Document Type: Original Clinical
Authors
1 Clinical and Experimental Internal Medicine Department, Medical Research Institute, Alexandria University.
2 Tropical Medicine Department, Alexandria University, Alexandria, Egypt.
3 Department of Epidemiology, High Institute of Public Health, Alexandria University.
4 Internal Medicine Department, Faculty of Medicine, Alexandria University, Alexandria, Egypt. Internal Medicine Department, Faculty of Medicine, Beirut Arab University, Beirut, Lebanon.
Abstract
Aim: HCV-induced cirrhosis is recognized as a leading cause of Hepatocellular Carcinoma (HCC) with a high annual incidence in Egypt. The role of serum amyloid A (SAA) has been highlighted in many inflammatory and neoplastic diseases. Accordingly, this study aimed to evaluate the potential of SAA as a biomarker for HCC in patients with HCV-induced cirrhosis and its capacity to predict HCC.
Patients and Methods: A comparative cross-sectional study was conducted on 90 HCV-induced cirrhotic patients. The patients were categorized into established HCC patients on top of HCV-induced cirrhosis (45 patients) and HCV-induced cirrhotic patients without HCC (45 patients). Besides taking history and conducting clinical, laboratory, and radiological examinations, SAA levels were recorded in all patients.
Results: Compared to non-HCC patients, most of the laboratory results were significantly deteriorated in cirrhotic HCC patients. HCC is developed substantially in patients with class C Child Paugh scores (p< 0.001). The mean SAA is elevated considerably in cirrhotic HCC patients than in cirrhotic non-HCC patients (70.38 ± 57.12 vs. 6.84 ± 1.91 ng/mL, respectively). At a cut-off value of >12 ng/mL, the sensitivity and specificity of SAA were 93.33% and 100%, respectively SAA, to diagnose patients with HCC in HCV-induced cirrhosis.
Conclusion: SAA is a highly sensitive and specific marker in diagnosing and predicting HCC development in HCV-cirrhotic patients.
Patients and Methods: A comparative cross-sectional study was conducted on 90 HCV-induced cirrhotic patients. The patients were categorized into established HCC patients on top of HCV-induced cirrhosis (45 patients) and HCV-induced cirrhotic patients without HCC (45 patients). Besides taking history and conducting clinical, laboratory, and radiological examinations, SAA levels were recorded in all patients.
Results: Compared to non-HCC patients, most of the laboratory results were significantly deteriorated in cirrhotic HCC patients. HCC is developed substantially in patients with class C Child Paugh scores (p< 0.001). The mean SAA is elevated considerably in cirrhotic HCC patients than in cirrhotic non-HCC patients (70.38 ± 57.12 vs. 6.84 ± 1.91 ng/mL, respectively). At a cut-off value of >12 ng/mL, the sensitivity and specificity of SAA were 93.33% and 100%, respectively SAA, to diagnose patients with HCC in HCV-induced cirrhosis.
Conclusion: SAA is a highly sensitive and specific marker in diagnosing and predicting HCC development in HCV-cirrhotic patients.
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