The data was presented as the mean

The data was presented as the mean (standard deviation) for continuous variables, and the frequency and percentage for ordinal and nominal variables. Continuous and categorical variables were assessed using t test and Chi-square test, respectively. A p value < 0.05 was considered statistically significant. All data were analyzed using SPSS version 20 (IBM, Armonk, NY, USA).
A total of 92 patients met the inclusion and exclusion criteria and were included in the study. Eight patients were lost to follow-up and did not attend for repeat PSA testing or TRUSBP and were excluded from the study. The mean age±standard deviation of the study population was 66.8 ± 6.9 years. Prostate cancer was detected in 37 patients. A comparison between Group 1 and Group 2 patients is presented in Table 1. Group 1 included 44 patients, while Group 2 included 42 patients. PCa was detected in 50% and 35.7% of Group 1 and Group 2 patients, respectively (p = 0.52). A drop in PSA level was detected in 27 (61%) patients and 21 (50%) patients of Group 1 and Group 2, respectively (p = 0.23). No statistically significant differences in histopathology results were detected between patients with and without a drop in PSA (Figure 1).
Group 1 patients had a statistically significant Δ PSA between PCa (+PCa) and non-PCa (–PCa) patients, –1.02 ± 2.9 and 1.03 ± 2.4, respectively (p = 0.008). No statistically significant Δ PSA was noted in Group 2 patients (p = 0.77; Table 2). A correlation between Δ PSA and Gleason score of PCa patients in both groups is presented in Table 3. No statistically significant Δ PSA in relation to Gleason score was found between both groups (p = 0.17).

Serum PSA is a nonspecific marker that can be elevated in noncancerous conditions. This prospective randomized study explores the common use of empiric antibiotic therapy for elevated PSA prior to TRUSBP and for the first time correlates prostate biopsy results, specifically Gleason score, to antibiotic use and the degree of change in PSA. Overall, empiric therapy with ciprofloxacin was not associated with statistically significant difference in mean Δ PSA before and after treatment. Paradoxically patients with PCa who received order Rimonabant had a significant reduction in their PSA level before biopsy (Δ PSA = −1.02 ± 2.9, p = 0.008).
An understanding of the motives behind the empiric use of antibiotics for high PSA is of great importance. Many urologists tend to use this management strategy principally because of the presence of numerous studies linking inflammation in the prostate to increased PSA levels. The extent of disruption of epithelial integrity caused by inflammatory infiltrate is the main etiology behind this observation. Subclinical prostatitis was detected in up to 40% of patients with an elevated PSA in one study. Carver et al also reported 32% chronic prostatitis National Institute of Health type-4 cases in a randomly chosen group of 300 men. However, while antibiotics might be useful in bacterial prostatitis, almost all cases of asymptomatic prostatitis (National Institute of Health Category 4) are not caused by bacteria, thereby not requiring treatment. Additionally, other studies failed to find a correlation between PSA and prostate inflammation, depicting prostate volume rather than inflammation as a major confounding factor causing PSA elevation.
Another reason that might support the use of antibiotics is to avoid unnecessary prostate biopsy. TRUSPB is the gold standard procedure for PCa diagnosis. It is indicated in the context of serum PSA elevation with or without abnormal DRE. Although this procedure is irreplaceable, it is still associated with various unavoidable complications such as sepsis, hematuria, and rectal bleeding. Fever and sepsis are perhaps the most influential causes of postbiopsy morbidity and the most common reason for hospitalization after TRUSBP. Severe infections were initially reported in < 1% of cases, but have increased as a consequence of antibiotic resistance. In a study of 455 patients undergoing TRUSBP, Al Rumaihi et al reported the occurrence of postbiopsy fever in 5.9% of cases. An obvious increase in the overall risk of postbiopsy infection has been noticed over the past decade. The principle reason for this observation is the unjustified use of antibiotics. An increasing rate of quinolone resistance is present as a dramatic 22% of men were found to have quinolone-resistant flora on prebiopsy rectal swabs. In a study by Song et al, extended spectrum of beta lactase producing Escherichia coli were isolated from blood samples of 95.9% of patients with postbiopsy infections. All these reasons support against the use of empiric antibiotics for high PSA, as such an act may increase the risk of postbiopsy infection with resistant organisms.