ASSOCIATION BETWEEN HEPATITIS B AND C WITH HEPATOCELLULAR CARCINOMA: A LITERATURE REVIEW

• Autor(a) principal: do Monte, Larissa Emilly Fiusa
• Data de Publicação: 2021
• Outros Autores: Barroso, Vanessa Ferreira, Simão, Isabela Coelho, Cavalcante, Karyne Costa, Pinheiro, Claudio Vinicius Araujo, de Figueiredo, Viviane Melo e Silva, Carneiro, Juliana Ramos, Leal, Plínio da Cunha
• Tipo de documento: Artigo
• Idioma: por; eng
• Título da fonte: Revista Uningá (Online)
• Texto Completo: https://revista.uninga.br/uninga/article/view/3954
• topic: Adulto; Fatores de risco; Hepatite B crônica; Hepatite C crônica; Neoplasia hepática; Hepatite B e C; Carcinoma; Adult; Chronic hepatitis B; Chronic hepatitis C; Liver neoplasm; Risk factors; Hepatitis B and C; Carcinoma

Hepatocellular carcinoma (HCC) is one of the most frequently diagnosed neoplasms. In addition, infection with hepatitis B virus (HBV) and hepatitis C virus (HCV) is associated with the development of HCC, although more genetic and pathophysiological studies are needed to consolidate the relationship. Thus, the aim of this study was to understand the association between HBV and HCV with HCC, and the association that can be established between antiviral therapy for HBV and HCV with this neoplasm. Therefore, a careful review of the literature published between 2016 and 2021 was developed in the databases of VHL and PubMed in Portuguese, English and Spanish. After applying filters and exclusion criteria, 21 articles were included in this review. In summary, the accumulation of mutations of the hepatitis B virus is inherently linked to the acceleration of the development of neoplasm. However, the association between PNPLA3 polymorphism rs738409 and HCC related to HCV is controversial in patients with cirrhosis. In addition, alpha-fetoprotein is the most used biomarker for HCC surveillance, but it has inadequate sensitivity and specificity, while prothrombin induced by vitamin K absence-II and Golgi protein 73 are more effective due to the reduction of false positive levels. Moreover, antiviral therapy with nucleotide analogues inhibits HBV replication, interfering with hepatocellular carcinogenesis. In relation to HCV, direct antiviral therapy reduces the risk of neoplasia because it presents high levels of sustained virological response.