Hepatites virais: B, C e D: atualização / Viral hepatitis: B, C and D: an update

JUSTIFICATIVA E OBJETIVOS: As hepatites causadas pelos vírus da hepatite B (VHB), vírus da hepatite C (VHC) e vírus da hepatite (VHD) têm como aspecto comum a transmissão por via parenteral e a possibilidade de cronificação. Revisar os aspectos clínico-epidemiológicos, diagnósticos, terapêuticos e profiláticos das infecções virais por tais agentes é o escopo do presente artigo. Realizou-se pesquisa bibliográfica nas bases de dados Scielo e Pubmed empregando-se os descritores hepatite B (hepatitis B); hepatite C (hepatitis C); hepatite D (hepatitis D) e hepatite G (hepatitis G), assim como livros texto, consensos e diretrizes relacionadas ao tema.CONTEÚDO: As formas agudas das hepatites B, C e D são usualmente benignas, podendo, sem embargo, ocorrerem quadros de hepatite fulminante. Em situações nas quais o sistema imunológico não é capaz de depurar o VHB e/ou VHC, há cronificação da infecção, com risco de desenvolvimento de cirrose e consequente insuficiência hepática crônica, bem como carcinoma hepatocelular. As hepatites B e D são imunopreveníveis, graças à vacina parao vírus B, mas, até o momento, não há imunoprofilaxia disponível para o vírus C.CONCLUSÃO: As hepatites pelos VHB e VHC constituem importantes desafios para a medicina atual, especialmente pela prevalência das infecções no planeta e pelo risco de desenvolvimento das complicações crônicas. Neste contexto, destaque-se a importância da avaliação diagnóstica, da instituição da terapêutica adequada e do emprego das medidas preventivas para tais infecções, elementos que devem ser solidamente conhecidas pelo clínico.

BACKGROUND AND OBJECTIVES: Hepatitis caused by hepatitis B virus (HBV), hepatitis C virus (HCV) and hepatitis D virus (HDV) have in common the transmission by parenteral route and the possibility of chronification. Reviewing the clinic, epidemiology, diagnose, therapeutics and prophylaxis of viral infections by these agents is the scope of this work. Bibliographic research was conducted both at databases Scielo and Pubmed through the chosen descriptors: hepatitis B, hepatitis C, hepatitis D and hepatitis G, and text books, consensus and guidelines related to the subject.CONTENTS: The acute viral B, C and D hepatitis are usually benign, though acute liver failure, fulminant hepatitis, may occur. In the cases when the immune system is unable to debug HBV and HCV the infection becomes chronic, cirrhosis with consequent chronic liver insufficiency and hepatocellular carcinomamay develop. HBV and HDV are immunopreventable, thanks to the hepatitis B virus vaccine, but at this point there's no immunoprophylaxis available for hepatitis C virus. CONCLUSION: HBV and HCV hepatitis are great challenges for medicine, particularly due to the prevalence of infections worldwide and the risk of chronic complications. In this context, diagnostic evaluation, adequate therapeutic care, and preventive measures must be soundly known by the physician.

Epidemiology and long-term consequences of hepatitis delta virus infection in the Yucpa Indians of Venezuela.

To define better the epidemiology and clinical impact of hepatitis delta virus (HDV) infection among hepatitis B virus (HBV) carriers in less developed countries, the authors prospectively studied a cohort of 216 Yucpa Indian HBV carriers in Venezuela. HBV carriers were followed regularly between 1983 and 1988 by physical examination, laboratory testing for liver enzymes and HBV and HDV markers, and epidemiologic history. Among the cohort, 74 (34%) were initially positive for HDV infection, and 35 additional persons became infected during the study. Risk factors for new HDV infection included living in southern Yucpa villages; being young adults (15-19 years) or young children (1-9 years), and living in a household with a person with acute HDV infection. Persons with HDV infection were at high risk of developing chronic liver disease; 56% of HDV-infected persons had moderate-to-severe chronic liver disease at the end of the study compared with none of the HBV carriers without HDV infection. Mortality rates were 6.9% and 8.8% per year, respectively, among initially HDV-positive HBV carriers and those with new HDV infection, because of rapidly progressive chronic liver disease and fulminant hepatitis; mortality was significantly lower in HBV carriers without HDV infection and in non-HBV carriers. HDV superinfection is a devastating disease in HBV carriers in tropical South America. Prevention of HBV infection with hepatitis B vaccine is the best available tool to reduce the impact of this problem.

Hepatitis viral delta

The etiologic agent of this severe form of hepatitis was identified by Rizzetto et al in Italy in 1977. The Delta virus resembles satellite viruses of plants which can not replicate without another specific virus. In this particular case hepatitis B virus is the helper agent. Clinically this form of hepatitis is characterized by two presentations: coinfeccion, which means simultaneous infection of a host with hepatitis B virus and hepatitis D virus. This variety of hepatitis can present with two distinct peaks of transaminases and usually resolves completely in most of the cases, however 0-4 percent can evolve to chronic hepatitis and 25 percent of the cases of fulminant hepatitis are due to this viral association. The diagnosis can be established demonstrating anti-HDV IgM or HDV-RNA or HDV antigen in the serum. In essence coinfection makers acute hepatic failure more common and the mortality is significantly higher than hepatitis B infections by itself. The second type of clinical presentation is superinfection, which means infection with the Delta virus of a patient previously infected with the hepatitis B virus (healthy carrier). Initially the patient develop a typical acute viral hepatitis in 50-70 percent of the cases, and 30-50 percent can have asymptomatic infection. The real problem with this presentation is that 20-90 percent of the cases evolved to chronicity: chronic active hepatitis and cirrhosis. The diagnosis can be made demonstrating anti-HDB IgM and anti-HDV IfG, although this last one is usually transitory. A liver biopsy can show HDV RNA or HDV antigen using special immunostainings...