Knockdown of growth differentiation factor-15 restrains prostate cancer through regulating MAPK/ERK signaling pathway.

Prostate cancer, prevalent among males, is influenced by various molecular factors, including Growth Differentiation Factor 15 (GDF15). Despite its recognized role in multiple tumor types, GDF15's specific involvement in prostate cancer remains insufficiently explored. This study investigates the regulatory function of GDF15 in prostate cancer. To explore GDF15's impact, we established GDF15 knockdown and overexpression models in prostate cancer cells. We quantified mRNA and protein levels using RT-PCR and Western blotting. Functional assays, including CCK8, Transwell, wound healing, and flow cytometry, were employed to evaluate cell proliferation, invasion, migration, and apoptosis. Additionally, the effect of GDF15 on tumor growth was assessed using a metastatic tumor model in nude mice. Elevated GDF15 expression was identified in prostate cancer tissues and cells. The knockdown of GDF15 led to the activation of the MAPK/ERK signaling pathway. C16PAF was found to counteract the inhibitory effects of sh-GDF15 on cell proliferation, invasion, migration, and apoptosis in LNCaP cells. It also reversed the sh-GDF15-induced alterations in the epithelial-mesenchymal transition (EMT) process. In vivo, C16PAF notably mitigated the sh-GDF15-induced suppression of tumor growth. The study demonstrated that sh-GDF15 inhibits cell proliferation, invasion, migration, EMT process, and tumor growth, while it promotes apoptosis. However, these effects were significantly reversed by C16PAF. The study underscores the potential of GDF15 as a target for novel therapeutic interventions in prostate cancer treatment and prevention. These findings illuminate GDF15's multifaceted role in prostate cancer pathogenesis and suggest its viability as a therapeutic target.

Androgen deprivation therapy plus apalutamide as neoadjuvant therapy prior radical prostatectomy for patients with unresectable prostate cancer.

Whether neoadjuvant therapy confers a survival benefit in advanced prostate cancer (PCa) remains uncertain. The primary endpoints of previous retrospective and phase II clinical studies that used neoadjuvant therapy, including androgen deprivation therapy combined with new-generation androgen receptor signaling inhibitors or chemotherapy, were pathological downstaging, progression-free survival, prostate-specific antigen relief, and local symptom improvement. To the best of our knowledge, no studies have explored the efficacy and safety of neoadjuvant therapy in improving the surgical resection rate in cases of unresectable primary tumors of PCa. We first designed this retrospective study to evaluate the potential value of apalutamide as neoadjuvant therapy in improving the resectability rate of radical prostatectomy (RP). We initially reported 7 patients with unresectable primary lesions who underwent neoadjuvant apalutamide treatment for a median of 4 months, and all of them successfully underwent RP treatment. Our study supported apalutamide as neoadjuvant therapy, which helped improve RP's success rate and did not significantly increase perioperative complications, and the neoadjuvant therapy was controllable. Our findings' clinical value and benefit for survival still need further clinical research to confirm.

[Significance of atypical small acinar proliferation and high-grade prostatic intraepithelial neoplasia in prostate biopsy in China].

OBJECTIVE: To assess the rates of atypical small acinar proliferation (ASAP) and high-grade prostatic intraepithelial neoplasia (HGPIN) detected in prostate biopsy in China and the risk of PCa found in subsequent repeat biopsy. METHODS: A total of 2,456 patients underwent TRUS-guided prostate biopsy with the samples of ASAP and/or HGPIN tissues in our hospital at least twice between July 2014 and June 2019. We analyzed the findings of digital rectal examination, prostate volumes, PSA levels, and the results of prostate biopsies. RESULTS: Initial prostate biopsies revealed 737 cases of PCa (30.0%), 215 cases of ASAP (8.8%), 98 cases of HGPIN (4.0%), and 18 cases of ASAP+HGPIN (0.7%). Totally, 313 of the patients met the inclusion criteria and included in this study. Of the 215 cases of ASAP confirmed in the first biopsy, 72 and 25 were diagnosed with PCa in the second and third biopsies, respectively, 83 with Gleason score (GS) 6, 14 with GS7, 57 with T1c and 40 with T2a tumors. Of the 98 cases of HGPIN confirmed in the first biopsy, 1 was diagnosed with PCa in the second and another 1 in the third biopsy, both with GS6 and T1c tumors. Of the 18 cases of ASAP+HGPIN confirmed in the first biopsy, 7 and 3 were diagnosed with PCa in the second and third biopsies, respectively, 7 with GS6, 3 with GS7, 6 with T1c and 4 with T2a tumors. CONCLUSIONS: ASAP is a significant risk factor for PCa and repeat prostate biopsy should be performed for patients diagnosed with ASAP in the first biopsy. Whether repeat biopsy is necessary for those diagnosed with HGPIN depends on other related clinical parameters./.

[Impact of immune inflammation on the proliferation and apoptosis of benign prostatic hyperplasia cells].

Objective: To investigate the impact of macrophage-induced immune inflammation on the proliferation and apoptosis of BPH cells and its possible mechanism. METHODS: Macrophages were stimulated with phorbol myristate acetate, co-cultured with BPH-1 cells, and then treated with the androgen receptor (AR) inhibitor or anti-CD40L antibody. The immunohistochemical biomarkers of the T lymphocytes (CD4 and CD8), B lymphocyte (CD20) and macrophages (CD68), AR, CD40/CD40L, and inflammatory factors IL-1, IL-6 and TNF-α were measured before and after treatment. The proliferation and apoptosis of the cells were observed by MTT assay, colony-forming assay and flow cytometry, and the expressions of cell apoptosis- and MAPK signaling pathway-related proteins were determined by qRT-PCR and Western blot. RESULTS: Significantly increased proliferation and decreased apoptosis of the cells, up-regulated expressions of Bcl-2, IL-1, IL-6, TNF-α, AR, CD40 and CD40L, and down-regulated expression of Bax were observed in the BPH-1 cells co-cultured with macrophages (the M-BPH-1 group) compared with those in the blank control (B-BPH-1) group (P < 0.01). In comparison with the BPH-1 cells treated with normal saline, those treated with either low-dose CD40L (L-CD40L) or high-dose CD40L (H-CD40L) showed markedly inhibited proliferation, increased apoptosis, up-regulated expression of Bax, and down-regulated expressions of Bcl-2, IL-1, IL-6 and TNF-α (P < 0.01), and those in the low- and high-dose AR (L-AR and H-AR) inhibitor groups exhibited remarkably reduced proliferation, increased apoptosis, down-regulated expressions of Bcl-2, IL-1, IL-6 and TNF-α, and up-regulated expression of Bax (P < 0.01). The phosphorylation levels of JNK, ERK and P38 were significantly elevated in the M-BPH-1 group, but declined in the H-CD40L and the H-AR inhibitor groups compared with those in the B-BPH-1 group, all in a concentration-dependent manner (P < 0.01). CONCLUSIONS: Macrophage-induced immune inflammation regulates AR and CD40/CD40L expressions and promotes the proliferation and inhibits the apoptosis of BPH-1 cells by activating the MAPK signaling pathway. /.

Influence of Androgen Receptor Antagonist MDV3100 Therapy on Rats With Benign Prostatic Hyperplasia.

PURPOSE: To probe the effect and mechanism of androgen receptor antagonist MDV3100 on benign prostatic hyperplasia (BPH) of rats. METHODS: BPH rat model was induced by testosterone propionate. Then antagomir-miR-21-3p or agomir-miR-21-3p was injected into rats before MDV3100 treatment. The prostate index was measured by weighing the wet weight of the rat prostate. The structural morphology of rat prostate was observed after hematoxylin & eosin staining. Immunohistochemistry was applied to evaluate the expression levels of Ki-6 and inflammatory cytokines (interleukin [IL]-6, IL-18, and tumor necrosis factor-α) in rat prostate tissues. Quantitative reverse transcription polymerase chain reaction was utilized for assessment of miR-21-3p expression, and Western blot for the performance of the phosphorylation levels of IKKα and p65. RESULTS: Injection of testosterone propionate caused increased prostate gland hyperplasia, heightened miR-21-3p level, and activated nuclear factor-kappa B (NF-κB) signaling pathway. Additionally, BPH was accompanied by inflammatory response, as evidenced by enhanced expressions of Ki-67 and inflammatory cytokines. MDV3100 exposure ameliorated BPH and suppressed miR-21-3p expression. Overexpression of miR-21-3p intensified BPH and inflammation level, while knockdown of miR-21-3p relieved BPH. The coeffect of miR-21-3p upregulation and MDV3100 subjection led to higher inflammatory response, elevated phosphorylation levels of IKKα and p65 than MDV3100 treatment alone. CONCLUSION: Androgen receptor antagonist MDV3100 alleviates BPH and inflammatory response through miR-21-3p downregulation and NF-κB signaling pathway blockade.

Macrophages affect immune inflammation and proliferation in benign prostatic hyperplasia via androgen receptor and CD40/CD40L signaling pathway.

OBJECTIVE: Considering the association of macrophage migration inhibitory factor with development of prostate diseases, this study aims to explore the effect and mechanism of macrophages (MAs) in inflammation and proliferation of benign prostate hyperplasia (BPH) cells. METHODS: Totally 85 prostate tissues (75 from BPH patients and 10 from brain death patients) were collected for determination of biomarkers of T lymphocyte (CD4 and CD8), B lymphocyte (CD20) and MAs (CD68), as well as androgen receptor (AR) and CD40/CD40L. MAs stimulated by phorbol myristate acetate (PMA) were cultured with BPH cells (BPH-1), followed by AR inhibitor or anti-CD40 L antibody treatment. Proliferation and cell apoptosis were observed by MTT assay, colony formation assay and flow cytometer. Expressions of apoptotic related proteins and MAPK signaling pathway-related proteins were determined by qRT-PCR and Western blot. RESULTS: BPH tissues had increased expressions of AR, CD40 and CD40 L, as well as elevated expressions of inflammation biomarkers (CD4, CD8, CD20 and CD68) in comparison to normal prostate tissues. MAs could increase the expressions of lymphocytes and inflammation biomarkers, in addition to promoting cell proliferation and inhibiting cell apoptosis. Cell proliferation and inflammation reaction could be attenuated by anti-CD40 L antibody and AR inhibitor in a concentration dependent manner through inhibiting the phosphorylation of JNK, ERK1/2 and p38. CONCLUSION: MAs regulate AR and CD40/CD40L expression to promote the inflammation and proliferation as well as inhibiting apoptosis of BPH-1 cells through activation of the MAPK signaling pathway. This conclusion may provide a therapeutic strategy for BPH patients.

Upregulation of GRIM-19 augments the sensitivity of prostate cancer cells to docetaxel by targeting Rad23b.

The gene associated with retinoid-interferon mortality (GRIM-19) has been reported to be correlated with drug resistance, whereas its functional role in prostate cancer (PC) is not fully understood. This study aims to clarify the potential role and molecular mechanisms of GRIM-19 on the response of PC cells to chemical drug docetaxel. mRNA and protein level of GRIM-19 expression in cells and tissues of PC were measured by quantitative real-time PCR and western blot, respectively. Knock-down of GRIM-19 in PC cells was performed using siRNA. Cell apoptosis was determined by flow cytometric analysis. DNA damage in PC cells was detected by γ-H2AX staining. GRIM-19 was downregulated in PC tissues and cell lines. Knock-down of GRIM-19 increased the resistance of PC cells to docetaxel, and overexpression of GRIM-19 promoted docetaxel-induced apoptotic death in PC cells. Mechanistically, GRIM-19 downregulated the expression of the survival gene Rad23b, which promoted DNA damage repair. Overexpression of Rad23b reversed GRIM-19-mediated response to docetaxel in PC cells. GRIM-19 promoted the sensitivity of PC cells to docetaxel by downregulating Rad23b, which may serve as a promising target to develop a better strategy of chemotherapy for PC.

Inhibition of miR-423-5p suppressed prostate cancer through targeting GRIM-19.

OBJECTIVE: To determine the effect of miR-423-5p on the progression of prostate cancer (PC). METHODS: miR-423-5p and GRIM-19 expressions were detected by qRT-PCR and western blot. PC cell proliferation was measured by MTT assay. PC cell apoptosis was detected by flow cytometry. Dual luciferase reporter assay was used to confirm the interaction between miR-423-5p and GRIM-19. RESULTS: Compared with normal prostate tissues and prostate epithelial cell HPrEC, miR-423-5p was up-regulated in human PC tissues and PC3 cells, whereas GRIM-19 expression was decreased. Inhibition of miR-423-5p suppressed PC3 cell proliferation, promoted PC3 cell apoptosis, and decreased anti-apoptosis protein BCL-2 expression. GRIM-19 was a target of miR-423-5p, and GRIM-19 was negatively regulated by miR-423-5p in PC3 cells. In addition, miR-423-5p knockdown inhibited the proliferation and promoted the apoptosis of PC3 cells through GRIM-19. In vivo experiments showed that miR-423-5p inhibitor administration reduced tumor volume, down-regulated miR-423-5p and GRIM-19 expressions in PC tissues of nude mice. CONCLUSION: Inhibition of miR-423-5p suppressed PC through targeting GRIM-19.

Circular RNA hsa_circ_0003221 (circPTK2) promotes the proliferation and migration of bladder cancer cells.

Emerging studies have shown that circular RNAs could be ideal biomarkers and even potential therapeutic targets for some tumors, including bladder cancer. However, only a few studies have investigated the circular RNAs in human bladder cancer. The key circular RNA molecules are closely related to bladder cancer and their roles remain largely unknown. Here, we investigated a novel circular RNA molecule, hsa-circ-0003221(circPTK2), which is differentially expressed in bladder carcinoma. Significant differential expression levels of circPTK2 were confirmed with quantitative PCR in 40 pairs of tissue and blood samples from patients with bladder carcinoma. Moreover, circPTK2 levels both in tissue and blood were significantly correlated with several clinicopathologic characteristics, including poor differentiation (P = 0.0103 in tissue, P = 0.024 in blood), N2-N3 lymph node metastasis (P = 0.0065 in tissue, P = 0.016 in blood), and T(II-III-IV) stage (P = 0.008 in tissue, P = 0.0003 in blood). Quantitative PCR results confirmed that circPTK2 is highly expressed in migrated cells separated by Transwell assay and in metastatic lymph nodes of tumors transplanted in nude mice. In vitro silence of circPTK2 by small interfering RNA inhibited the proliferation and migration of bladder cancer cells. On the contrary, circPTK2 overexpression promoted proliferation and migration. This study showed that circPTK2 promotes proliferation and migration of cells and may be a novel potential biomarker and therapeutic target for bladder cancer diagnosis and therapy.

[Effects of simvastatin on the proliferation and apoptosis of prostatic epithelial RWPE-1 cells].

OBJECTIVE: To investigate the effects of simvastatin on the proliferation and apoptosis of prostatic epithelial RWPE-1 cells. METHODS: RWPE-1 cells cultured in vitro were treated with simvastatin at 0, 10, 20, and 40 µmol/L for 24, 48, and 72 hours followed by determination of their proliferation by MTT assay, and their apoptosis by flow cytometry. The mRNA and protein expressions of Bcl-2, Bax, and Cx43 were detected by fluorescence quantitative RT-PCR and Western blot, respectively. RESULTS: After 72 hours of treatment with simvastatin at 10, 20, and 40 µmol/L, the inhibition rates of the RWPE-1 cells were (21.07 ± 6.41)%, (34.87 ± 9.65)%, and (47.18 ± 10.88)%, respectively, significantly higher than (1.21 ± 0.54)% in the control group (P < 0.05) and in a dose-dependent manner (P < 0.05); the cell apoptosis rates were (0.066 ± 0.016)%, (0.126 ± 0.023)%, and (0.192 ± 0.025)%, respectively, remarkably higher than (0.015 ± 0.005)% in the control (P < 0.05) and also in a dose-dependent manner (P < 0.05); the mRNA and protein expressions of Bcl-2 were decreasing while those of Bax and Cx43 increasing with the increased concentration of simvastatin (P < 0.05). The expression of Cx43 was correlated negatively with that of Bcl-2 but positively with that of Bax. CONCLUSION: Simvastatin inhibits the proliferation of prostate epithelial cells and induce their apoptosis by acting on the gap junctional intercellular communication.

[Oral medication of statins retards the progression of benign prostatic hyperplasia and lower urinary tract symptoms].

OBJECTIVE: To determine whether oral statins can delay the progression of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). METHODS: We conducted a retrospective cohort study of 50-69-year-old males who came for physical examination in our hospital between January 2003 and December 2008. We designed the inclusion criteria, followed them up for 5 years, and investigated the relationship of oral statins with the clinical progression of BPH and LUTS. RESULTS: Totally, 653 men met the inclusion criteria and were included in this study, of whom 283 were treated with oral statins (group 1) while the other 370 with none (group 2). There were no statistically significant differences between the two groups in age and baseline IPSS, Qmax, and prostate volume (PV) (P > 0.05). During the follow-up, 24 cases in group 1 and 35 cases in group 2 were excluded for obvious dys-uria. A gradual increase was observed in IPSS in both groups 1 and 2 year by year from the baseline to the 5th year of follow-up, but significantly lower in the former group (4.27 +/- 1.16, 4.63 +/- 1.05, 5.27 +/- 0.96, 6.41 +/- 1.04, 7.21 +/- 1.21, and 7.93 +/-1.50) than in the latter (4.24 +/- 1.35, 5.26 +/- 1.23, 6.84 +/- 1.20, 8.75 +/- 1.84, 10.82 +/- 3.01, and 12.98 +/- 4.21) (P < 0.01); a gradual decrease was seen in Qmax, though markedly higher in group 1 ([26.56 +/- 2.09], [24.06 +/- 1.94], [21.33 +/- 1.66], [19.24 +/- 1.54], [17.44 +/- 1.53], and [16.27 +/- 1.37] ml/s) than in group 2 ([26.74 +/- 2.40], [23.62 +/- 2.01], [20.63 +/- 1.69], [17.72 +/- 1.48], [14.82 +/- 1.11], and [11.86 +/- 1.24] ml/s) (P < 0.01); and a gradual increase was found in PV, but remarkably smaller in the former group ([19.82 +/- 4.94], [22.60 +/- 4.99], [25.80 +/- 5.20], [27.92 +/- 5.05], [29.11 +/- 5.24], and [29.97 +/- 5.26] ml) than in the latter ([20.21 +/- 4.78], [24.30 +/- 4.98], [28.50 +/- 5.14], [32.84 +/- 4.77], [36.99 +/- 4.78], and [40.90 +/- 4.78] ml) (P < 0.01). Longer medication of statins was associated with better efficacy. CONCLUSION: Oral statins can significantly delay the clinical progression of BPH and LUTS.

ImmunoCyt™ and cytology for diagnosis of bladder carcinoma: a meta analysis.

BACKGROUND: Currently, cystoscopy and urine cytology are standard modalities in therapy monitoring and follow-up of bladder carcinoma (BC). Cystoscopy is an invasive and uncomfortable procedure while cytology has a limited value because it is operator-dependent and has low sensitivity. This study was to assess the accuracy of ImmunoCyt in detecting BC by comparing it with cytology using systemic analyses of studies published in both English and Chinese. METHODS: Cochrane systematic evaluation was used to search through MEDLINE, EMBASE, Cochrane Library, CMCC, and CNKI for studies regarding ImmunoCyt and cytology for detection of BC. Data were extracted and analyzed by the software MetaDiSc 1.4. RESULTS: In total 42 relevant studies were searched, of which 15 were enrolled and 12 491 patients were included. Heterogeneity, except for threshold effects, was found within these studies. A meta-analysis was performed using the random effect model. Pooled accuracy indicators like sensitivity, specificity, and diagnostic odds ratio of ImmunoCyt™ and cytology were 0.75 (0.73-0.77) vs. 0.45 (0.43-0.48), 0.73 (0.72-0.74) vs. 0.97 (0.96-0.97), and 10.97 (7.53-15.99) vs. 16.40 (10.57-25.46), respectively. The sensitivity of both was increased with the increase of tumor grade and stage. The area under summary receiver operating characteristics curve was 0.834 4 and 0.853 4 and the Q index 0.766 7 and 0.785 3 for ImmunoCyt and cytology, respectively. Combination of both can obviously improve the accuracy of diagnosis. CONCLUSIONS: ImmunoCyt has a high sensitivity in detecting BC, but its specificity is low. As an important adjunct, ImmunoCyt™ can not replace cytology, but combined with cytology it could improve sensitivity with high specificity in the detection and postoperative monitoring of BC.

[Prophylatic antibiotic use in percutaneous nephrolithotomy: a meta-analysis].

OBJECTIVE: To determine whether antibiotic prophylaxis can reduce the risk of postoperative infective complications in patients undergoing percutaneous nephrolithotomy (PCNL) who have sterile preoperative urine. METHODS: MEDLINE, EMBASE, Cochrane Collaboration Reviews, CMCC and CNKI were searched for RCTs comparing antibiotic prophylaxis with placebo (or blank controls) for patients undergoing PCNL with preoperative sterile urine. The search strategy was made according to the Collaborative Review Group search strategy. Data were extracted by 2 reviewers using the designed extraction form. The software RevMan 4.2 was used to review management and data analysis. RESULTS: A total of 9 trails, 1 placebo controlled, 3 non treatment controlled, and 5 active controlled, involving 1018 patients, met the inclusion criteria. Prophylactic antibiotic use in patients at low risk undergoing PCNL significantly decreased fever (RR = 0.71, 95% CI: 0.54-0.92, P = 0.009), bacteriuria (RR = 0.39, 95%CI: 0.23-0.67, P = 0.0006) and bacteremia incidence (RR = 0.43, 95%CI: 0.25-0.73, P = 0.002). Effective antibiotic classes included quinolone which significantly decreased bacteriuria incidence (RR = 0.31, 95%CI: 0.12-0.82, P = 0.010) and nitrofurantoin which significantly decreased fever incidence (RR = 0.38, 95%CI: 0.24-0.61, P = 0.005). Extended course significantly decreased fever incidence (RR = 0.64, 95%CI: 0.47-0.87, P = 0.004) and bacteriuria incidence (RR = 0.35, 95%CI: 0.18-0.71, P = 0.003). CONCLUSIONS: Prophylactic antibiotics can significantly decrease the incidence of postoperative infective complications. A significant decrease in bacteriuria incidence can be achieved with quinolones. Extended course is effective in decreasing fever, and bacteriuria incidence.

[Meta-analysis of fluorescence in situ hybridization and cytology for diagnosis of bladder cancer].

BACKGROUND AND OBJECTIVE: Currently, cystoscopy and urine cytology are standard modalities in therapy monitoring and follow-up of bladder cancer. Cystoscopy is an invasive and uncomfortable procedure while cytology has a limited value because it is operator-dependent and has a low sensitivity. This study was to assess the accuracy of fluorescence in situ hybridization(FISH) in detecting bladder cancer by comparing it with cytology using systemic analyses of studies published in both English and Chinese. METHODS: Cochrane systematic evaluation was used to search through MEDLINE, EMBASE, Cochrane Library, CMCC and CNKI for studies regarding FISH and cytology in the detection of bladder cancer. Data were extracted and analyzed using software MetaDiSc1.4. RESULTS: In total 242 relevant studies were searched, of which 12 studies were enrolled and 3430 patients were included. Heterogeneity, except for threshold effects, was found within these studies. A meta-analysis was performed using the random effect model. Pooled accuracy indicators like sensitivity, specificity, positive likelihood ratio (LR), negative LR and diagnostic odds ratio of FISH and cytology were 74% (71%-77%) vs. 57% (54%-61%), 88 % (86%-90%) vs. 85 % (83%-87%), 6.18 (3.56-10.73) vs. 4.15 (2.78-6.20), 0.29 (0.19-0.45) vs. 0.51(0.41-0.63) and 24.17 (9.33-62.64) vs. 9.59 (5.91-15.57), respectively. The sensitivity of both FISH and cytology were increased with the increase of tumor grade and stage. The areas under summary receiver operating characteristics (SROC) curve were 0.8938 and 0.7847, and the Q indices were 0.8247 and 0.7226 for FISH and cytology, respectively. CONCLUSIONS: FISH has a high accuracy in detecting bladder cancer. But its sensitivity in detecting high-stage bladder cancer is lower than that of cytology. Although FISH can not replace traditional urine cytology, it can be used as an important adjunct in the preoperative detection and postoperative monitoring of bladder cancer.

[Meta-analysis of antibiotic prophylaxis for postoperative bacteriuria in patients undergoing transrectal prostatic biopsy].

OBJECTIVE: To investigate whether antibiotic prophylaxis can reduce the risk of postoperative bacteriuria in patients undergoing transrectal prostatic biopsy (TPB) who have sterile preoperative urine. METHODS: MEDLINE, EMBASE, Cochrane Collaboration Reviews, CMCC, and CNKI were searched for randomized controlled trials (RCTs) comparing antibiotic prophylaxis with placebo/blank controls for patients undergoing TPB with preoperative sterile urine. The search strategy was made according to the Collaborative Review Group search strategy. Data were extracted by two reviewers using the designed extraction form. The software RevMan4.2 was used to review management and data analysis. RESULTS: 67 relevant RCTs were found, of which 12 qualified ones were included into the analysis. Antibiotic prophylaxis significantly decreased the rate of bacteriuria within the period 1 week after TPB (corresponding pooled relative risk (RR) and 95% CI was 0.32 (0.23 - 0.46, P < 0.01). The effective antibiotics included quinolones and quinolones combined with nitroimidazole, with the pooled RR and 95% CI of 0.31 (0.18 - 0.53, P < 0.01) and 0.32 (0.17 - 0.60, P = 0.0004) respectively. There was no significant difference in the effect between short treatment course protocol and long course protocol (P = 0.41). CONCLUSION: Prophylactic antibiotics can significantly decrease the incidence of post-TPB bacteriuria. A significant decrease in bacteriuria incidence can be achieved with a range of antibiotic agents, including quinolones and-quinolones combined with nitroimidazole. Treatment protocols of any duration are effective.

Meta-analysis of antibiotic prophylaxis use in transrectal prostatic biopsy.

OBJECTIVE: To determine whether antibiotic prophylaxis can reduce the risk of postoperative infective complications in men undergoing transrectal prostatic biopsy (TPB) who had sterile preoperative urine. METHODS: MEDLINE, EMBASE, Cochrane Collaboration Reviews, Chinese Medical Current Contents (CMCC), and National Knowledge Infrastructure (CNKI) were searched for randomized controlled trials that compared the effect of antibiotic prophylaxis with placebo or active controls for men undergoing TPB with preoperative sterile urine. Two reviewers independently extracted the data of patient characteristics and outcomes based on a prospectively developed protocol. RESULTS: A total of 12 trials (3 placebo controlled, 3 non-treatment controlled, and 6 actively controlled) involving 1 987 patients, met the inclusion criteria. Prophylactic antibiotic use in patients at low risk undergoing TPB significantly decreased bacteriuria and middle degree fever incidence, but could not decrease the incidence of bacteremia. The relative risk for post-TPB bacteriuria, middle degree fever, and bacteremia were 0.32 (95%CI 0.23 to 0.46), 0.37 (95%CI 0.17 to 0.77), and 0.96 (95%CI 0.61 to 1.50), respectively. Effective antibiotic classes included quinolone, co-quinolone and nitroimidazole, and co-trimethoprim and sulfamethoxazole. Treatment protocols of any duration were effective. CONCLUSION: Antibiotic prophylaxis obviously decreases the incidence of bacteriuria and middle degree fever but not bacteremia in men with preoperative sterile urine undergoing TPB. A significant decrease in bacteriuria incidence can be achieved with a range of antibiotic agents, including quinolones and co-quinolone and nitroimidazole. Treatment protocols of any duration are effective with no heterogeneity.

[Progress in the studies of alpha1-adrenoceptor blocker for concurrent benign prostatic hyperplasia and hypertension].

The epidemiological survey shows that primary hypertension is one of the independent risk factors in the development and the progress of BPH, 25 percent of old male patients aged 60 or more suffer from the two diseases at the same time, which grievously affects their quality of life. There is little literature about the appropriate therapeutic regimen of BPH associated hypertension. The article reviews the progress in the studies of alpha1-adrenoceptor blocker for BPH associated hypertension, and explores the main problems facing us and ventures the prospects for the development in this field.