Nonablative transurethral Erbium:YAG laser treatment for chronic prostatitis/chronic pelvic pain syndrome: A prospective comparative study.

AIMS: This prospective study aimed to compare the clinical outcomes between the use of Erbium:YAG (Er:YAG) laser in a nonablative mode, to the use of the pharmacological treatment of oral tadalafil for the treatment of chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). METHODS: The laser group received two sessions of Erbium:YAG laser, administered intraurethrally in a long, nonablative train of long pulses (SMOOTH™ mode), applied at the level of the male prostatic urethra. Tadalafil group received oral tadalafil at a dose of 5 mg/day, consecutively for 2 months. Effectiveness was assessed using the International Prostate Symptom Score (IPSS) questionnaire, VAS (visual analogue scale) pain score, and maximum urethral flow at follow-up visits up to 12 months after initiating treatment. Adverse effects were recorded after each treatment and follow-up sessions. RESULTS: The results show a significant decrease in the IPSS score in both groups up to the 12-month follow-up. The increase in Q-max was evident up to 3-months follow-up in the tadalafil group and up to 6 months in the laser group. The decrease in the VAS pain score was also significant in both treatment groups, lasting up to 3 months in the tadalafil group and up to 6 months in the laser group. CONCLUSIONS: The nonablative Er:YAG SMOOTH™ laser seems to be a promising treatment for this widely occurring condition. More studies are needed to confirm its safety and efficacy.

Prostatitis crónica: Aporte del contraste endovenoso en fase tardía para su caracterización en resonancia magnética multiparamétrica de próstata / Chronic Prostatitis: Contrast Contribution in Late Phase for its Characterization in Multiparametric-Magnetic Resonance Imaging of the Prostate

Resumen Objetivo: El objetivo de este estudio es demostrar la utilidad de una secuencia tardía post-contraste en la resonancia magnética multiparamétrica de próstata (RMMP) para caracterizar lesiones PI-RADS II. Materiales y métodos: Se analizaron en forma retrospectiva las RMMP realizadas entre enero de 2015 y diciembre de 2016. El protocolo de la RMMP fue basado en las recomendaciones del PI-RADS versión 2, y se agregó una adquisición tardía luego del dinámico post-contraste. Los reportes fueron revisados bajo la versión 2.1. Resultados: Se seleccionaron 31 pacientes que presentaron lesiones categorizadas como PI-RADS II en la zona periférica, los cuales se encontraban en seguimiento del antígeno prostático específico y presentaron confirmación histológica de prostatitis crónica. Se evidenció un realce tardío de la lesión en todos los pacientes. Según los resultados histopatológicos, 30 presentaban prostatitis crónica y el restante tejido benigno (tejido fibromuscular). Discusión: La prostatitis crónica no muestra realce temprano, y presenta realce tardío debido al tejido conectivo fibroso que la compone. En la RMMP, la prostatitis puede imitar el cáncer de próstata. Agregar una adquisición tardía solo adiciona 150 segundos al estudio y podría ayudar a resolver aquellos casos inciertos categorizados como PI-RADS III empleando las secuencias convencionales, debido a que el realce tardío de la lesión es altamente sugestivo de un proceso inflamatorio (PI-RADS II). Conclusión: La presencia de realce tardío es una herramienta útil para realizar un adecuado diagnóstico de una lesión PI-RADS II en la zona periférica, pudiendo evitar una biopsia innecesaria.

Abstract Objective: The aim of this study is to demonstrate the utility of a post-contrast late sequence in multiparametric magnetic resonance imaging (RMMP) to characterize PI-RADS II lesions. Materials and methods: The RMMPs performed between January 2015 and December 2016 were retrospectively analyzed. The RMMP protocol was based on the recommendations of the PI-RADS version 2, and a late acquisition was added, after the dynamic post-contrast. The reports were reviewed under the version 2.1. Results: 31 patients with PI-RADS II lesions in the peripheral zone were selected, who were in prostate specific antigen follow-up and had histological confirmation of chronic prostatitis. A late enhancement of the lesion was evidenced in all patients. According to the histopathological results, 30 had chronic prostatitis and the remaining benign tissue (fibromuscular tissue). Discussion: Chronic prostatitis does not show early enhancement, and presents late enhancement due to its fibrous connective tissue. In RMMP, prostatitis may mimic prostate cancer. Adding a late sequence only adds 150 seconds to the study and could help to resolve those uncertain cases categorized as PI-RADS III using traditional sequences because the late enhancement of the lesion is highly suggestive of an inflammatory process (PI-RADS II). Conclusion: The presence of late enhancement is a useful tool to perform an adequate diagnosis of a PI-RADS II lesion in the peripheral zone, helping to avoid an unnecessary biopsy.

Chronic prostatitis alters the prostatic microenvironment and accelerates preneoplastic lesions in C57BL/6 mice.

BACKGROUND: Chronic prostatitis has been supposed to be associated with preneoplastic lesions and cancer development. The objective of this study was to examine how chronic inflammation results in a prostatic microenvironment and gene mutation in C57BL/6 mice. METHODS: Immune and bacterial prostatitis mouse models were created through abdominal subcutaneous injection of rat prostate extract protein immunization (EAP group) or transurethral instillation of uropathogenic E. coli 1677 (E. coli group). Prostate histology, serum cytokine level, and genome-wide exome (GWE) sequences were examined 1, 3, and 6 months after immunization or injection. RESULT: In the EAP and E. coli groups, immune cell infiltrations were observed in the first and last months of the entire experiment. After 3 months, obvious proliferative inflammatory atrophy (PIA) and prostatic intraepithelial neoplasia (PIN) were observed accompanied with fibrosis hyperplasia in stroma. The decrease in basal cells (Cytokeratin (CK) 5+/p63+) and the accumulation of luminal epithelial cells (CK8+) in the PIA or PIN area indicated that the basal cells were damaged or transformed into different luminal cells. Hic1, Zfp148, and Mfge8 gene mutations were detected in chronic prostatitis somatic cells. CONCLUSION: Chronic prostatitis induced by prostate extract protein immunization or E. coli infection caused a reactive prostatic inflammation microenvironment and resulted in tissue damage, aberrant atrophy, hyperplasia, and somatic genome mutation.

Chronic prostatitis alters the prostatic microenvironment and accelerates preneoplastic lesions in C57BL/6 mice

BACKGROUND: Chronic prostatitis has been supposed to be associated with preneoplastic lesions and cancer development. The objective of this study was to examine how chronic inflammation results in a prostatic microenvironment and gene mutation in C57BL/6 mice. METHODS: Immune and bacterial prostatitis mouse models were created through abdominal subcutaneous injection of rat prostate extract protein immunization (EAP group) or transurethral instillation of uropathogenic E. coli 1677 (E. coli group). Prostate histology, serum cytokine level, and genome-wide exome (GWE) sequences were examined 1, 3, and 6 months after immunization or injection. RESULT: In the EAP and E. coli groups, immune cell infiltrations were observed in the first and last months of the entire experiment. After 3 months, obvious proliferative inflammatory atrophy (PIA) and prostatic intraepithelial neoplasia (PIN) were observed accompanied with fibrosis hyperplasia in stroma. The decrease in basal cells (Cytokeratin (CK) 5+/p63+) and the accumulation of luminal epithelial cells (CK8+) in the PIA or PIN area indicated that the basal cells were damaged or transformed into different luminal cells. Hic1, Zfp148, and Mfge8 gene mutations were detected in chronic prostatitis somatic cells. CONCLUSION: Chronic prostatitis induced by prostate extract protein immunization or E. coli infection caused a reactive prostatic inflammation microenvironment and resulted in tissue damage, aberrant atrophy, hyperplasia, and somatic genome mutation.

Immunological Mechanisms Underlying Chronic Pelvic Pain and Prostate Inflammation in Chronic Pelvic Pain Syndrome.

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is the most common urologic morbidity in men younger than 50 years and is characterized by a diverse range of pain and inflammatory symptoms, both in type and severity, that involve the region of the pelvis, perineum, scrotum, rectum, testes, penis, and lower back. In most patients, pain is accompanied by inflammation in the absence of an invading infectious agent. Since CP/CPPS etiology is still not well established, available therapeutic options for patients are far from satisfactory for either physicians or patients. During the past two decades, chronic inflammation has been deeply explored as the cause of CP/CPPS. In this review article, we summarize the current knowledge regarding immunological mechanisms underlying chronic pelvic pain and prostate inflammation in CP/CPPS. Cumulative evidence obtained from both human disease and animal models indicate that several factors may trigger chronic inflammation in the form of autoimmunity against prostate, fostering chronic prostate recruitment of Th1 cells, and different other leukocytes, including mast cells, which might be the main actors in the consequent development of chronic pelvic pain. Thus, the local inflammatory milieu and the secretion of inflammatory mediators may induce neural sensitization leading to chronic pelvic pain development. Although scientific advances are encouraging, additional studies are urgently needed to establish the relationship between prostatitis development, mast cell recruitment to the prostate, and the precise mechanisms by which they would induce pelvic pain.

Transcutaneous electrical nerve stimulation (TENS) in the symptomatic management of chronic prostatitis/chronic pelvic pain syndrome: a placebo-control randomized trial

OBJECTIVE: The aim of the study was to investigate the therapeutic efficacy of transcutaneous electrical nerve stimulation (TENS) in the symptomatic management of chronic prostatitis pain/chronic pelvic pain syndrome. DESIGN: A pretest, posttest randomized double blind design was used in data collection. PARTICIPANT: Twenty-four patients diagnosed with chronic prostatitis- category IIIA and IIIB of the National Institute of Health Chronic Pain (NIH-CP) were referred for physiotherapy from the Urology department. Intervention: Pre treatment pain level was assessed using the NIH-CP (pain domain) index. The TENS group received TENS treatment, 5 times per week for a period of 4 weeks (mean treatment frequency, intensity, pulse width and duration of 60Hz, 100µS, 25mA and 20 minutes respectively). The Analgesic group received no TENS treatment but continued analgesics; the Control group received no TENS and Analgesic but placebo. All subjects were placed on antibiotics throughout the treatment period. Outcome measures: Post-treatment pain level was also assessed using NIH-CP pain index. RESULT: Findings of the study revealed significant effect of TENS on chronic prostatitis pain at p < 0.05. CONCLUSION: TENS is an effective means of non-invasive symptomatic management of chronic prostatitis pain.