Mean Serum PSA Levels Research Articles

Seminal Plasma Prostate-Specific Antigen Level in Benign Prostatic Hyperplasia

Introduction: We evaluated the role of the seminal plasma PSA level in the prediction of the response to α-blocker treatment in patients with benign prostatic hyperplasia. Materials and Methods: 18 male patients with lower urinary tract symptoms were enrolled in the study. After their blood was sampled for PSA, ejaculates of all the subjects were obtained. Serum and seminal plasma PSA levels were calculated by Active PSA IRMA kit. Patients were given 4 mg/day doxazosin for a period of 6 weeks, following which their International Prostate Symptom Score (IPSS) evaluation was repeated. The correlation between serum PSA, seminal plasma PSA and PSA density levels and the percentage improvement in IPSS was investigated. Results: The mean serum PSA level, the mean PSA density and the mean seminal PSA level of the patients were 2.7 ± 1.2 ng/ml, 0.05 ± 0.02 ng/ml/cm³ and 0.7 ± 0.39 g/l, respectively. The percentage improvement in IPSS varied from 26.9 to 53.5%. Serum PSA and serum PSA density were not useful in the prediction of the response to α-blocker treatment, but the seminal PSA levels correlated with the percentage improvement in the IPSS (p = 0.017). Conclusions: Seminal plasma PSA has been found to be a better predictor of the response to α-blocker treatment when compared to serum PSA and PSA density.

Prostate-Specific Antigen Induces Proliferation of Peripheral Blood Lymphocytes and Cytokine Secretion in Benign Prostate Hypertrophy Patients

Purpose: The etiology of benign prostatic hypertrophy (BPH) is still obscure. Data supporting an interaction connecting prostate hyperplasia and immune dysregulation is accumulating lately. The aim of the study was to assess the cellular immune responses to PSA by measuring the in vitro potential of PSA to induce proliferation and cytokine secretion in peripheral blood lymphocytes (PBLs) of BPH patients. Materials and Methods: PBLs were extracted from fresh blood of 36 BPH patients and 11 age-matched controls. The PBLs were incubated with PSA. Proliferation of the cultured PBLs was determined by thymidine incorporation. Secretion of cytokines to the culture medium was measured either by biological assay (IL-2) or by ELISA (IL-4, IL-10, IFNγ, TNFα). Results: Twelve of the 36 BPH patients responded to PSA, whereas none of the 11 controls responded (p = 0.04). The proliferative response of PBLs from BPH patients was significantly higher as compared to PBLs of controls (p = 0.03). The mean total prostate volume and the transition zone volume were 51% and 54% bigger, respectively, among the responders to PSA as compared to the nonresponders (p < 0.05), whereas the mean serum PSA level did not differ significantly. PBLs of BPH patients secreted significantly higher levels of TNFα, both spontaneously and in response to PSA, as compared to controls (p = 0.003). Conclusions: These findings show that PSA is able to induce proliferation of PBLs in vitro in BPH patients. Moreover, the higher spontaneous and PSA-induced secretion of TNFα in BPH patients may reflect a role for this proinflammatory cytokine in vivo. Based on these observations, we suggest that autoimmune dysregulation might have a role in BPH.

Salvage surgery or salvage radiotherapy for locally recurrent prostate cancer

Objectives. To evaluate the efficacy and toxicity of salvage radiation or surgery for locally recurrent tumor after initial treatment for clinically localized prostate cancer. Methods. The treatment records of 70 patients with local treatment failure after definitive therapy for clinically localized prostate cancer were reviewed. Initial treatment consisted of external beam radiation therapy (RT) in 27 patients and radical retropubic prostatectomy (RP) in 43 patients. Results. The mean serum PSA levels were similar in both groups before initial treatment: 8.5 and 10.5 ng/mL for the salvage RP and salvage RT groups, respectively ( P = 0.09). However, at the time of salvage treatment, the mean serum PSA levels were 9.1 and 1.1 ng/mL for the salvage RP and salvage RT groups, respectively ( P = 0.0001). The mean time from tumor recurrence to salvage treatment was 15.6 months for the salvage RP group and 4.9 months for the salvage RT group ( P = 0.0001). Although there was no statistical difference in the disease-free survival rate ( P = 0.38), a trend for better disease control in the salvage RT group was evident (74.4% versus 44.4%). Patients treated with salvage RP had a higher rate of urinary incontinence than those undergoing salvage RT: 63% and 32.6%, respectively ( P = 0.01). Conclusions. The disease-free survival rate was similar between patients receiving salvage RP or RT, despite the significantly higher serum PSA levels at the time of treatment and the delay in time to treatment for the salvage RP patients. Salvage RP is associated with a high rate of urinary incontinence. Earlier identification of tumor recurrence after RT may improve the efficacy and safety of salvage RP.