Department of Urology, Faculty of Medical Sciences, University of Fukui, Eiheiji, Japan.
Int J Urol. 2024 Sep;31(9):968-974. doi: 10.1111/iju.15518. Epub 2024 Jun 27.
Benign prostatic hyperplasia, a prevalent condition in aging men, is characterized by the proliferation of prostatic epithelial and stromal cells, which leads to bladder outlet obstruction and the exacerbation of lower urinary tract symptoms. There is increasing evidence that chronic prostatic inflammation contributes to the pathogenesis and progression of benign prostatic hyperplasia. This review explores the complex relationship between chronic inflammation and benign prostatic hyperplasia, focusing on the underlying mechanisms, clinical implications, and current therapeutic approaches. The pathophysiology of benign prostatic hyperplasia is multifaceted, involving factors such as hormonal changes, hypoxia, urine reflux into prostatic ducts and stroma, autoimmune responses, and infection-induced inflammation. Inflammatory cytokines, particularly interleukin-17 and interleukin-8, may play key roles in tissue remodeling and smooth muscle contraction within the prostate, thereby influencing benign prostatic hyperplasia progression. Current therapies for benign prostatic hyperplasia include α1-blockers, phosphodiesterase 5 inhibitors, 5α-reductase inhibitors, and plant-based treatments (e.g., pollen extract). These therapies aim to alleviate symptoms by reducing prostatic inflammation, improving blood flow, and inhibiting hormonal pathways involved in prostatic enlargement. However, patients with chronic prostatic inflammation often experience more severe lower urinary tract symptoms and may be resistant to conventional treatments. This resistance has prompted the exploration of alternative therapies targeting inflammation. Chronic prostatic inflammation plays a central role in the pathogenesis and severity of benign prostatic hyperplasia. An understanding of its mechanisms will enable the development of more effective treatments to improve the quality of life among patients with benign prostatic hyperplasia.
良性前列腺增生是一种常见于老年男性的疾病，其特征是前列腺上皮和基质细胞的增殖，导致膀胱出口梗阻和下尿路症状加重。越来越多的证据表明，慢性前列腺炎症有助于良性前列腺增生的发病机制和进展。本综述探讨了慢性炎症与良性前列腺增生之间的复杂关系，重点介绍了潜在机制、临床意义和当前治疗方法。良性前列腺增生的病理生理学是多方面的，涉及激素变化、缺氧、尿液反流到前列腺导管和基质、自身免疫反应和感染引起的炎症等因素。炎症细胞因子，特别是白细胞介素-17 和白细胞介素-8，可能在前列腺组织重塑和平滑肌收缩中发挥关键作用，从而影响良性前列腺增生的进展。目前治疗良性前列腺增生的方法包括α1-阻滞剂、磷酸二酯酶 5 抑制剂、5α-还原酶抑制剂和植物治疗（如花粉提取物）。这些疗法旨在通过减轻前列腺炎症、改善血液流动和抑制前列腺增大相关的激素途径来缓解症状。然而，患有慢性前列腺炎症的患者通常会经历更严重的下尿路症状，并且可能对常规治疗产生抵抗。这种抵抗促使人们探索针对炎症的替代治疗方法。慢性前列腺炎症在良性前列腺增生的发病机制和严重程度中起着核心作用。对其机制的理解将使我们能够开发更有效的治疗方法，从而提高良性前列腺增生患者的生活质量。
