Prostate is an immune-competent organ normally populated by inflammatory cells. Prostatic inflammation origin can be multi-factorial and there are some emerging evidences on its possible role as a factor involved in prostate cancer (PC) pathogenesis and progression.This review critically analyzes the role of inflammation as a prognostic factor for progression and aggressiveness of PC. We verified the last 10 years literature data on the association between inflammation and PC aggressiveness, or PC response to therapies.Several studies tried to correlate different inflammatory factors with the aggressiveness and metastatization of PC; all data sustain the role of inflammation in PC progression but they also produce confusion to identify a reliable clinical prognostic marker.Data on patients submitted to radical prostatectomy (RP) showed that cases with marked intraprostatic tissue inflammation are associated with higher rate of biochemical progression; systemic inflammation markers appear to have a significant prognostic value.Analyzing data on patients submitted to radiotherapy (RT) emerges a significant association between high neuthrophil to lymphocyte ratio (NLR) and decreased progression free survival and overall survival; also plateled to lymphocyte ratio (PLR) and C-reactive protein (CRP) have been proposed as significant prognostic factors for progression and overall survival.In patients submitted to androgen deprivation therapy (ADT), inflammation may drive castration resistant PC (CRPC) development by activation of STAT3 in PC cells. NLR has been proposed as independent predictor of overall survival in CRPC submitted to chemotherapy.Most of data are focused on markers related to systemic inflammation such as NLR and CRP, more than specifically to chronic prostatic inflammation. The suggestion is that these inflammatory parameters, also if not specific for prostatic inflammation and possibly influenced by several factors other than PC, can integrate with established prognostic factors.
Our aim was to systematically evaluate the benefits of degarelix as antagonist versus agonists of gonadotropin-releasing hormones (GnRH) for the treatment of advanced prostate cancer (PC). This comparison was performed either in terms of biochemical or oncological or safety profiles. To this end we, carried out a systematic review and meta-analysis of the literature.We selected only studies directly and prospectively analyzing the two treatments in the same population (randomized phase III studies). We followed the Preferred Reporting Items for Systematic Reviews and meta-analyses process for reporting studies.After we eliminated studies according to the exclusion criteria, 9 publications were considered relevant to this review. These articles described 5 clinical trials that were eligible for inclusion. The follow-up duration in all trials did not exceed 364 days. This meta-analysis and review comprised a total of 1719 men, 1061 randomized to degarelix versus 658 to GnRH agonists treatment for advanced PC. Oncological results were evaluated only in 1 trial (CS21:408 cases) and they were not the primary endpoints of the study. Treatment emerging adverse events were reported in 61.4% and 58.8% of patients in the degarelix and GnRH agonists group, respectively (odds ratio, OR = 1.17; 95% confidence interval, 95% CI: 0.78–1.77, P > 0.1). Treatment related severe cardiovascular side effects were reported (trial CS21-30-35) in 1.6% and 3.6% of patients in the degarelix and GnRH agonists group, respectively (OR = 0.55, 95% CI: 0.26–1.14, P > 0.1).Our analysis evidences relevant limitations in particular for the comparative evaluation of the efficacy and the oncological results related to degarelix.
Background Chronic kidney disease (CKD) is a highly prevalent condition. Urologic disorders are known causes of CKD, but often remain undiagnosed and underestimated also for their insidious onset and slow progression. We aimed to evaluate the prevalence of urological unrecognized diseases in CKD patients by uroflowmetry. Methods We enrolled consecutive stable CKD outpatients. The patients carried out two questionnaires, the International Prostate Symptom Score and Incontinence Questionnaire-Short Form, and they also underwent uroflowmetry, evaluating max flow rate ( Q max ), voiding time and voided volume values. Results A total of 83 patients (43 males, mean age of 59.8 ± 13.3 years) were enrolled. Our study showed 28 males and 10 females with a significant reduction of Q max (P < 0.001) while 21 females reported a significant increase of Q max (P < 0.001) with a prevalence of 49.5% of functional urological disease. Moreover, we showed a significant association between Q max and creatinine (P = 0.013), estimated glomerular filtration rate (P = 0.029) and voiding volume (P = 0.05). We have not shown significant associations with age (P = 0.215), body mass index (P = 0.793), systolic blood pressure (P = 0.642) or diastolic blood pressure (P = 0.305). Moreover, Pearson’s chi-squared test showed a significant association between Q max altered with CKD (χ 2 = 1.885, P = 0.170) and recurrent infection (χ 2 = 8.886, P = 0.012), while we have not shown an association with proteinuria (χ 2 = 0.484, P = 0.785), diabetes (χ 2 = 0.334, P = 0.563) or hypertension (χ 2 = 1.885, P = 0.170). Conclusions We showed an elevated prevalence of urological diseases in nephropathic patients; therefore, we suggest to include uroflowmetry in CKD patient assessment, considering the non-invasiveness, repeatability and low cost of examination. Uroflowmetry could be used to identify previously unrecognized urological diseases, which may prevent the onset of CKD or progression to end-stage renal disease and reduce the costs of management.
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