Smoking exacerbates lower urinary tract symptoms and chronic prostatic inflammation in patients with benign prostatic hyperplasia.

Inamura S1, Kobayashi H1, Tsutsumiuchi M1, Itoga A1, Seki M1, Taga M1, Tsuchiyama K1, Fukushima M1, Aoki Y1, Ito H1, Yokoyama O1

Research Type

Basic Science / Translational

Abstract Category

Male Lower Urinary Tract Symptoms (LUTS) / Voiding Dysfunction

Abstract 702
Prevalence, Etiology and Quality of Life
Scientific Podium Short Oral Session 34
Friday 6th September 2019
15:15 - 15:22
Hall G1
Benign Prostatic Hyperplasia (BPH) Detrusor Overactivity Pathophysiology
1.Department of Urology, Faculty of Medical Sciences, University of Fukui

So Inamura



Hypothesis / aims of study
Smoking, a major public health problem worldwide, causes a variety of illnesses and exacerbates lower urinary tract symptoms (LUTS). The effects of smoking cessation on LUTS are still unclear. Herein we assessed the impact of smoking on LUTS and the effectiveness of smoking cessation on LUTS in patients with benign prostatic hyperplasia (BPH).
Study design, materials and methods
We retrospectively analyzed the cases of 118 BPH patients who underwent transurethral prostatic surgery. Their smoking history was confirmed. We classified the patients into the non-smokers (n=45 ), former smokers (n=62), and current smokers (n=11) and assessed the relationship between smoking history and clinical parameters: International Prostatic Symptom Score (IPSS), uroflowmetry, pressure flow study results, the magnitude of prostatic inflammation, serum C-reactive protein (CRP) level, and serum prostate specific antigen (PSA) level. We evaluated the relationships between the clinical parameters and the patients' smoking duration, duration of smoking cessation, and Brinkman index values. We used prostatic tissue obtained from the patients' surgery to quantify the magnitude of prostatic inflammation histologically, based on the abundance ratio of high endothelial venule (HEV)-like vessels. HEV-like vessels can be detected by immunostaining with MECA-79. At the same time, we detected all vessels in the tissue by immunostaining with CD34. We then counted the number of MECA-79+ vessels and that of CD34+ vessels and calculated the MECA-79+ / CD34+ vessel ratio. We previously demonstrated that the MECA-79+/CD34+ vessel ratio is a reliable marker of chronic inflammation [1].
The IPSS straining scores of the non-smokers were significantly lower than those of the smokers (1.710 ± 1.690 vs. 2.600 ± 1.902, p=0.029), and the non-smokers' scores for weak stream, voiding subscore, and total score tended to be lower than those of the smokers (weak stream 3.350 ± 1.798 vs. 3.980 ± 1.291, p=0.058; voiding subscore 7.510 ± 4.426 vs. 9.320 ± 4.322, p=0.057; total score 17.110 ± 8.386 vs. 20.400 ± 7.724, p=0.060). In the pressure flow study, there were negative correlations between duration of smoking and strong desire to void (SDV), and between urgency and bladder volume at the initial detrusor overactivity (DO) (SDV: correlation coefficient -0.314, p=0.013, Fig. 1A; urgency: correlation coefficient -0.349, p=0.008, Fig. 1B; bladder volume at initial DO: correlation coefficient -0.417, p=0.021, Fig. 1C). Maximum cystic capacity (MCC) tended to be negatively correlated with the duration of smoking (correlation coefficient -0.227, p=0.055).Serum PSA level and serum CRP level was positively correlated with the duration of smoking (serum PSA level: correlation coefficient 0.212, p=0.047, serum CRP level: correlarion coefficient 0.216, p=0.049). We next focused on the former smokers and examined the relationship between smoking cessation and clinical parameters. The duration of smoking cessation was significantly negatively correlated with the magnitude of chronic prostatic inflammation (correlation coefficient −0.253, p=0.027, Fig. 1D). In the pressure-flow study, the duration of smoking cessation was positively correlated with urgency and MCC (urgency: correlation coefficient 0.286, p=0.030, MCC: correlation coefficient 0.241, p=0.050). SDV and BOOI tended to be correlated with duration of smoking cessation (SDV: correlation coefficient 0.241, p=0.051, BOOI: correlarion coefficient -0.260, p=0.062).
Interpretation of results
Our analyses demonstrated that smoking is associated with the exacerbation of both storage and voiding dysfunction, and they suggest that the effect of smoking on the lower urinary tract could be reversible. Smoking is well known to cause blood flow disorder and oxidative stress systemically. We thus hypothesize that such adverse effects of smoking cause the exacerbation of LUTS and chronic inflammation.
Concluding message
Our results demonstrate that smoking exacerbated LUTS and chronic prostatic inflammation, and we observed the effectiveness of smoking cessation on LUTS. To the best of our knowledge, this is the first report demonstrating a relationship between smoking and chronic prostatic inflammation.
Figure 1 (A - C) correlation between the duration of smoking and clinical parameters , (D)correlation between the duration of smoking cessation and the magnitude of chronic prostatic inflammation.
  1. Inamura S, Shinagawa T, Hoshino H, Sakai Y, Imamura Y, Yokoyama O, Kobayashi M. Appearance of high endothelial venule-like vessels in benign prostatic hyperplasia is associated with lower urinary tract symptoms. Prostate. 2017 77: 794-802.
Funding None Clinical Trial No Subjects Human Ethics Committee he Ethics Committee of the Faculty of Medical Sciences, University of Fukui, Japan Helsinki Yes Informed Consent Yes