P-0074 The Influence of Hepatitis D Virus in the Occurrence of Hepatocellular Carcinoma (HCC)

Abstract

IntroductionThe natural course of HDV liver infection is still under evaluation. Some authors suggest that the ability of HDV to suppress HBV replication, known as promoter of hepatic carcinogenesis, could represent a protective mechanism to lower the risk of HCC development in case of co-infection. Conversely, there are data demonstrating that patients with florid infections from both HBV and HDV could develop HCC more frequent and at a younger age than those infected by HBV alone, indicating that HDV infection causes HCC possibly indirectly by inducing inflammation and cirrhosis. We aimed to investigate the influence of hepatitis D virus in the occurrence of HCC compared to HBV monoinfection in southeast of Romania. MethodsWe compared the clinical features of 38 patients diagnosed with HCC and HVB-HVD co-infection and we compared results with a control group of 38 patients with HCC and HBV monoinfection. We noted the demographic data (age, sex, BMI) the presence of underlying cirrhosis and the Child-Pugh classification, the history of antiviral treatment, the viral loads, the tumor markers (AFP) and the tumor features (multiple, TNM classification). ResultsThe age of patients diagnosed with HCC and co-infection was significantly younger than those of the control group (58.2±4.1 vs.63.28±9.61, p=0.032, CI 95% 12.35-33.78.). The presence of cirrhosis correlated better with co-infection rather than monoinfection (p=0.002, CI 95% 34.251-78.377) and the Child-Pugh classification showed a more frequent presence of stages B and C in patients with HCC and co-infection than in controls (p=0.028 and p=0.033). The antiviral treatment with interferons didn't reveal any influence in HCC clinical course in co-infected patients, while in patients with monoinfection, the history of nucleoside/tide analogues showed to be protective (p=0.040). HBV monoinfected patients with high viral loads>106 correlated better with the occurrence of HCC compared to patients with mono and co-infections with low viral loads. Also high viral loads of both viruses correlated better with the presence of HCC (p=0.005) Alpha-fetoprotein level >200 IU/mL was more common in controls (p= 0.044) and didn't correlate with HVD infection. TNM classification showed more stage III-IV in HBV monoinfected patients (p=0.009). ConclusionThe younger age detected in our patients, the presence of decompensate underlying cirrhosis (stages Child B/C), the absence of response to treatment and earlier TNM stage confirm that HDV infection causes accelerated and more severe necroinflammation, fibrosis and earlier cirrhosis, mechanisms through which HVD increases the risk of HCC occurrence.