B-121 Evaluation of the use of Serum Amyloid A (SAA) as a diagnostic biomarker in prostate cancer

Abstract

Prostate cancer (PCa) is a major health challenge in men and has contributed to a high rate of cancer-related death worldwide. Many risk factors for PCa are primarily related to age, family history, and ethnicity, but recent literature suggests that inflammation plays an active role in PCa development. Serum amyloid A (SAA) is an acute-phase protein involved in inflammation and is produced by the liver. It is an inflammatory biomarker that is significantly upregulated in many inflammatory diseases. This underscores its importance in monitoring expression levels during PCa disease pathogenesis. Thus, we evaluated serum levels of Serum Amyloid A (SAA) in PCa patients compared with healthy controls. This cross-sectional case–control study involved fifty (50) prostate cancer patients attending the Nnamdi Azikiwe University Teaching Hospital (NAUTH), Nnewi, Anambra State, Nigeria. Forty (40) age-matched healthy controls were randomly selected from the same community. Consent was obtained from these participants, and data on age and family history were collected using a questionnaire. Venous blood samples were collected and analyzed for total prostate-specific antigen (tPSA) and serum amyloid A (SAA) using Enzyme-linked immunosorbent assay (ELISA) techniques. Data were analysed using Student’s t-test and Pearson correlation, with statistical significance set at p = 0.05. This study found a significant serum tPSA level in the test group (prostate cancer patients) (57.22 ± 36.59 ng/mL) compared with healthy controls (2.28 ± 1.12 ng/mL; p < 0.001) as expected. The serum SAA levels were elevated similarly in both the test group (prostate cancer patients) (96.68 ± 61.90 mg/L) and the healthy controls (93.64 ± 29.14 mg/L). There was no statistical difference (p = 0.776) when both groups were compared. Findings from this study showed that SAA, as an inflammatory biomarker, cannot be used holistically as a diagnostic tool in PCa. patients. This is because the current study found no association between SAA and PCa, as there were similarly elevated levels of SAA in both the PCa patients and healthy controls. Leveraging this report, this work strengthens and guides future PCa studies toward the identification of more specific biomarker-related parameters.