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Letter to the Editor

Letter to the Editor regarding the article “Association of elevated interleukin-17 and angiopoietin-2 with prostate size in benign prostatic hyperplasia”

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Pages 83-84 | Received 08 Aug 2017, Accepted 10 Aug 2017, Published online: 28 Aug 2017

Dear Editor,

We read with great interest the currently published manuscript by Arivazhagan et al. [Citation1] on the association of Angiopoietin-2 (ANGPT2) and ınterleukin-17 (IL-17) with prostate enlargement. Being one of the most common diseases disturbing aging males with lower urinary tract symptoms reducing the quality of life, BPH/LUTS is of keen interest to the researchers. Beyond the clinical relevance of BPH/LUTS, the studies for enhancing our understanding of the underlying pathophysiology is also precious, since the exact cause and effect mechanisms have not been elucidated yet. Therefore, we congratulate the authors for the present paper evaluating the possible link between somewhat inflammation markers and prostate enlargement.

The authors enrolled patients diagnosed with BPH undergoing transurethral resection of the prostate (TUR-P) and age-matched controls. They compared ANGPT2 and IL-17 level between groups and concluded that patients with BPH have higher ANGPT2 and IL-17 level than control group, as well as a positive correlation, was found between two inflammation descriptives. This is a concise, well-documented study but we want to make some contributions and further discuss some important considerations. According to several studies, inflammation is likely to be important involved in the pathophysiology of BPH [Citation2,Citation3]. Additionally, the close relationship between prostate enlargement and inflammation related situations such as obesity, dyslipidemia, diabetes mellitus, metabolic syndrome is well documented in many studies [Citation4,Citation5]. In this regard, the data analysis of the present study including those compounding factors into the multivariate logistic regression analysis would identify the role of the aforementioned inflammatory markers more accurately.

The clinical relevance of these inflammatory markers in urology practice is also a topic that deserves attention. As future perspectives:

  1. Establishment of the level of these markers in resected prostatic tissues either benign or malignant, the association of those in BPH parameters (improvement in maximal urethral flow rate, IPSS, post void residual volume, etc.) would enable urologists to find out clinical implications of these inflammatory markers in prostatic diseases.

  2. Cumulative production of reactive oxygen species (ROS) commonly produced from inflammatory cells through either endogenous or exogenous insult plays a significant role in age-related diseases. Thus it is reasonable to suggest oxidative stress mechanisms as a part of the elucidation of BPH pathogenesis. The results of this study should provoke the researchers accumulating their interest on the potential association of reactive oxygen specifies and BPH/LUTS.

Consequently, the current study represents reliable data for the potential association of angiogenesis and inflammation with the most common benign neoplasm, BPH, in aging male. It is evident that further well-designed studies are needed to better understand the implication of inflammation related markers in underlying pathophysiological mechanisms of benign prostate hyperplasia.

Disclosure statement

No potential conflict of interest was reported by the authors.

References

  • Arivazhagan J, Nandeesha H, Dorairajan LN, et al. Association of elevated interleukin-17 and angiopoietin-2 with prostate size in benign prostatic hyperplasia. Aging Male. 2017;20:115–118.
  • Norström MM, Rådestad E, Sundberg B, et al. Progression of benign prostatic hyperplasia is associated with pro-inflammatory mediators and chronic activation of prostate-infiltrating lymphocytes. Oncotarget. 2016;7:23581–23593.
  • Russo GI, Cimino S, Castelli T, et al. Benign prostatic hyperplasia, metabolic syndrome and non-alcoholic fatty liver disease: ıs metaflammation the link? Prostate. 2016;76:1528–1535.
  • Gacci M, Corona G, Vignozzi L, et al. Metabolic syndrome and benign prostatic enlargement: a systematic review and meta-analysis. BJU Int. 2015;115:24–31.
  • Pashootan P, Ploussard G, Cocaul A, et al. Association between metabolic syndrome and severity of lower urinary tract symptoms (LUTS): an observational study in a 4666 European men cohort. BJU Int. 2015;116:124–130.

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