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作 者:张洪团[1] 徐勇[1] 畅继武[1] 张志宏[1] 刘冉录[1] 马宝杰[1]
机构地区:[1]天津医科大学第二医院泌尿外科,天津300211
出 处:《中华男科学杂志》2012年第3期208-211,共4页National Journal of Andrology
摘 要:目的:探讨BPH患者组织学前列腺炎与PSA、前列腺体积、PSA密度(PSAD)、IPSS、最大尿流率(Qmax)及残余尿量(PVR)的相关性。方法:手术切除或经尿道前列腺电切术(TURP)治疗的BPH患者673例。按照是否伴有组织学前列腺炎将患者分为两组:A组:BPH伴组织学前列腺炎;B组:BPH不伴有组织学前列腺炎。比较两组患者PSA、前列腺体积、PSAD、IPSS、Qmax及PVR。结果:A组PSA水平为(5.64±2.48)μg/L,前列腺体积(43.66±13.11)ml,PSAD 0.129±0.048,IPSS(24.72±5.39)分,Qmax(6.94±3.23)ml/s,PVR(124.90±49.80)ml;B组PSA水平为(4.97±1.99)μg/L,前列腺体积(40.41±11.44)ml,PSAD 0.123±0.034,IPSS(23.40±6.21)分,Qmax(7.75±3.52)ml/s,PVR(112.73±50.03)ml。A组PSA水平、前列腺体积、IPSS和PVR均明显高于B组(P<0.05);A组Qmax明显低于B组(P<0.05);PSAD两组间差异无统计学意义(P>0.05)。结论:组织学前列腺炎能明显增加患者的PSA水平、前列腺体积、IPSS和PVR,降低患者Qmax。但是组织学前列腺炎与PSAD无关;组织学前列腺炎是影响BPH临床进展的重要因素。Objective: To explore the correlation of histologically proven prostatitis with the level of prostate specific antigen (PSA), prostate volume, PSA density (PSAD), international prostate symptom score (IPSS), maximum flow rate (Qmax) and postvoid residual volume (PVR) in men with symptoms of benign prostate hyperplasia (BPH). Methods : Totally 673 patients surgically treated for BPH were divided into Groups A and B in accordance with histological findings, the former including those with histological prostatitis, and the latter without it. Comparisons were made between the two groups in the PSA level, prostate volume, PSAD, IPSS, Qmax and PVR. Results: The PSA level, prostate volume, IPSS and PVR were significantly higher in Group A ([5.64 ±2.48 ] p,g/L, [43.66±13.11] ml, 24.72±5.39and [124. 90 ± 49. 801 ml) than inB ([4.97±1.99] μg/L, [40.41±11.44] ml, 23.40± 6.21 and [ 112.73 ± 50.03 ] ml) ( P 〈 0.05 ), while Qmax markedly lower in the former ( [ 6.94 ± 3.231 ml/s) than in the latter ( [ 7.75 ± 3.52 ] ml/s) (P 〈 0.05 ), but PSAD showed no statistically significant difference between the two groups (0. 129 ± 0. 048 vs 0. 123 ± 0. 034, P 〉 0.05 ). Conclusion : Histological prostatitis can significantly increase the PSA level, prostate volume, IPSS and PVR, and reduce the Qmax of the patient, but is not correlated with PSAD. It is an important factor influencing the clinical progression of BPH. Natl J Androl, 2012, 18 (3) : 208 -211
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