Session: PD02: Benign Prostatic Hyperplasia: Basic Research & Pathophysiology
PD02-10: The humoral immunity activation causes the bladder outlet obstruction related with prostate through the different mechanism from the prostate volume
Fukushima Medical University Department of Urology
Introduction: The prostate volume and morphological features of the prostate are well known to be associated with bladder outlet obstruction (BOO) in the male patients. However, the causative agents and factors of BOO are multifactorial and incompletely understood. This study aims to find out the novel mechanism underlying bladder outlet obstruction (BOO) except for prostate volume and morphological features by comprehensive gene expression analysis (CGEA) Methods: A total of 31 patients who had a diagnosis of benign by the random prostate biopsy were enrolled in this study. CGEA was performed with prostate specimens obtained by the biopsy. The patients were divided into control group (prostate volume < 30 mL) and benign prostatic enlargement (BPE) group (prostate volume = 30 mL). Hierarchical clustering was performed to identify the clusters with similar gene expression by the genes indicated significantly different between two groups by t-test. The uroflowmetry parameters were compared among each cluster. The protocol was approved by the ethics committee of Fukushima Medical University Results: CGEA selected 12 genes with significant difference in mean converted value between control and BPE (P <0.01) from 11,907 genes. Hierarchical clustering analysis using these 12 genes categorized three different clusters: the control (n=8), the BPE (n=11) and BPE with inflammatory (n=12) clusters. As compared BPE cluster, the BPE with inflammatory cluster have activation of humoral immunity (increased VSIG2 gene), more suppression of estrogen receptor signaling (reduced ELK4 gene) and more decreased angiogenesis (reduced MME gene). The maximum flow rate was significantly lower in the BPE with inflammatory cluster than in the control cluster (P=0.03). There was no significant difference about the maximum flow rate between control cluster and BPE cluster. Conclusions: Our results suggested that humoral immunity activation, estrogen receptor signaling suppression and decreased angiogenesis reduced maximal urinary flow rate in the patients with large prostate volume. The activation of humoral immunity in addition to the change of estrogen receptor signaling and angiogenesis causes BOO related with prostate through the different mechanism from the prostate volume. SOURCE OF Funding: None
