Man Li-Bo, Li Gui-Zhong, Huang Guang-Lin, Wang Jian-Wei, Liu Bao-Yue
Department of Urology, Beijing Jishuitan Hospital, Beijing 100035, China.
Zhonghua Nan Ke Xue. 2012 Aug;18(8):710-4.
To investigate the relationship of the histopathologic grade and extent of prostatic inflammation with the level of serum PSA in patients with type IV prostatitis.
We performed transrectal ultrasound-guided prostate biopsy for 120 patients suspected of prostate cancer and included in this study only those with benign prostate hyperplasia (BPH) and prostatitis (n = 46), excluding the cases with prostate cancer and those with BPH but no prostatitis. We evaluated the relationship between prostatic inflammation and serum PSA levels based on the three-grade pathohistologic criteria for the extent, location and aggressiveness of prostatic inflammation. The serum tPSA levels, fPSA levels, % fPSA, and PSAD were compared among different groups.
As for the extent of inflammation, 35 of the 46 included cases were grade I (tPSA: [8.46 +/- 4.09] microg/L; fPSA: [1.75 +/- 0.93] microg/L; PSAD: 0.15 +/- 0.11), 7 were grade II (tPSA: [15.26 +/- 5.26] microg/L; fPSA: [2.54 +/- 0.72] microg/L; PSAD: 0.26 +/- 0.07) and 4 were grade III (tPSA: [21.05 +/- 7.58] microg/L; fPSA: [3. 19 +/- 1.13] microg/L; PSAD: 0.42 +/- 0.19), with statistically significant differences among the three groups in the levels of tPSA (P = 0.001), fPSA (P = 0.008) and PSAD (P < 0.001). Regarding the location of inflammation, 19 cases were grade I, 17 were grade II and 10 were grade II, with no significant differences in tPSA, fPSA and %fPSA among the three grades (P > 0.05). As for the aggressiveness of inflammation, 32 cases were grade I (tPSA: [8.37 +/- 4.07] microg/L; fPSA: [1.76 +/- 0.93] microg/L; PSAD: 0.14 +/- 0.11), 10 were grade II (tPSA: [13.30 +/- 5.69] microg/L; fPSA: [3.27 +/- 2.21] microg/L ; PSAD: 0.25 +/- 0.06) and 4 were grade III (tPSA: [21.05 +/- 7.58] microg/L; fPSA: [3.19 +/- 1.13] microg/L; PSAD: 0.42 +/- 0.19), with statistically significant differences among the three grades in the levels of tPSA (P = 0.002), fPSA (P = 0.024) and PSAD (P < 0.001). The extent of inflammation was positively correlated with the levels of tPSA (r = 0.6, P < 0.001), fPSA (r = 0.5, P = 0.001) and PSAD (r = 0.6, P < 0.001), and so was the aggressiveness of inflammation (tPSA: r = 0.5, P < 0.001; fPSA: r = 0.4, P = 0.008; PSAD: r = 0.7, P < 0.001), but a negative correlation was found between the aggressiveness of inflammation and %fPSA (r = -0.4, P = 0.013).
The aggressiveness and extent of prostatic inflammation in asymptomatic prostatitis patients are significantly correlated with the level of serum PSA, which may help pathologists to avoid unnecessary repeated biopsies for patients with high-grade prostatitis.
探讨IV型前列腺炎患者前列腺炎症的组织病理学分级及范围与血清PSA水平的关系。
对120例疑似前列腺癌患者行经直肠超声引导下前列腺穿刺活检，本研究仅纳入良性前列腺增生（BPH）和前列腺炎患者（n = 46），排除前列腺癌患者及有BPH但无前列腺炎的患者。根据前列腺炎症范围、部位及侵袭性的三级病理组织学标准，评估前列腺炎症与血清PSA水平的关系。比较不同组间血清总PSA（tPSA）水平、游离PSA（fPSA）水平、fPSA百分比及前列腺特异抗原密度（PSAD）。
就炎症范围而言，46例纳入病例中，35例为I级（tPSA：[8.46±4.09]μg/L；fPSA：[1.75±0.93]μg/L；PSAD：0.15±0.11），7例为II级（tPSA：[15.26±5.26]μg/L；fPSA：[2.54±0.72]μg/L；PSAD：0.26±0.07），4例为III级（tPSA：[21.05±7.58]μg/L；fPSA：[3.19±1.13]μg/L；PSAD：0.42±0.19），三组间tPSA水平（P = 0.001）、fPSA水平（P = 0.008）及PSAD（P < 0.001）差异有统计学意义。就炎症部位而言，19例为I级，17例为II级，10例为III级，三级间tPSA、fPSA及fPSA百分比差异无统计学意义（P > 0.05）。就炎症侵袭性而言，32例为I级（tPSA：[8.37±4.07]μg/L；fPSA：[1.76±0.93]μg/L；PSAD：0.14±0.11），10例为II级（tPSA：[13.30±5.69]μg/L；fPSA：[3.27±2.21]μg/L；PSAD：0.25±0.06），4例为III级（tPSA：[21.05±7.58]μg/L；fPSA：[3.19±1.13]μg/L；PSAD：0.42±0.19），三级间tPSA水平（P = 0.002）、fPSA水平（P = 0.024）及PSAD（P < 0.001）差异有统计学意义。炎症范围与tPSA水平（r = 0.6，P < 0.001）、fPSA水平（r = 0.5，P = 0.001）及PSAD（r = 0.6，P < 0.001）呈正相关，炎症侵袭性与tPSA水平（r = 0.5，P < 0.001）、fPSA水平（r = 0.4，P = 0.008）及PSAD（r = 0.7，P < 0.001）也呈正相关，但炎症侵袭性与fPSA百分比呈负相关（r = -0.4，P = 0.013）。
无症状前列腺炎患者前列腺炎症的侵袭性及范围与血清PSA水平显著相关，这可能有助于病理学家避免对高级别前列腺炎患者进行不必要的重复活检。
