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Fazli H R, Mohamadkhani A, Godarzi H R, Pourshams A, Jafarinia M. Protective Effect of Dehydroepiandrosterone (DHEA) On Pancreatic Cancer Through C-Reactive Protein (CRP) Production Inhibition. rbmb.net 2024; 13 (2) :174-183
URL: http://rbmb.net/article-1-1406-en.html
URL: http://rbmb.net/article-1-1406-en.html
Liver and Pancreatobiliary Diseases Research Center, Digestive Disease Research Institute, Shariati Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Abstract: (548 Views)
Background: The relationship between inflammation and pancreatic cancer (PC) has been previously explored, but the precise role of inflammatory markers in disease risk and progression remains unclear. This case-control study aimed to investigate the association between C-reactive protein (CRP), systemic inflammation marker, and dehydroepiandrosterone (DHEA), systemic cytokines regulator, in relation to pancreatic cancer risk.
Methods: Serum levels of DHEA and CRP were measured in 50 pancreatic cancer patients and 50 age and sex-matched healthy controls using enzyme-linked immunosorbent assay (ELISA) and latex particle-enhanced immunoturbidimetric assay, respectively. Data analysis was performed using STATA software.
Results: The results showed that while DHEA levels were lower in pancreatic cancer patients compared to healthy subjects, the difference did not reach statistical significance (p=0.74). Conversely, CRP levels were significantly elevated in pancreatic cancer patients (p=0.001). Subgroup analysis based on sex revealed significant differences in DHEA and CRP concentrations between male patients and controls. Furthermore, a marginally significant inverse relationship was observed between log CRP and DHEA levels in pancreatic cancer patients (p=0.054). Risk assessment analysis, adjusted for age and sex, demonstrated an increased risk of pancreatic cancer associated with elevated log CRP levels (p=0.001; OR=1.671), and a decreased risk associated with higher DHEA levels (p=0.024, OR=0.479).
Conclusions: our findings highlight the direct association of pancreatic cancer with CRP and the inverse relationship with DHEA, suggesting the involvement of inflammation in pancreatic cancer development. Moreover, the observed inverse correlation between CRP and DHEA among pancreatic cancer patients suggests a potential inhibitory effect of DHEA on CRP levels.
Methods: Serum levels of DHEA and CRP were measured in 50 pancreatic cancer patients and 50 age and sex-matched healthy controls using enzyme-linked immunosorbent assay (ELISA) and latex particle-enhanced immunoturbidimetric assay, respectively. Data analysis was performed using STATA software.
Results: The results showed that while DHEA levels were lower in pancreatic cancer patients compared to healthy subjects, the difference did not reach statistical significance (p=0.74). Conversely, CRP levels were significantly elevated in pancreatic cancer patients (p=0.001). Subgroup analysis based on sex revealed significant differences in DHEA and CRP concentrations between male patients and controls. Furthermore, a marginally significant inverse relationship was observed between log CRP and DHEA levels in pancreatic cancer patients (p=0.054). Risk assessment analysis, adjusted for age and sex, demonstrated an increased risk of pancreatic cancer associated with elevated log CRP levels (p=0.001; OR=1.671), and a decreased risk associated with higher DHEA levels (p=0.024, OR=0.479).
Conclusions: our findings highlight the direct association of pancreatic cancer with CRP and the inverse relationship with DHEA, suggesting the involvement of inflammation in pancreatic cancer development. Moreover, the observed inverse correlation between CRP and DHEA among pancreatic cancer patients suggests a potential inhibitory effect of DHEA on CRP levels.
Keywords: C-reactive protein, Dehydroepiandrosterone, Inflammation, Risk factors. Pancreatic cancers.
Type of Article: Original Article |
Subject:
Molecular Biology
Received: 2024/06/2 | Accepted: 2024/11/18 | Published: 2025/01/4
Received: 2024/06/2 | Accepted: 2024/11/18 | Published: 2025/01/4
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