Effect of direct-acting antiviral drugs on portal circulation hemodynamics in cirrhotic patients infected with HCV

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Abstract

Background: Liver cirrhosis (LC) is the most common cause of portal hypertension. In chronic hepatitis C patients who are treated with direct-acting antiviral therapy (DAAS), the progression of cirrhosis can be reversed with treatment. Portal hypertension is also expected to improve with a virological response. Aim: To evaluate the effect of direct-acting antiviral therapy on portal circulation hemodynamics in cirrhotic patients infected with HCV. Methods: This study included 78 consecutive patients with chronic HCV-related liver disease. They were treated by a sofosbuvir-based regimen in combination with daclatasavir. All patients were subjected to routine investigations (complete blood count, liver and renal function tests), hepatitis B surface antigen, α feto protein, PCR of HCV RNA, imaging (abdominal ultrasound and colored Doppler and duplex examination for the assessment portal hypertension) before starting treatment and after 1 year. Results: There was a significant improvement in Doppler parameters such as portal vein (PV) diameter, PV velocity, PV cross-sectional area, portal congestive index, splenic vein diameter, and spleen span; the decrease in portal pressure occur in about 55% of the patients; several factors are associated with non-response as a history of bilharziasis, patients from a rural area, presence of splenomegaly and varices, low HB level, low platelet count, and high level of fibrosis. Conclusion: Sustained virological response to direct-acting antiviral therapy is associated with a reduction in portal pressure in patients with liver cirrhosis and clinically significant portal hypertension.

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Hassnine, A. A., Soliman, W., Elsayed, A. M., Higazi, M. M., Saied, M., & Abdelraheem, E. M. (2022). Effect of direct-acting antiviral drugs on portal circulation hemodynamics in cirrhotic patients infected with HCV. Egyptian Liver Journal, 12(1). https://doi.org/10.1186/s43066-022-00181-4

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