Complex relationship between chronic inflammation and BPH

[madman]

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 a1-blockers, phosphodiesterase 5 inhibitors, 5a-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.




ASSOCIATION BETWEEN CHRONIC INFLAMMATION AND BPH


RELATIONSHIP BETWEEN PROSTATIC ENLARGEMENT AND PROSTATIC INFLAMMATION


PROSTATIC INFLAMMATION AND BLADDER OUTLET OBSTRUCTION (BOO)


RELATIONSHIP BETWEEN STORAGE DYSFUNCTION AND PROSTATIC INFLAMMATION


PATHOPHYSIOLOGY OF PROSTATIC INFLAMMATION INFECTION


HORMONAL INFLUENCE

Generally, androgens are considered key factors in prostatic enlargement. Testosterone is converted to dihydrotestosterone and acts on androgen receptors to promote cell division within the prostate, contributing to increased prostate volume.6 The anti-inflammatory effects of androgens have been identified in various organs. For example, dihydrotestosterone can suppress the production of cytokines and chemokines such as IL-1, IL-6, and IL-8 by modulating NF–jB orIjB signaling.22 However, few studies have evaluated the effects of androgen on prostatic inflammation. Thus, we suspect that altered androgen levels in the prostate affect the severity of prostatic inflammation; further studies are necessary to explore this hypothesis.


PELVIC ISCHEMIA


URINE REFLUX


AUTOIMMUNITY


CHRONIC PROSTATIC INFLAMMATION AND LUTS




POTENTIAL THERAPEUTIC APPROACHES FOR PROSTATIC INFLAMMATION

-Assessment of prostatic inflammation

-Antibiotics

-a1-blockers

-Phosphodiesterase 5 inhibitors

-5ARIs

-Pollen extract

-Nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids




CONCLUSIONS

Chronic prostatic inflammation can worsen urinary and storage symptoms, potentially decreasing the quality of life in patients with BPH. Efforts to understand the mechanisms underlying chronic inflammation should be a key component of BPH research; further advancements in this area are expected regarding pathophysiological mechanisms and novel treatment methods.