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This research seeks to evaluate the effects of direct-acting antivirals on vascular invasion in hepatocellular carcinoma using imaging techniques.

February 12, 2026Open Access

Vascular invasion patterns in hepatocellular carcinoma following direct acting antiviral therapy: CT and MRI assessment

Key Points

This research seeks to evaluate the effects of direct-acting antivirals on vascular invasion in hepatocellular carcinoma using imaging techniques.
Conducted a case-control study with 102 patients with hepatitis C virus-related HCC.
Divided patients into two groups: one receiving direct-acting antivirals (DAA) and another not receiving treatment.
Utilized computerized tomography (CT) and magnetic resonance imaging (MRI) for assessment.
Microvascular invasion occurred in 31.37% of treated patients versus 9.8% of untreated patients.
Portal vein invasion was noted in 45.1% of treated patients compared to 17.65% in untreated patients.
Lesion sizes were significantly larger in the treated group than in the untreated group.

Abstract

Abstract Background The effects of direct-acting antivirals (DAA) on vascular invasion in hepatocellular carcinoma (HCC) remain controversial. This study aimed to assess the impact of DAA on vascular invasion of HCC via imaging by computerized tomography (CT) and magnetic resonance imaging (MRI). Methods This case–control study was conducted on 102 consecutive proven patients with hepatitis C virus (HCV) related HCC. Patients were divided into two equal groups; of whom 51 received DAAs agents (group I, treated), while 51 patients not received DAA agents (group II, not treated). Group I received two different regimens of DAA agents, 12 weeks of sofosbuvir (400 mg)/velpatasvir (100 mg) (27 patients) and 12 weeks of sofosubuvir 400 g/daclatasvir 60 g (24 patients). Results Microvascular invasion (MVI) occurred in 16 (31.37%) patients in group I, and 5 (9.8%) patients in group II. Portal vein invasion occurred in 23 (45.1%) patients in group I, and 9 (17.65%) patients in group II. The rate of both microvascular and portal vein invasions was significantly higher in group I than in group II ( P = 0.01) and ( P = 0.003), respectively. Size of lesions was significantly higher in group I than group II ( P < 0.001) and site of lesions was significantly different between both groups 9bilopar was higher in group I) ( P < 0.001). Number of focal lesions was insignificantly different between both groups. Regarding enhancement pattern, the rate of peripheral and homogenous enhancement was similar in both groups ( P = 0.092) and ( P = 0.618), respectively. But heterogeneous and no enhancement were significantly important between both groups ( P < 0.001) and ( P < 0.001), respectively. Group I was associated with more nodal deposits ( P = 0.002) and pulmonary deposits ( P = 0.046) compared to the other group. The rate of bone deposits was similar in both groups ( P = 0.715). Conclusions DAAs agents were associated with differences in the characteristics and distribution of HCC. DAAs were associated with an increase in the rate of microvascular and portal vein invasions, lesion size, and presence of nodal and pulmonary deposits.

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