Chronic prostatic inflammation is one of the significant factors in the exacerbation of the severity of lower urinary tract symptom (LUTS). Various methods have been used to assess the magnitude of prostatic inflammation. It was reported that the serum C-reactive protein (CRP) level was associated with the severity of LUTS, particularly storage symptoms in patients with benign prostatic hyperplasia (BPH) [1]. However, it is unclear whether the CRP level truly reflects the magnitude of prostatic inflammation. Our previous report demonstrated that the number of high endothelial venule (HEV)-like vessels was a remarkable histological marker that can be used to quantify the magnitude of chronic inflammation, and we showed that chronic prostatic inflammation exacerbated the severity of LUTS particularly voiding dysfunction by using urodynamic study (UDS) [2]. 
Here we assessed the relationship between the magnitude of chronic prostatic inflammation and the serum CRP level. By using UDS parameters, we also evaluated the impact of CRP on the severity of LUTS.

We examined the tissue specimens obtained from 121 BPH patients who underwent transurethral resection of the prostate (TURP) or holmium laser enucleation of the prostate (HoLEP) and pre-surgery measurement of the serum CRP level. The tissue specimen were immunostained for CD34 and MECA-79 to determine the HEV-like vessel number. Patients with any type of pre-operative bacterial infection and patients taking an anti-inflammatory drug such as NSAIDs or steroids were excluded. We quantified the magnitude of prostatic inflammation histologically by determining the number of HEV-like vessels in each specimen, and we evaluated the relationship between the number of HEV-like vessels and the serum CRP level. We divided the patients into two groups based on the median serum CRP level (0.05 mg/dL) and compared the groups’ clinical parameters: the International Prostate Symptom Score (IPSS), the Overactive Bladder Symptom Score (OABSS), prostatic volume, serum prostate-specific antigen (PSA), and uroflowmetry and pressure-flow study.

There was no correlation between the number of HEV-like vessels and the serum CRP level (correlation coefficient= - 0.038, p=0.388; Fig. 1). The serum CRP levels were well correlated with each item of the OABSS (daytime frequency score: correlation coefficient= 0.520, p=0.009; nighttime frequency score: correlation coefficient= 0.425, p=0.027; urgency score: correlation coefficient= 0.477, p=0.014; urgency urinary incontinence score: correlation coefficient=0.593, p=0.002). The proportion of detrusor overactivity (DO) in the higher-CRP group was significantly higher than that of the lower-CRP group (65.0% vs. 34.3%, p=0.009; Fig. 2). Chronic prostatic inflammation assessed by the number of HEV-like vessels was not associated with the proportion of DO. Higher CRP level was significantly associated with the existence of DO in univariable and multivariable analyses (univariable: odds ratio: 3.550, p=0.011; multivariable: odds ratio: 6.450, p=0.009).

We demonstrated that the serum CRP level was not a marker of chronic prostatic inflammation, but the serum CRP level was significantly associated with storage dysfunction. It is unclear how CRP is associated with storage dysfunction. We hypothesized that CRP itself might be related to aggravating factors of OAB. Further studies are required to determine the relationship between CRP and storage dysfunction.

To the best of our knowledge, this is the first report to demonstrate that the serum CRP level is not associated with the magnitude of chronic prostatic inflammation, but that the serum CRP level is significantly associated with the severity of storage dysfunction by using UDS parameters.

Hung SF et al. Increased serum C-reactive protein level is associated with increased storage lower urinary tract symptoms in men with benign prostatic hyperplasia. PLoS ONE 2014; 9: e85588.
Inamura S et al. Appearance of high endothelial venule-like vessels in benign prostatic hyperplasia is associated with lower urinary tract symptoms. Prostate. 2017 77: 794-802.