癌的准确性和特异性。结果:(1)前列腺癌患者TPSA和PSAD值均明显高于前列腺增生患者(P0.01),F/TPSA明显低于前列腺增生患者(P0.01);(2)TPSA阈值定为4 ng/ml时,诊断前列腺癌的敏感性、特异性分别为56.23%、80.10%。F/TPSA阈值定为0.15时,诊断前列腺癌的敏感性、特异性分别为88.10%、69.10%,PSAD阈值定为0.20时,诊断前列腺癌的敏感性、特异性分别为88.60%、88.30%。结论:TPSA、F/TPSA和PSAD在前列腺癌诊断中均有一定的价值,且PSAD诊断前列腺癌的敏感性、特异性优于TPSA、F/TPSA,是诊断前列腺癌更为理想的指标。     

前列腺PI-RADS V2.1评分联合血清PSA相关指标对灰区前列腺癌的诊断价值研究

摘要 目的：探讨前列腺影像报告和数据系统第2.1版（PI-RADS V2.1）评分联合血清前列腺特异抗原（PSA）相关指标对灰区前列腺癌的诊断价值。方法：回顾性分析2016年1月至2019年12月的187例经病理证实且PSA为灰区（4-10 ng/mL）的前列腺癌或前列腺增生患者资料。根据病理结果分为前列腺癌（PCa）组与前列腺增生组（BPH）组。由两名经验丰富的MRI诊断医师通过盲法对所有患者MRI图像进行PI-RADS V2.1评分,统计并计算血清PSA相关指标：总前列腺特异抗原（t-PSA）、游离前列腺特异抗原（f-PSA）、游离前列腺特异抗原与总前列腺特异抗原比值（f-PSA/t-PSA）、前列腺特异抗原密度（PSAD）。采用t检验比较各项指标在两组间的差异性,并使用受试者工作曲线（ROC）分析各项指标对灰区前列腺癌的诊断效能。结果：PI-RADS V2.1评分与PSAD在PCa与BPH组之间的差异具有统计学意义（P＜0.05）,而t-PSA、f-PSA、f-PSA/t-PSA在PCa与BPH组之间的差异均无统计学意义（P＞0.05）。根据ROC曲线分析,PI-RADS V2.1评分、PSAD、PI-RADS V2.1评分联合PSAD诊断灰区前列腺癌的曲线下面积（AUC）分别为0.814、0.671及0.838,且PI-RADS V2.1评分联合PSAD的AUC显著高于单独应用PI-RADS V2.1评分（Z=1.989,P＜0.05）与PSAD（Z=3.174,P＜0.05）。结论：PI-RADS V2.1评分与PSAD对诊断灰区前列腺癌具有较高诊断效能,且联合PI-RADS V2.1评分与PSAD能进一步提高诊断效能。     

经直肠剪切波弹性成像技术联合血清CEA、PSA、FPSA对前列腺良恶性病变的鉴别诊断价值研究

摘要 目的：研究经直肠剪切波弹性成像技术（TRSWE）联合血清癌胚抗原（CEA）、前列腺特异性抗原（PSA）、游离前列腺特异性抗原（FPSA）对前列腺良恶性病变的鉴别诊断价值。方法：选取合肥市第二人民医院2019年1月～2022年6月收治的90例前列腺病变患者,根据病理检查分为前列腺癌组（47例）和前列腺良性病变组（43例）。对所有前列腺病变患者均行TRSWE检查,分析前列腺良恶性病变的图像差异以及弹性模量最大值（Emax）、弹性模量平均值（Emean）。检测所有前列腺病变患者的血清CEA、PSA、FPSA水平并进行对比。采用受试者工作特征（ROC）曲线分析明确Emax值、Emean值以及血清CEA、PSA、FPSA水平联合诊断前列腺良恶性病变的效能。结果：前列腺癌组Emax值、Emean值均高于前列腺良性病变组（均P＜0.05）。前列腺癌组血清CEA、PSA及FPSA水平均高于前列腺良性病变组（均P＜0.05）。经ROC曲线分析发现,Emax值、Emean值以及血清CEA、PSA、FPSA水平联合检测诊断前列腺良恶性病变的效能优于上述5项指标单独检测。结论：TRSWE联合血清CEA、PSA、FPSA对前列腺良恶性病变的鉴别诊断价值较高,可有效提升前列腺癌的检出率,可能值得临床推广应用。     

术前中性粒细胞绝对值/淋巴细胞比值联合血清瘦素、睾酮对前列腺癌根治术后生化复发的评估价值

摘要 目的：探讨术前中性粒细胞绝对值/淋巴细胞比值（NLR）联合血清瘦素、睾酮对前列腺癌（PCa）根治术后生化复发的评估价值。方法：选取2018年1月～2020年1月于我院接受根治性切除术治疗的82例PCa患者。术前均检测NLR、血清瘦素、睾酮水平。术后对所有患者均进行2年随访观察,按照是否发生生化复发分为复发组（n=34）以及无复发组（n=48）。比较两组NLR、血清瘦素、睾酮水平差异。收集患者临床资料,采用多因素Logistic回归分析PCa根治术后生化复发的影响因素。采用受试者工作特征（ROC）曲线分析NLR以及血清瘦素、睾酮预测PCa根治术后生化复发的评估价值。结果：复发组术前NLR以及瘦素水平均高于无复发组（P＜0.05）,而睾酮水平低于无复发组（P＜0.05）。复发组术前前列腺特异抗原（PSA）≥10 ng/mL、TNM分期T2期人数占比以及Gleason评分均高于无复发组（P＜0.05）。多因素Logistic回归分析显示,术前PSA≥10 ng/mL、TNM分期T2期、Gleason评分较高、术前NLR较高、瘦素水平较高、睾酮水平较低是PCa根治术后生化复发的危险因素（P＜0.05）。ROC曲线分析显示,联合检测术前NLR、血清瘦素、睾酮水平预测PCa根治术后生化复发的ROC曲线下面积为0.897,高于三项指标单独检测的0.678、0.712、0.733。结论：PCa根治术后生化复发受术前PSA、NLR、血清瘦素、睾酮水平、TNM分期、Gleason评分等因素影响,术前NLR联合血清瘦素、睾酮对PCa根治术后生化复发的预测价值较高。     

前列腺癌生物标记与早期诊断

前列腺癌发病率高,肿瘤晚期难以治愈,这就致使早期诊断变得尤为重要。生物标记应用于诊断和治疗已经有50年的历史了,当今前列腺特异性抗原(PSA)作为唯一应用于临床的标记,一套依赖于PSA的诊断系统已经建立。然而标记本身的缺陷限制了系统的应用。基因组学和蛋白质组学技术的发展大大加速了前列腺癌相关生物分子的研究,为发现前列腺癌的生物标记提供了广阔的前景。以前列腺癌发生的遗传背景为基础,对目前的检测标记以及检测标记的标准作了介绍。     

Optimisation de l’utilisation du PSA

PSA is a tumor marker usually determined for prostate cancer at diagnosis for its pronostic value and at therapy follow-up. But lack of specificity of PSA for prostate cancer and variability between assays demonstrated by the quality program survey make this marker not valuable in mass screening program. Market control of Afssaps on analysis devices of PSA showed a correct harmonization for total PSA. Biological tools available and easy to perform could improve ability of PSA for early detection of prostate cancer at a curable stage without induction of unnecessary biopsies prescribed because elevated total PSA values.     

Improved prostate cancer detection with a human kallikrein 11 and percentage free PSA-based artificial neural network

Human kallikrein 11 (hK11) was evaluated in a percentage free PSA-based artificial neural network (ANN) to reduce unnecessary prostate biopsies. Serum samples from 357 patients with (n=132) and without (n=225) prostate cancer (PCa) were analyzed and ANN models were constructed and compared to all parameters. The discriminatory power of hK11 was lower than that of PSA, but receiver operator characteristic (ROC) analyses demonstrated significantly larger areas under the curves for the ANN compared to all other parameters. ANNs with hK11 may lead to a further reduction in unnecessary prostate biopsies, especially when analyzing patients with less than 15% free PSA.     

Prostate cancer: risk assessment and diagnostic approaches

The successful treatment of prostate cancer relies on detection of the disease at its earliest stages. Although prostate-specific antigen (PSA)-based screening has been a significant advance in the early diagnosis of prostate cancer, identifying specific genetic alterations in a given family or patient will allow more appropriate screening for early disease. Mapping and identification of specific prostate cancer susceptibility genes is slowly becoming a reality. Other prostate cancer risks include a family history, race, and possibly serum markers such as insulin-like growth factor-I (IGF-I). Once a high-risk man is identified, transrectal ultrasound (TRUS)-guided biopsies are the standard to diagnose prostate cancer. Although TRUS is an advance over traditional digitally directed biopsies, it represents a random sampling of the prostate since most lesions cannot be visualized. Newer modalities such as ultrasound contrast agents, pattern recognition, and artificial neural networks (ANNs), applied to TRUS images, may improve diagnostic accuracy. If a man at risk for prostate cancer has undergone a negative TRUS biopsy, the decision for the need for additional biopsies is problematic. Use of PSA derivatives such as free and total PSA and the initial biopsy abnormalities such as atypia or high-grade prostatic intraepithelial neoplasia may define those patients in need of follow-up biopsy.     

Newer potential biomarkers in prostate cancer

Prostate-specific antigen (PSA) screening has led to a significant rise in the number of men diagnosed with prostate cancer and an associated increase in biopsies performed. Despite its limitations, including a positive predictive value of only 25%-40%, PSA remains the only generally accepted biomarker for prostate cancer. There is a need for better tools to not only identify men with prostate cancer, but also to recognize those with potentially lethal disease who will benefit from intervention. A great deal of work has been done worldwide to improve our knowledge of the genetics behind prostate cancer and the specificity of PSA by developing assays for different PSA isoforms. Common genetic alterations in prostate cancer patients have been identified, including CpG hypermethylation of GSPT1 and TMPRSS2:ERG gene fusion. Serum and urine detection of RNA biomarkers (eg, PCA3) and prostate cancer tissue protein antibodies (eg, EPCA) are being evaluated for detection and prognostic tools. This article reviews some of the promising developments in biomarkers.     

Cancer de la prostate : la maladie localisée

Localized prostate cancer is characterized by a tumor confined to the prostate gland at clinical evaluation. Since the onset of PSA screening, the detection of localized prostate cancer has increased. Prognosis factors are clinical stadification, PSA value, PSA doubling time, tumor volume related to needle biopsy pathologic findings (Gleason score, percentage biopsies involved). Treatment depends on tumor prognosis, symptoms and performance status of the patient. Localized prostate cancer can be treated by surgery (radical prostatectomy, high intensity focused ultrasound) or radiotherapy (conformational radiation therapy, brachytherapy). Active follow-up can be proposed to very low risk patients.     

Developing a Follow-Up Strategy for Patients with PSA Ranging from 4 to 10 ng/ml via a New Model to Reduce Unnecessary Prostate Biopsies

Objective

The aim of this study was to develop a follow-up strategy based on the new model to reduce unnecessary prostate biopsies in patients with prostate specific antigen (PSA) ranging from 4 to 10 ng/ml.

Methods

A total of 436 patients with PSA ranging from 4 to 10 ng/ml who had undergone transrectal ultrasound (TRUS)-guided prostate biopsy were evaluated during the first stage. Age, PSA, free PSA (fPSA), digital rectal examination (DRE) findings, ultrasonic hypoechoic mass, ultrasonic microcalcifications, prostate volume (PV) and PSA density (PSAD) were considered as predictive factors. A multiple logistic regression analysis involving a backward elimination selection procedure was applied to select independent predictors. After a comprehensive analysis of all results, we developed a new model to assess the risk of prostate cancer and an effective follow-up strategy.

Results

Age, PSA, PV, fPSA, rate of abnormal DRE findings and rate of hypoechoic masses detected by TRUS were included in our model. A significantly greater area under the receiver-operating characteristic curve was obtained in our model when compared with using PSA alone (0.782 vs. 0.566). Patients were grouped according to the value of prostate cancer risk (PCaR). In the second stage of our study, patients with PCaR>0.52 were recommended to undergo biopsies immediately while the rest of the patients continued close follow-up observation. Compared with the first stage, the detection rate of PCa in the second stage was significantly increased (33.0% vs 21.1%, p = 0.012). There was no significant difference between the two stages in distribution of the Gleason score (p = 0.808).

Conclusions

We developed a follow-up strategy based on the new model, which reduced unnecessary prostate biopsies without delaying patients’ diagnoses and treatments.     

Trends in Prostate Specific Antigen (PSA) testing and prostate cancer incidence and mortality in Australia: A critical analysis

BackgroundPopulation trends in PSA testing and prostate cancer incidence do not perfectly correspond. We aimed to better understand relationships between trends in PSA testing, prostate cancer incidence and mortality in Australia and factors that influence them.MethodsWe calculated and described standardised time trends in PSA tests, prostate biopsies, treatment of benign prostatic hypertrophy (BPH) and prostate cancer incidence and mortality in Australia in men aged 45–74, 75–84, and 85 + years.ResultsPSA testing increased from its introduction in 1989 to a peak in 2008 before declining in men aged 45–84 years. Prostate biopsies and cancer incidence fell from 1995 to 2000 in parallel with decrease in trans-urethral resections of the prostate (TURP) and, latterly, changes in pharmaceutical management of BPH. After 2000, changes in biopsies and incidence paralleled changes in PSA screening in men 45–84 years, while in men ≥85 years biopsy rates stabilised, and incidence fell. Prostate cancer mortality in men aged 45–74 years remained low throughout. Mortality in men 75–84 years gradually increased until mid 1990s, then gradually decreased. Mortality in men ≥ 85 years increased until mid 1990s, then stabilised.ConclusionAge specific prostate cancer incidence largely mirrors PSA testing rates. Most deviation from this pattern may be explained by less use of TURP in management of BPH and consequent less incidental cancer detection in TURP tissue specimens. Mortality from prostate cancer initially rose and then fell below what it was when PSA testing began. Its initial rise and fall may be explained by a possible initial tendency to over-attribute deaths of uncertain cause in older men with a diagnosis of prostate cancer to prostate cancer. Decreases in mortality rates were many fold smaller than the increases in incidence, suggesting substantial overdiagnosis of prostate cancer after introduction of PSA testing.     

On the clinical usefulness of the free-to-total prostate-specific antigen ratio

The free-to-total prostate-specific antigen ratio (F/T PSA) is associated with the presence of prostate cancer and is thus used as an indicator for suspicion of prostate cancer and as a determinant for biopsy. We reviewed a recent retrospective series of 966 consecutive prostate biopsies where F/T PSA was blindly determined and did not influence biopsy indication. We simulated the association of F/T PSA with biopsy outcome and its impact as a biopsy determinant. When adopting an F/T PSA cutoff of 10%, 13%, 16% or 20% among random sextant biopsies in the 4-10 ng/mL total PSA range, the sensitivity was 15%, 37%, 55% and 72% and the specificity 89%, 80%, 64% and 44%, respectively. Using F/T PSA as a biopsy determinant, from 1.7 to 2.6 cancer biopsies would have been delayed to avoid 10 benign biopsies. As this balance is not acceptable, F/T PSA has no role as a biopsy indicator and its clinical use is questionable.     

Use of choline tracers in the prostate carcinoma management

Prostate cancer is the second most frequently diagnosed cancer in men. This incidence has increased because of the introduction of screening with prostate-specific antigen (PSA) and the use of improved biopsy techniques. Choline PET/CT cannot be recommended as a first-line screening procedure for primary prostate cancer. PET/CT has a limited sensitivity due to its dependency on tumor configuration and size, and a limited specificity in differentiation between prostate cancer and benign pathologies. PET/CT could be useful in the detection of malignant lymph nodes in case of nodes greater than 5 mm in diameter. An application of choline PET/CT may be to increase the detection rate of clinically suspected prostate cancer with multiple negative prostate biopsies. Choline PET/CT has proved to be useful for restaging patients with prostate cancer with biochemical failure. Studies have shown that the positive detection rate of choline PET/CT increases with increasing PSA values. The definition of a PSA cut-off value to refer prostate carcinoma with biochemical recurrence would be helpful for the clinical management of these patients. Several PSA cut-off values have been proposed by literature. The routine use of choline PET/CT cannot be recommended only in patients with an absolute PSA value of < 1 ng/mL. Moreover, the sensitivity of ¹⁸F-Fluorocholine (FCH) PET/CT is significantly higher in patients with a PSA velocity > 2 ng/mL per year or a PSA-doubling time ≤ 6 months. In case of early bone metastases ¹⁸F-FCH could be superior to ¹⁸F-sodium fluoride due to the absence of bone reaction and remodelling.     

Atypical prostatic glandular proliferations on needle biopsy: Diagnostic implications, use of immunohistochemistry, and clinical significance

In recent times, PSA screening and a substantial increase in prostate needle biopsies have not only resulted in detection of minute foci of cancer but have also very likely resulted in increased detection of atypical glandular proliferations. Not uncommonly, there are only a limited number of atypical glands in these biopsies, and these require careful evaluation to enable an accurate diagnosis. We describe diagnostic implications, use of immunohistochemistry, and clinical significance of these lesions. Foci of atypical glands, also labeled atypical small acinar proliferation of uncertain significance, have features suspicious for but not diagnostic of cancer. Atypical foci include a broad group of lesions of differing clinical significance. These include benign, small acinar proliferations mimicking prostate cancer and atypical glandular proliferations suspicious for carcinoma. Definite diagnosis requires accurate histopathologic assessment and judicious use of immunohistochemistry. Patients with atypical glands on prostate needle biopsy have a high risk for harboring cancer and therefore have an increased risk for having cancer detected in subsequent biopsies.