Abstract

ObjectiveWe conducted experiments to elucidate the impact of ischemic change on benign prostatic hyperplasia (BPH) using immunohistochemistry. MethodsMedical records of consecutive patients over 60 years of age who underwent transurethral resection of the prostate for BPH between January 2009 and September 2012 were evaluated. As vascular risk factors, the presence or absence of diabetes mellitus, hypertension, current smoking, obesity, dyslipidemia, and diseases related to bladder function were investigated. As BPH-related factors, International Prostate Symptom Score, quality of life, maximal flow rate, postvoid residual volume, prostate-specific antigen, prostate volume, prostate calculi, and medication state for BPH were investigated. Immunohistochemistry was performed for hypoxia-inducible factor (HIF-1α), sex hormone receptors, and smooth muscle actin. Additionally, microvessel density (MVD) and diffuse fibrosis (DF) were evaluated. ResultsA total of 101 patients were included and HIF-1α expression in stroma and glands were observed in 56 (55.4%) and 34 (33.7%) cases, respectively. There was no significant association between HIF-1α expression and vascular risk factors or BPH-related variables. However, there was a significant correlation between the HIF-1α expression in stroma and higher MVD. HIF-1α expression in the stroma was also significantly correlated with higher expressions of the androgen and progesterone receptors in the stroma. DF was frequently found in cases with higher HIF-1α expression in the stroma than in those with lower HIF-1α expression. ConclusionIn patients with response to ischemic changes of the prostate, HIF-1α expression could be confirmed, and the expression of the androgen receptor was significantly lower in these patients. Chronic ischemic damage in the prostate can progress to a condition that is refractory to pharmacologic therapy. Chronic ischemic damage, which can progress to refractory phase to pharmacologic therapy, is correlated with the hormonal status of prostate.

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