Considerations about the use of antivirals in patients with primary biliary cholangitis and hepatitis B virus early infection

Rodríguez-Orozco, Alain R.

doi:10.1016/j.medcli.2020.06.053

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Rodríguez-Orozco" "autores" => array:1 [ 0 => array:4 [ "nombre" => "Alain R." "apellidos" => "Rodríguez-Orozco" "email" => array:1 [ 0 => "alain.rodriguez@umich.mx" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:2 [ "etiqueta" => "b" "identificador" => "aff0010" ] ] ] ] "afiliaciones" => array:2 [ 0 => array:3 [ "entidad" => "Faculty of Medicine and Biological Sciences “Dr. Ignacio Chávez”, University of San Nicolás de Hidalgo, Morelia, Mexico" "etiqueta" => "a" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Instituto de Investigación Científica en Temas de Familia, Alergia e Inmunología, Morelia, Mexico" "etiqueta" => "b" "identificador" => "aff0010" ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Consideraciones sobre el empleo de antivirales en pacientes con colangitis biliar primaria e infeccion inicial por virus de la hepatitis B" ] ] "textoCompleto" => "There are many factors implicated in the autoimmune damage progression in patients with previous primary biliary cholangitis (PBC) and early Hepatitis B viral infection such as the generation of autoantibodies, biliary innate immune response via dsRNA-recognizing receptors, upregulation of the expression of certain molecules mediated by interferon gamma and tumor necrosis factor and upregulation of NF-kappa B induced by pathogen-associated molecular patterns,<a class="elsevierStyleCrossRef" href="#bib0030">1</a> endogenous retroviral protein acting as autoantigens and stimulation of inflammatory citokines as interleukine 6. TLRs (Toll-like receptors) are involved in the pathogenesis and progression of autoimmune liver disease and TLR-mediated immune response are able to downregulate HBV replication and pathogens have developed strategies to suppress or evade the TLR system in the liver.<a class="elsevierStyleCrossRef" href="#bib0035">2</a> Then TLR gene polymorphisms may play a role in development of HBV-related severe liver diseases. Based on the molecular mimicry hypothesis, viral proteins that are similar to the liver autoantigens can induce immune cross reactions. The aim of these study was to report a case of a woman with primary biliary cholangitis and severe acute infection with HBV in which the early use of tenofovir lead to the elimination of the virus and to stop the progression to liver failure and limiting cholangitis.A 35-year-old Mexican woman with previous diagnosis of PBC two years ago confirmed by biopsy, and history of promiscuity, who lived with a high socioeconomic level, presented skin and eye jaundice, asthenia, diffuse abdominal pain, itching and nausea, aspartate aminotransferase 184IU/L, alanine aminotransferase 128IU/L, ASAT/ALAT ratio=1.4375, total bilirubin 4.45mg/dL, alkaline phosphatase 309IU/L, prolonged prothrombin time (18.6s, 1.7 times above the control, prothrombin concentration (50%), International Normalized Ratio of 1.8, albumin (2.6g/dL), (41,000platelets/mm3), antinuclear antibodies 1:640, anti-mitochondrial antibodies 1:160, Anti-mitochondrial M2 antibodies 241.8ue. Child Pugh score 9, F3 fibrosis score (FibroScan), hepatitis B virus core antigen 2.1ue (positive), IgG antibodies against hepatitis B virus core antigen<0.4eu (negative), Hepatitis B surface antigen 0.02ui (negative), Anti-Antigen S hepatitis B virus antibodies 0.0ui (negative), total antibodies against hepatitis C virus negative and HIV virus negative. The diagnosis of primary biliary cholangitis and Hepatitis B early infection was made. For treatment, it was ordered 15mg/kg/day of ursodeoxycholic acid and 300mg of tenofovir daily and fat-soluble vitamins and calcium as nutritional supplements. The use of the antiviral was discussed with the patient and accepted by her. Maximum HBV DNA load was 92,000IU/mL. Ten months later, complete virological suppression was reached defined by HBV DNA load<20IU/ml, and the following results were reported antinuclear antibodies 1:160, anti-mitochondrial antibodies 1:80, Anti-mitochondrial M2 antibodies 169.8ue, aspartate aminotransferase 64IU/L alanine aminotransferase 53IU/L ASAT/ALAT ratio=1.2075, total bilirubin 1.45mg/dL and F3 fibrosis score (FibroScan).The patients with fulminant hepatitis who show positive serum anti-HBc IgM antibodies due to HBV infection appear to be not an uncommon finding.<a class="elsevierStyleCrossRef" href="#bib0040">3</a> There are several reports that show the effects of hepatotrophic viruses on autoinmune liver disease appearance and exacerbation. For example, inhibiting and/or eradicating hepatitis C virus (HCV) and the hepatitis B (HBV) viral replication with direct-acting antivirals would remove specific stimulation of host immunity in a previous immunosuppressed host.<a class="elsevierStyleCrossRef" href="#bib0045">4</a> The use of direct antivirals could be effects upon autoantibody production. This strategy has been used in patients with HCV infection and previous autoinmune liver diseases but there is not consensus in patients with HBV infection and autoinmune liver diseases.Chronic hepatitis viruses, mainly hepatitis C virus infection has been linked to the development of autoimmunity but the use of antivirals could be effects limiting cholangitis.<a class="elsevierStyleCrossRef" href="#bib0050">5</a> The addition of antivirals in patients with primary biliary cholangitis and HBV early infection should be highly influenced by a complete evaluation of the immunological profile, liver function, comorbidities and life style to considerer the risk of progression to fulminant hepatitis and/or liver failure. Studies with larger cohorts are required, but it will be difficult to do so it is difficult to find a representative number of patients, that is why the doctor's decisions with the patient will continue to determine therapeutic behavior.FundingNone.Conflict of interestThe author declares that he has no conflict of interest." "textoCompletoSecciones" => array:1 [ "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Funding" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Conflict of interest" ] 2 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "The author read the instruction for authors and he is agreed with the submitted version of the paper, and all who have been acknowledged as contributors or as providers of personal communications have agreed to their inclusion. The material is original and it has been neither published elsewhere nor submitted for publication simultaneously and in case of acceptance, the paper will not be published elsewhere." ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0030" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Interferon gamma accelerates NF-kappaB activation of biliary epithelial cells induced by Toll-like receptor and ligand interaction" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:3 [ 0 => "K. Harada" 1 => "K. Isse" 2 => "Y. 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Mason" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Rev Port Cardiol" "fecha" => "2011" "volumen" => "13" "paginaInicial" => "101" "paginaFinal" => "107" ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/00257753/0000015700000005/v1_202108280531/S0025775320305509/v1_202108280531/en/main.assets" "Apartado" => array:4 [ "identificador" => "66430" "tipo" => "SECCION" "es" => array:2 [ "titulo" => "Cartas al Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "es" ] "PDF" => "https://static.elsevier.es/multimedia/00257753/0000015700000005/v1_202108280531/S0025775320305509/v1_202108280531/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0025775320305509?idApp=UINPBA00004N"]

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