Korean J Urol.  2008 Nov;49(11):997-1002. 10.4111/kju.2008.49.11.997.

The Effect of Chronic Prostatic Inflammation on Acute Urinary Retention in the Setting of Benign Prostatic Hyperplasia

• Cha WH
• Jang TJ
• Kim KH
• Seo YJ
• Lee KS

• KMID: 1328171
• DOI: http://doi.org/10.4111/kju.2008.49.11.997

Abstract

PURPOSE: The aim of this study was to evaluate the effect of chronic prostatic inflammation on acute urinary retention(AUR) in the setting of benign prostatic hyperplasia(BPH).
MATERIALS AND METHODS
A total of 132 male patients admitted to our clinic with BPH-related AUR or BPH-related lower urinary tract symptoms (LUTS) were included in this study. These patients were divided into two groups. Group 1 consisted of 58 patients with AUR who underwent transurethral resection of the prostate(TURP), and group 2 consisted of 74 patients with LUTS who underwent TURP. Prostatic infarction, morphology, inflammation were examined. Prostatic infarction was evaluated according to the presence or absence of infarction. Prostatic morphology was assessed according to three categories: mainly glandular hyperplasia, stromal hyperplasia, or a mixture of glandular and stromal hyperplasia. Prostatic inflammation was assessed according to three categories: mild, moderate, and severe.
RESULTS
Prostatic infarction was observed in 8.6% of the patients in group 1 and in 8.1% of the patients in group 2(p=1.000). Glandular, stromal, and mixed hyperplasia were detected in 36.2%, 5.2%, and 58.6% of the patients in group 1 and in 35.1%, 6.8%, and 58.1% of the patients in group 2, respectively(p=0.222). Mild, moderate, and severe chronic prostatic inflammation were observed in 39.7%, 31.0%, and 29.3% of the patients in group 1 and in 73.0%, 20.3%, and 6.7% of the patients in group 2, respectively(p<0.001). CONCLULSIONS: Chronic prostatic inflammation may play an important role on AUR developing secondary to BPH.

Keyword

Urinary retention; Prostate; Infarction; Morphology; Inflammation

MeSH Terms

Male
Humans

Figure

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  Fig. 1. Post-glandular prostatic infarction and disrupted epithelium were detected in 5 patients in Group 1 and in 6 patients in Group 2, respectively. No significant differences were noted between the two groups (H&E, x200).

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  Fig. 2. The prostatic tissue shows glandular hyperplasia (A) (x200), stromal hyperplasia (B) (x200), and mixture hyperplasia (C) (x200). No significant differences were noted between the two groups (H&E).

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  Fig. 3. The prostatic tissue shows severe inflammation (A) and mild inflammation (B) in the stroma, along with involvement of the glandular epithelium. The inflammatory infiltrate was predominantly lymphocytic. Prostatic inflammation (A) was more pronounced in group 1 than it was in group 2 (H&E, x200).

Reference

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