Addressing an Unmet Need in Postprostatectomy Care: Perspectives on Urovaxom

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Urogenit Tract Infect. 2025;20(2):118-119
Publication date (electronic) : 2025 August 31
doi : https://doi.org/10.14777/uti.2550030015
Department of Urology, Biomedical Research Institute, Pusan National University Hospital, Pusan National University School of Medicine, Busan, Korea
Corresponding author: Byeong Jin Kang Department of Urology, Biomedical Research Institute, Pusan National University Hospital, Pusan National University School of Medicine, 179, Gudeok-ro, Seo-gu, Busan 49241, Korea Email: uropean86@gmail.com, uropean86@pusan.ac.kr
Received 2025 June 30; Revised 2025 August 4; Accepted 2025 August 5.

To the editor,

I read with great interest the study by Kang et al. [1] evaluating the efficacy of Urovaxom in patients experiencing chronic pelvic pain syndrome (CPPS) following radical prostatectomy (RP). The study highlights an important yet underexplored aspect of survivorship in prostate cancer patients.

Despite growing clinical recognition, the pathophysiology of post-RP CPPS remains poorly understood. In the context of RP, pelvic plexus nerve injury, sterile postsurgical inflammation, and altered bladder dynamics have all been implicated in the development of persistent pelvic pain. Psychological stressors related to cancer treatment and survivorship may further contribute to symptom chronicity [2,3]. Animal studies have shown that localized prostatic inflammation can induce sustained pelvic pain and heightened neural innervation, consistent with mechanisms of neuroimmune sensitization [4]. A deeper understanding of these interacting immunologic and neurologic factors is essential for the development of mechanism-based therapies for post-RP CPPS.

In this context, the use of Urovaxom—a bacterial lysate with immunomodulatory properties—represents a promising approach. Its potential to modulate innate and adaptive immune responses may help restore immune balance, reduce neuroinflammation, and alleviate pain and urinary symptoms, as evidenced by significant reductions in National Institutes of Health Chronic Prostatitis Symptom Index, International Prostate Symptom Score, and Overactive Bladder Symptom Score in this study. This is consistent with findings that immune-based interventions can reduce sensory hypersensitivity in CPPS models [1,5,6].

I encourage future investigations to integrate mechanistic endpoints—such as inflammatory cytokine profiles or neuroimaging biomarkers—into randomized controlled trials. Understanding who responds best to agents like Urovaxom may depend on further defining the immune and neurologic subtypes of post-RP CPPS.

In summary, Kang et al. [1] provide an important contribution to a clinically relevant but underexplored field. Their findings may serve as a catalyst for mechanistic and translational studies aimed at personalizing care for post-RP CPPS.

Notes

Conflict of Interest

BJK, a member of the Editorial Board of Urogenital Tract Infection, is the corresponding author of this letter. However, he played no role whatsoever in the editorial evaluation of this article or the decision to publish it. Except for that, the author has nothing to disclose.

References

1. Kang JK, Ha YS, Park S, Kwon TG, Kim TH. Efficacy of Urovaxom for improving chronic pelvic pain syndrome symptoms in prostate cancer patients who underwent radical prostatectomy: a multicenter, prospective cohort study. Urogenit Tract Infect 2025;20:42–7.
2. Pontari M, Ruggieri M. Mechanisms in prostatitis/chronic pelvic pain syndrome. J Urol 2004;172:839–45.
3. Breser M, Salazar F, Rivero V, Motrich R. Immunological mechanisms underlying chronic pelvic pain and prostate inflammation in chronic pelvic pain syndrome. Front Immunol 2017;8:898.
4. Rudick C, Schaeffer A, Thumbikat P. Experimental autoimmune prostatitis induces chronic pelvic pain. Am J Physiol Regul Integr Comp Physiol 2008;294:R1268–75.
5. Chen L, Bian Z, Chen J, Meng J, Zhang M, Liang C. Immunological alterations in patients with chronic prostatitis/chronic pelvic pain syndrome and experimental autoimmune prostatitis model: a systematic review and meta-analysis. Cytokine 2021;141:155440.
6. Motrich RD, Breser ML, Sanchez LR, Godoy GJ, Prinz I, Rivero VE. IL-17 is not essential for inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome. Pain 2016;157:585–97.

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