Підвищений рівень ПСА у пацієнтів із поєднанням хронічного простатиту й доброякісної гіперплазії передміхурової залози: варіанти лікування та оптимізація діагностики раку (Огляд літератури)

The relationship between chronic prostatitis (CP), which often coexists with benign prostatic hyperplasia (BPH), and elevated prostate-specific antigen (PSA) levels presents a clinical challenge, often complicating the decision-making process regarding prostate cancer (PCa) diagnosis. This overlap creates significant clinical challenges, as distinguishing between benign inflammatory conditions and malignancy is critical for determining the appropriate course of action. The treatment options for elevated PSA in the context of CP are not clearly defined in current guidelines. While most studies suggest that antibiotics are the most typical management strategy in such cases, the choice of antibiotic and optimal treatment duration remain unclear. Some research has explored the use of fluoroquinolones and other broad-spectrum antibiotics, but consensus on the most effective regimen is lacking. Additionally, there is limited evidence regarding the long-term outcomes of antibiotic therapy in these cases. Although most studies have shown that PSA levels decrease following antibiotic treatment, it remains uncertain whether this reduction improves the accuracy of PCa diagnosis. A drop in PSA may reflect the resolution of inflammation rather than the absence of cancer, posing a risk of overlooking malignancies. Another significant challenge is that inflammatory processes in the prostate can deteriorate and complicate histological analysis, further obscuring PCa diagnosis. Inflammation may alter tissue architecture, making it harder to detect malignant cells and increasing the risk of both false-positive and false-negative findings. This complicates the interpretation of prostate biopsies and may delay appropriate cancer treatment. Emerging research has started to focus on novel biomarkers, such as Prostate Health Index (PHI), 4Kscore, and urinary markers like PCA3 and TMPRSS2:ERG, which may offer additional diagnostic value beyond PSA alone. These markers have shown promise in differentiating CP from PCa, but their clinical utility requires further validation through large-scale studies. In conclusion, the relationship between CP, PSA levels, and PCa remains complex and poorly defined. Future research should aim to establish standardized treatment protocols for PSA elevation in patients with CP and BPH, clarify the role of antibiotics, and explore the integration of new biomarkers into routine clinical practice. This review highlights the importance of individualized diagnostic strategies and the integration of novel biomarkers to optimize patient management, reduce unnecessary biopsies, and improve clinical outcomes. Ongoing research remains crucial for refining these approaches and establishing evidence-based guidelines for the diagnosis and treatment of CP and PCa.