Benign prostatic hyperplasia (BPH) is a common age-related condition characterized by stromal and epithelial proliferation within the prostate and is influenced by androgen signaling, ageing, obesity, metabolic dysfunction, and inflammation. Increasing interest has focused on whether the gut microbiota may contribute to these processes through a putative gut-prostate axis. The human gut contains a complex microbial ecosystem comprising thousands of bacterial species whose metabolites and immune-modulatory activities influence host physiology. Alterations in microbial composition and function have been associated with numerous chronic inflammatory and metabolic disorders. Emerging clinical and preclinical evidence suggests that gut dysbiosis may also be associated with prostate enlargement and lower urinary tract symptoms. Proposed mechanisms include altered production of short-chain fatty acids, impaired intestinal barrier integrity with increased lipopolysaccharide translocation, Toll-like receptor signaling, changes in tryptophan and serotonin metabolism, vagal pathways, and systemic cytokine-mediated inflammation. However, current evidence remains largely associative and mechanistic, with relatively few human studies directly linking alterations in the gut microbiota to BPH pathogenesis. This narrative review examines current evidence supporting the gut-prostate axis in BPH, evaluates potential biological mechanisms such as the vagus nerve and tryptophan, discusses dietary influences on microbiota composition, and highlights limitations in the existing literature together with priorities for future research and therapeutic development.

Recurrent urinary tract infections (rUTIs) represent one of the most common infectious conditions worldwide, yet their pathophysiology extends far beyond repeated episodes of acute bacterial cystitis. Increasing evidence indicates that recurrence may arise through overlapping mechanisms including reinfection from intestinal or periurethral reservoirs, intracellular bacterial persistence, microbial dysbiosis, impaired mucosal immunity and chronic inflammatory remodelling of the bladder microenvironment. Current diagnostic frameworks remain largely based on symptom-based definitions and standard urine culture, approaches that incompletely capture the biological complexity of recurrent disease. This limitation is evident even at the definitional level, where clinically pragmatic categories often fail to reflect the heterogeneous mechanisms underlying recurrence. Advances in expanded urine culture techniques, metagenomics and metabolomics have reshaped the understanding of the urinary tract as a dynamic ecological system interconnected with vaginal, intestinal and prostatic microbial compartments. These approaches have identified diverse microbial communities, virulence-associated functional profiles and host-microbe interactions linked to recurrence-prone phenotypes. Significant challenges continue to persist in elucidating the biological mechanisms driving recurrence. Addressing these gaps is essential to improve disease characterization and support the development of more effective diagnostic and therapeutic approaches.

Chronic non-bacterial prostatitis (CNP), a prevalent and debilitating urological disorder affecting 8.4% of men aged 15-60 years, presents significant clinical challenges due to the paucity of targeted therapies and poor patient adherence. To address this unmet medical need, we developed an innovative multifunctional nanoplatform (QM (Zn) NPs) by integrating Ti3C2 MXene with a quercetin-zinc coordination complex (Que-Zn) for precision CNP therapy. This system leverages chondroitin sulfate (Chs)-mediated CD44 targeting to achieve selective accumulation in inflamed prostate tissue, thereby enhancing Zn[2+] bioavailability while enabling co-delivery of MXene and Que-Zn therapeutic payloads. Upon localization, QM (Zn) NPs orchestrate a coordinated therapeutic cascade: MXene scavenges reactive oxygen species (ROS) via electron-deficient sites, while Que-Zn drives M1-to-M2 macrophage repolarization and facilitates Zn[2+] cellular uptake. The accumulated intracellular Zn[2+] critically upregulates metallothionein 1 (Mt1), activating the IKK/NF-κB/IκB axis to resolve inflammation and oxidative damage. Transcriptomic analysis unequivocally identified Mt1 as the pivotal mediator of Zn[2+]-driven microenvironment reprogramming. Notably, QM (Zn) NPs not only significantly alleviated pelvic pain by mitigating neuronal oxidative stress but also exhibited excellent biocompatibility. This work pioneers a targeted nano-theranostic strategy that synergistically restores zinc homeostasis, quenches ROS, and reprograms immune responses, thereby establishing a transformative paradigm for CNP management.

Pancreatic calcification is a hallmark structural change of chronic pancreatitis. However, few reports have described extensive diffuse pancreatic calcification that develops within a relatively short period after acute pancreatitis and is incidentally detected during urological evaluations. We report the case of a 34-year-old man who presented with urinary frequency, gross hematuria, and the passage of sand-like material in his urine. He had smoked five cigarettes per day and consumed alcohol on approximately 10 occasions per month since the age of 29 years, when abnormal liver function was noted on routine tests, and he developed acute pancreatitis at the age of 31 years. Computed tomography (CT) and magnetic resonance cholangiopancreatography performed at that time revealed no pancreatic calcifications. At the current presentation, he was diagnosed with acute bacterial prostatitis, and a urine culture yielded Escherichia coli. A kidneys, ureters, and bladder (KUB) radiograph performed to evaluate suspected urolithiasis incidentally revealed multiple calcified densities in the pancreatic region. Moreover, noncontrast CT demonstrated extensive diffuse calcifications involving the entire pancreas, with mild pancreatic enlargement. Serum calcium, IgG4, intact parathyroid hormone, and HbA1c levels were within the normal ranges, suggesting that alcohol consumption and smoking were the most likely etiological factors. This case suggests that extensive calcific chronic pancreatitis can develop within a relatively short period following acute pancreatitis. Clinicians evaluating KUB radiographs and CTs performed for urological indications should systematically check for clinically significant incidental findings outside the urinary tract.

In recent years we have witnessed increasing interest for the role of microbiota in the pathophysiology and management of prostatic diseases. However, there are several aspects to comprehend. Here, we aim to assess the gut microbiota composition and faecal microbiota-derived short-chain fatty acids production (SCFAs) in the pathogenesis of CP/CPPS. All patients with CP/CPPS attending our urology centre, were enrolled in this study, and underwent urological examination, microbiological evaluation, intestinal microbiota analysis and measurement of interleukins in semen. A cohort of subjects who had undergone intestinal microbiota investigation for various reasons but did not exhibit any symptoms of urological disease, was used as control group. Laboratory data from the two groups were analysed in terms of gut microbiota composition and levels of SCFAs. We enrolled 37 patients and 45 controls. In the CP/CPPS patient group, the mean levels of interleukins were: IL-8 934 pg/ml, IL-10 64 pg/ml, IL-6 871 pg/ml. In this patient group, we found higher levels of Bifidobacteriaceae and Bacteroidaceae and lower levels of Prevotella and Lactobacillus with a Firmicutes/Bacteroides mean ratio at 0.27. The control group had a normal Firmicutes/Bacteroides mean ratio (1.6). The two groups showed a significant difference in total SCFAs levels (p = 0.001) and in particular regarding indole-3-propionic acid (p = 0.003) and butyric acid (p < 0.001). A statistically significant correlation was found between the levels of IL-8 and a decreasing SCFAs production (p < 0.001). A difference in gut microbiota between patients with CP/CPPS and controls, together with a reduction in faecal levels of microbiota-derived short-chain fatty acids and decreased IL-8 levels in semen, might be part of the pathophysiological mechanism in CP/CPPS.

Prostatic calculi are frequently detected on transrectal ultrasound (TRUS) and computed tomography (CT), yet their clinical relevance in prostatitis remains uncertain. To systematically evaluate the association between prostatic calculi and prostatitis-related outcomes in adult men. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses-compliant systematic review was conducted. PubMed, Ovid Embase, CINAHL, and Google Scholar were searched for studies published between January 1, 2015 and October 31, 2025. Eligible studies assessed prostatic calculi by presence, burden, location, or density and compared outcomes with men without calculi or with lower burden. Outcomes included prostatitis diagnoses, validated symptom measures (National Institutes of Health-chronic prostatitis symptom index [NIH-CPSI], International Prostate Symptom Score [IPSS], International Index of Erectile Function - 5), inflammatory markers, and treatment response. Risk of bias was assessed using the Critical Appraisal Skills Programme tool. A total of 198 records were identified, of which 10 studies were included. Most were cross-sectional, with one prospective CP/chronic pelvic pain syndrome cohort. Greater calcification burden and peri-urethral distribution were associated with higher NIH-CPSI and IPSS scores and less favorable symptom improvement following medical therapy. CT-based cohorts reported associations between higher-density calculi and worse lower urinary tract symptoms, erectile dysfunction, pelvic pain, and reduced quality of life. A prostatectomy series demonstrated bacterial biofilm within calcifications, providing biological plausibility. Prostatic calculi - particularly when extensive or peri-urethral - are associated with increased symptom burden and may identify men with more refractory disease. However, current evidence is observational and heterogeneous, with incomplete confounder control. Standardized imaging classifications and prospective studies are required to clarify causal relationships and inform management strategies.

Acute and chronic bacterial prostatitis are clinically significant entities that can be difficult to diagnose and appropriately treat. Herein, we review when to suspect these clinical conditions, how to diagnose them, and how to effectively treat them based on the extant literature. Our aim was to equip the practicing clinician with the ability to proficiently diagnose and manage acute and chronic bacterial prostatitis, particularly in older patients.

Purple urine bag syndrome (PUBS) is an infrequent and generally asymptomatic condition characterized by the purple coloration of urine in patients with a urinary catheter, secondary to bacterial metabolism of tryptophan and the production of pigments. We describe the case of an 82-year-old male with a history of benign prostatic hyperplasia, arterial hypertension, and chronic Foley catheter use, who presented for a preoperative consultation without symptoms, exhibiting purple urine of 48 hours' duration. The urine culture showed growth of extended-spectrum beta-lactamase-producing Klebsiella pneumoniae. Given the absence of urinary or systemic symptoms, it was decided not to administer antibiotics and to only replace the urinary drainage system. The patient progressed favorably, with resolution of the color change. PUBS, although striking, is a benign finding associated with asymptomatic bacteriuria, and its management should avoid unnecessary antibiotic use.

Prostatitis is an inflammatory disease of the prostate gland that can present with lower abdominal pain, urinary incontinence, and sexual dysfunction. The diagnosis of prostatitis encompasses two main conditions: acute bacterial prostatitis (ABP) and chronic bacterial prostatitis (CBP). Urinary dysfunction is a key factor in the pathogenesis of chronic prostatitis. Overactive contraction of the urinary sphincter can cause bladder outlet obstruction and residual urine, which can lead to urinary reflux into the prostate. Alpha-1-adrenergic receptor antagonists (alpha blockers) are a class of drugs that inhibit smooth muscle contraction in the prostate and bladder neck. Tamsulosin is the first selective 1-adrenergic receptor antagonist, primarily the 1A and 1D subtypes, which are found in the smooth muscle of the prostate, bladder neck, and prostatic urethra. Blockade of these receptors reduces smooth muscle tone in these structures, which, in turn, improves urine flow from the bladder. We carried out a systematic review of the literature to evaluate the efficacy of tamsulosin in the treatment of acute and chronic bacterial and abacterial prostatitis, as well as chronic pelvic pain syndrome (CPPS). A search for clinical trials was carried out in the PubMed database, the clinical trials registry clinicaltrials.gov, and the Russian electronic library elibrary.ru by two independent researchers using keywords describing treatments that potentially included tamsulosin. The search yielded information on 21 publications, 20 of which were included in the systematic review. Five studies were non-comparative, meaning they analyzed only patients receiving tamsulosin in addition to background therapy. The remaining studies had different comparison groups and could include active strategies such as antibacterial, analgesic, anti-inflammatory, herbal (urological) medications, and others. Treatment duration ranged from 4 to 52 weeks. The prescribed dose of tamsulosin was 0.4 mg orally once daily. Most studies used the NIH-CPSI (National Institute of Health Chronic Prostatitis Symptom Index) scores to evaluate outcomes. The average age of the participants ranged from 28.9 to 59.1 years. The quality of the included studies was highly variable. Of the 20 studies included in this review, 19 examined the use of tamsulosin in patients with CP/CPPS. Positive treatment outcomes were observed in all studies using tamsulosin. Increases in maximum urinary flow rate, significant symptom regression, as measured by standardized scales, and improvements in quality of life were observed. The greatest differences in symptom regression were observed early in treatment, up to 45 days. This is likely due to the fact that urinary dysfunction, pain, and decreased quality of life become more prominent early in the disease course. The safety of the treatment was assessed in 15 of the 20 studies. No standardized scales were used to assess safety. The safety of tamsulosin was assessed based on the reporting of adverse reactions. The development of serious adverse reactions (defined in Roszdravnadzor Order No. 1071 of February 15, 2017) was reported in two studies, but it was not possible to reliably link them to tamsulosin use. CONCLUSION: The results of this systematic review confirm that tamsulosin is an effective drug for inclusion in combination treatment regimens for various forms of prostatitis, including CBP, chronic abacterial prostatitis, and CPPS. Its use significantly reduces symptoms such as pain and dysuria, which in turn improves patients' quality of life.