The influence of asymptomatic inflammatory prostatitis on the onset and progression of lower urinary tract symptoms in men with histologic benign prostatic hyperplasia
Rikiya Taoka, Yoshiyuki Kakehi
Department of Urology, Faculty of Medicine, Kagawa University, Takamatsu, Kagawa, Japan
The influence of asymptomatic inflammatory prostatitis on the onset and progression of lower urinary tract symptoms in men with histologic benign prostatic hyperplasia
Rikiya Taoka, Yoshiyuki Kakehi
Department of Urology, Faculty of Medicine, Kagawa University, Takamatsu, Kagawa, Japan
摘要 Benign prostatic hyperplasia (BPH) is a condition that greatly affects the quality of life of middle-aged and elderly men. Histopathologically, hyperplastic changes frequently occur in the prostate tissue of elderly men, the incidence of which has been reported to reach approximately 80% in men in their 70s. In clinical practice, approximately 25% of men with histologic BPH are assumed to experience lower urinary tract symptoms (LUTS) and receive some kind of treatment. In other words, there are some men with histologic BPH who do not exhibit LUTS. For that reason, many factors, such as the change in hormonal environment, the immune or autoimmune response, the alteration of gene expression, and so on, are thought to affect the onset and progression of LUTS in men with histologic BPH. One such factor that has long drawn attention is the presence of asymptomatic histological inflammation, which very often accompanies symptomatic BPH. Recent studies have suggested that asymptomatic histological inflammation causes repeated destruction, healing, and regeneration of the prostate tissue, leading to the enlargement of prostatic nodules, while at the same time causing stromal tissuepredominant remodeling of the prostate tissue, which can increase urination resistance and result in the condition changing from asymptomatic BPH to symptomatic BPH. In future, the biomolecular clarification of the significance of asymptomatic histological inflammation in the prostate tissue could help develop new treatment strategies for BPH accompanied by LUTS.
Abstract: Benign prostatic hyperplasia (BPH) is a condition that greatly affects the quality of life of middle-aged and elderly men. Histopathologically, hyperplastic changes frequently occur in the prostate tissue of elderly men, the incidence of which has been reported to reach approximately 80% in men in their 70s. In clinical practice, approximately 25% of men with histologic BPH are assumed to experience lower urinary tract symptoms (LUTS) and receive some kind of treatment. In other words, there are some men with histologic BPH who do not exhibit LUTS. For that reason, many factors, such as the change in hormonal environment, the immune or autoimmune response, the alteration of gene expression, and so on, are thought to affect the onset and progression of LUTS in men with histologic BPH. One such factor that has long drawn attention is the presence of asymptomatic histological inflammation, which very often accompanies symptomatic BPH. Recent studies have suggested that asymptomatic histological inflammation causes repeated destruction, healing, and regeneration of the prostate tissue, leading to the enlargement of prostatic nodules, while at the same time causing stromal tissuepredominant remodeling of the prostate tissue, which can increase urination resistance and result in the condition changing from asymptomatic BPH to symptomatic BPH. In future, the biomolecular clarification of the significance of asymptomatic histological inflammation in the prostate tissue could help develop new treatment strategies for BPH accompanied by LUTS.
Rikiya Taoka, Yoshiyuki Kakehi. The influence of asymptomatic inflammatory prostatitis on the onset and progression of lower urinary tract symptoms in men with histologic benign prostatic hyperplasia[J]. Asian Journal of Urology, 2017, 4(3): 158-163.
Rikiya Taoka, Yoshiyuki Kakehi. The influence of asymptomatic inflammatory prostatitis on the onset and progression of lower urinary tract symptoms in men with histologic benign prostatic hyperplasia. Asian Journal of Urology, 2017, 4(3): 158-163.
[1] Berry SJ, Coffey DS, Walsh PC, Ewing LL. The development of human benign prostatic hyperplasia with age. J Urol 2015;132:474-9. [2] Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA. Campbell-Walsh urology. 10th ed, vol. 3. Elsevier; 2011. p. 2585. [3] Roehrborn CG. Pathology of benign prostatic hyperplasia. Int J Impot Res 2008;(Suppl. 3):S11-8. [4] Oesterling JE. Benign prostatic hyperplasia:a review of its histogenesis and natural history. Prostate 1996;(Suppl. 6):67-73. [5] Taoka R, Tsukuda F, Ishikawa M, Haba R, Kakehi Y. Association of prostatic inflammation with down-regulation of macrophage inhibitory cytokine-1 gene in symptomatic benign prostatic hyperplasia. J Urol 2004;171:2330-5. [6] Collins MM, Meigs JB, Barry MJ, Walker CE, Giovannucci E, Kawachi I. Prevalence and correlates of prostatitis in the health professionals follow-up study cohort. J Urol 2002;167:1363-6. [7] Nickel JC, Elhilali M, Vallancien G. Benign prostatic hyperplasia (BPH) and prostatitis:prevalence of painful ejaculation in men with clinical BPH. BJU Int 2005;95:571-4. [8] Pontari MA. Chronic prostatitis/chronic pelvic pain syndrome in elderly men:toward better understanding and treatment. Drugs Aging 2003;20:1111-25. [9] Krieger JN, Nyberg Jr L, Nickel JC. NIH consensus definition and classification of prostatitis. JAMA 1999;282:236-7. [10] Crawford ED, Wilson SS, McConnell JD, Slawin KM, Lieber MC, Smith JA, et al. Baseline factors as predictors of clinical progression of benign prostatic hyperplasia in men treated with placebo. J Urol 2006;175:1422-6. [11] Nickel JC, Roehrborn CG, O'leary MP, Bostwick DG, Somerville MC, Rittmaster RS. Examination of the relationship between symptoms of prostatitis and histological inflammation:baseline data from the REDUCE chemoprevention trial. J Urol 2007;178:896-900. [12] Nickel JC, Roehrborn CG, Castro-Santamaria R, Freedland SJ, Moreira DM. Chronic prostate inflammation is associated with severity and progression of benign prostatic hyperplasia, lower urinary tract symptoms and risk of acute urinary retention. J Urol 2016;196:1493-8. [13] Nickel JC, Downey J, Young I, Boag S. Asymptomatic inflammation and/or infection in benign prostatic hyperplasia. BJU Int 1999;84:976-81. [14] Kramer G, Mitteregger D, Marberger M. Is benign prostatic hyperplasia (BPH) an immune inflammatory disease? Eur Urol 2007;51:1202-16. [15] Ficarra V, Rossanese M, Zazzara M, Giannarini G, Abbinante M, Bartoletti R, et al. The role of inflammation in lower urinary tract symptoms (LUTS) due to benign prostatic hyperplasia (BPH) and its potential impact on medical therapy. Curr Urol Rep 2014;15:463. [16] Gacci M, Corona G, Vignozzi L, Salvi M, Serni S, De Nunzio C, et al. Metabolic syndrome and benign prostatic enlargement:a systematic review and meta-analysis. BJU Int 2015;115:24-31. [17] Gacci M, Vignozzi L, Sebastianelli A, Salvi M, Giannessi C, De Nunzio C, et al. Metabolic syndrome and lower urinary tract symptoms:the role of inflammation. Prostate Cancer Prostatic Dis 2013;16:101-6. [18] Vignozzi L, Morelli A, Corona G, Sebastianelli A, Serni S, Gacci M, et al. Testosterone protects the lower urinary tract from metabolic syndrome-induced alterations. Horm Mol Biol Clin Investig 2012;11:329-37. [19] Vignozzi L, Gacci M, Cellai I, Santi R, Corona G, Morelli A, et al. Fat boosts, while androgen receptor activation counteracts, BPH-associated prostate inflammation. Prostate 2013;73:789-800. [20] Gandaglia G, Briganti A, Gontero P, Mondaini N, Novara G, Salonia A, et al. The role of chronic prostatic inflammation in the pathogenesis and progression of benign prostatic hyperplasia (BPH). BJU Int 2013;112:432-41. [21] Prakash K, Pirozzi G, Elashoff M, Munger W, Waga I, Dhir R, et al. Symptomatic and asymptomatic benign prostatic hyperplasia:molecular differentiation by using microarrays. Proc Natl Acad Sci U S A 2002;99:7598-603. [22] Kakehi Y, Segawa T, Wu XX, Kulkarni P, Dhir R, Getzenberg RH. Down-regulation of macrophage inhibitory cytokine-1/prostate derived factor in benign prostatic hyperplasia. Prostate 2004;59:351-6. [23] Paralkar VM, Vail AL, Grasser WA, Brown TA, Xu H, Vukicevic S, et al. Cloning and characterization of a novel member of the transforming growth factor-beta/bone morphogenetic protein family. J Biol Chem 1998;273:13760-7. [24] Kamijo T, Sato S, Kitamura T. Effect of cernitin pollen-extract on experimental nonbacterial prostatitis in rats. Prostate 2001;49:122-31. [25] Taniguchi S, Taoka R, Inui M, Sugimoto M, Kakehi Y. Influence of inflammation and aging on macrophage inhibitory cytokine-1 gene expression in rat ventral prostate. Urology 2009;73:410-4. [26] Tsunemori H, Sugimoto M, Xia Z, Taoka R, Oka M, Kakehi Y. Effect of the phytotherapeutic agent Eviprostat on inflammatory changes and cytokine production in a rat model of nonbacterial prostatitis. Urology 2011;77:e15-20. [27] Sugimoto M, Oka M, Tsunemori H, Yamashita M, Kakehi Y. Effect of a phytotherapeutic agent, Eviprostat®, on prostatic and urinary cytokines/chemokines in a rat model of nonbacterial prostatitis. Prostate 2011;71:438-44. [28] Shibuya S, Xia Z, Sugimoto M, Ueda N, Haba R, Kakehi Y. The phytotherapeutic agent, eviprostat, suppresses stromal proliferation and inflammation even after establishment of nonbacterial prostatitis in the rat prostate. Urology 2014;83:528-34. [29] Roumeguère T, Zouaoui Boudjeltia K, Babar S, Nuyens V, Rousseau A, Van Antwerpen P, et al. Effects of phosphodiesterase inhibitors on the inflammatory response of endothelial cells stimulated by myeloperoxidase-modified low-density lipoprotein or tumor necrosis factor alpha. Eur Urol 2010;57:522-8. [30] Vignozzi L, Gacci M, Cellai I, Morelli A, Maneschi E, Comeglio P, et al. PDE5 inhibitors blunt inflammation in human BPH:a potential mechanism of action for PDE5 inhibitors in LUTS. Prostate 2013;73:1391-402. [31] Vignozzi L, Filippi S, Morelli A, Comeglio P, Cellai I, Sarchielli E, et al. Testosterone/estradiol ratio regulates NO-induced bladder relaxation and responsiveness to PDE5 inhibitors. J Sex Med 2012;9:3028-40. [32] Morelli A, Comeglio P, Filippi S, Sarchielli E, Vignozzi L, Maneschi E, et al. Mechanism of action of phosphodiesterase type 5 inhibition in metabolic syndrome-associated prostate alterations:an experimental study in the rabbit. Prostate 2013;73:428-41. [33] American Urological Association guideline:management of benign prostatic hyperplasia (BPH). https://www.auanet.org/education/guidelines/benign-prostatic-hyperplasia.cfm. [34] European Association of Urology guideline:treatment of nonneurogenic male LUTS. http://uroweb.org/guideline/treatment-of-non-neurogenic-male-luts/#1. [35] Yamanishi T, Yasuda K, Kamai T, Tsujii T, Sakakibara R, Uchiyama T, et al. Single-blind, randomized controlled study of the clinical and urodynamic effects of an a-blocker (naftopidil) and phytotherapy (eviprostat) in the treatment of benign prostatic hyperplasia. Int J Urol 2004;11:501-9. [36] Homma Y, Araki I, Igawa Y, Ozono S, Gotoh M, Yamanishi T, et al. Clinical guideline for male lower urinary tract symptoms. Int J Urol 2009;16:775-90.
Christopher Hartman, Nikhil Gupta, David Leavitt, David Hoenig, Zeph Okeke, Arthur Smith. Advances in percutaneous stone surgery[J]. Asian Journal of Urology, 2015, 2(1): 26
-32
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