Shabana, H., Elgamal, S., Menessy, A., Abdel-Khalek, E., Abozeid, F., Askar, M., Mohsen, M., El-Desoky, A. (2024). Hepatocellular carcinoma before and after the era of direct-acting antiviral therapy for chronic hepatitis C: Dose the story differ?. Medical Journal of Viral Hepatitis, 8.1(1), 17-22. doi: 10.21608/mjvh.2024.350728
Hany Shabana; Salah Elgamal; Ayman Menessy; Ehab Abdel-Khalek; Fatma Abozeid; Marwa Askar; Mohammed Mohsen; Abd- Elmohsen El-Desoky. "Hepatocellular carcinoma before and after the era of direct-acting antiviral therapy for chronic hepatitis C: Dose the story differ?". Medical Journal of Viral Hepatitis, 8.1, 1, 2024, 17-22. doi: 10.21608/mjvh.2024.350728
Shabana, H., Elgamal, S., Menessy, A., Abdel-Khalek, E., Abozeid, F., Askar, M., Mohsen, M., El-Desoky, A. (2024). 'Hepatocellular carcinoma before and after the era of direct-acting antiviral therapy for chronic hepatitis C: Dose the story differ?', Medical Journal of Viral Hepatitis, 8.1(1), pp. 17-22. doi: 10.21608/mjvh.2024.350728
Shabana, H., Elgamal, S., Menessy, A., Abdel-Khalek, E., Abozeid, F., Askar, M., Mohsen, M., El-Desoky, A. Hepatocellular carcinoma before and after the era of direct-acting antiviral therapy for chronic hepatitis C: Dose the story differ?. Medical Journal of Viral Hepatitis, 2024; 8.1(1): 17-22. doi: 10.21608/mjvh.2024.350728
Hepatocellular carcinoma before and after the era of direct-acting antiviral therapy for chronic hepatitis C: Dose the story differ?
1Hepatology and Gastroenterology Unit, Internal Medicine dept., Faculty of Medicine, Mansoura Univ., Egypt.
2Hepatology and Gastroenterology Unit, Internal Medicine dept., Faculty of Medicine, Mansoura Univ., Egypt
3Clinical pathology dept., Mansoura New General Hospital, Ministry of Health, Egypt.
4Diagnostic Radiology dept., Mansoura University Hospital, Faculty of Medicine, Mansoura Univ., Egypt
Abstract
Background. Hepatitis C virus (HCV) infection is a leading cause of liver cancer globally. Treating chronic HCV with direct-acting antivirals (DAAs) in cirrhotic patients has raised concerns about their effect on HCC development and progr-ession. Objective: To compare the characteristics of de novo HCC in chronic HCV cirrhotic patients who achieved susta-ined virological response (SVR) with DAAs therapy, with that of HCC which developed in chronic HCV cirrhotic patients who did not receive DAAs or PEG interferon-based treatments. Methods The study included 200 chronic HCV cirrhotic patients divided into two groups: group 1 with 100 patients who developed de novo HCC post-SVR following DAAs, and group 2 with 100 HCV-related HCC patients who developed HCC without prior antiviral therapy. Non-invasive HCC diagnosis was based on EASL guidelines. Baseline demogr-aphic, clinical, and laboratory data were collected. The Child-Turcotte-Pugh (CTP) score, class, and Barcelona Clinic Liver Cancer (BCLC) staging system were determined (stages 0/A as early stages, while BCLC stages B/C/D as late stages of HCC). The types of DAAs used for chronic HCV treatment were also recorded. Results. Post-DAAs HCC was diagnosed approximately 4.3 years post-SVR, characterized by multi-focal or diffuse infiltration compared to HCV-related HCC. The tumor diameter in post-DAAs HCC was larger versus in HCV-related HCC (p= 0.002). Linear regression analysis indicated that DAAs therapy was a significant predictor of a larger tumor diameter. Malignant portal vein thrombosis (PVT) was more prevalent in post-DAAs HCC compared to HCV-related HCC (p= 0.001). CTP score was significantly lower in post-DAAs HCC compared to HCV-related HCC (p < .001). Post-DAAs HCC was diagnosed at later BCLC stages than HCV-related HCC. The serum AFP level was insignificantly higher in post-DAAs HCC than in HCV-related HCC. Platelets were significantly higher in post-DAAs HCC than in HCV-related HCC (p= 0.001). ALT levels were significantly lower in post-DAAs HCC compared to HCV-related HCC (p=0.02). Conclusion Post-DAAs HCC had larger size, a more diffuse pattern, and a higher rate of malignant PVT compared to HCV-related HCC. It was diagnosed at later BCLC stages but had lower CTP scores, lower ALT levels, and higher platelet counts.
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