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Inflammatory mediators in the development and progression of benign prostatic hyperplasia

Key Points

  • Epidemiological data suggest a causal link between benign prostatic hyperplasia (BPH) and prostatic inflammation

  • Stimuli including infectious agents, urinary reflux, metabolic syndrome, the ageing process and autoimmune responses can trigger dysregulation of the prostate immune system through several molecular pathways involving the development of inflammatory infiltrates

  • Tissue damage and chronic tissue healing could result in the development of BPH nodules

  • Several drugs targeting prostatic inflammation have been tested for the management of BPH and its symptoms, but concerns regarding their efficacy and safety limit their use in clinical practice

  • Targeting prostate inflammation could offer a target for new treatment strategies in patients with BPH

Abstract

Benign prostatic hyperplasia (BPH) is the most common urological disease in elderly men. Epidemiological data suggest a causal link between this condition and prostatic inflammation. The prostate is an immune-competent organ characterized by the presence of a complex immune system. Several stimuli, including infectious agents, urinary reflux, metabolic syndrome, the ageing process, and autoimmune response, have been described as triggers for the dysregulation of the prostatic immune system via different molecular pathways involving the development of inflammatory infiltrates. From a pathophysiological standpoint, subsequent tissue damage and chronic tissue healing could result in the development of BPH nodules.

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Figure 1: The central role of chronic prostate inflammation in the development and progression of BPH–LUTS.

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De Nunzio, C., Presicce, F. & Tubaro, A. Inflammatory mediators in the development and progression of benign prostatic hyperplasia. Nat Rev Urol 13, 613–626 (2016). https://doi.org/10.1038/nrurol.2016.168

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