Background: The relationship between Chronic Prostatitis (CP) and Benign Prostatic Hyperplasia (BPH) has been increasingly studied due to the potential overlap in their pathophysiological mechanisms. This study aims to elucidate the histopathological correlations between inflammation and BPH, emphasizing the roles of inflammatory mediators, hormonal influences, and immune responses in the progression of BPH. Methods: An ambispective study was conducted from May 2004 to July 2011, analysing prostatic specimens from patients undergoing Transurethral Resection of Prostate (TURP) and open prostatectomy for benign prostatic enlargement. Specimens were fixed, processed, and stained for histopathological examination. Standard statistical methods were employed for data analysis. Results: Out of 391 prostatic specimens examined, 369 were diagnosed with BPH. Chronic prostatitis was the most common non-neoplastic lesion associated with BPH, observed in 50.4% of cases. Histopathological findings frequently showed inflammatory cell infiltration, glandular disruption, and stromal fibrosis. Notable associations included glandular changes due to inflammation and varying degrees of fibrosis. Discussion: The findings confirm a significant histopathological interplay between chronic prostatitis and benign prostatic hyperplasia. Chronic inflammation appears to contribute to prostatic tissue proliferation and hyperplasia, suggesting that inflammatory pathways may be integral to the pathogenesis and symptomatology of BPH. Conclusion: Understanding the complex interactions between inflammatory processes and prostatic tissue growth can enhance the diagnostic and therapeutic approaches for patients with BPH, potentially leading to targeted treatments that address these underlying processes. Continued research into the molecular and cellular mechanisms of inflammation in BPH is essential for developing more effective management strategies.
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