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  • 1.
    Bruggmann, P.
    et al.
    Arud Ctr Addict Med, Zurich, Switzerland.
    Berg, T.
    Univ Leipzig, Leipzig, Germany.
    Ovrehus, A. L. H.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Moreno, C.
    Erasme Univ Hosp, Univ Libre Brussels, Brussels, Belgium.
    Brandao Mello, C. E.
    Dept Gastroenterol, Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
    Roudot-Thoraval, F.
    Dept Sante Publ, Hop Henri Mondor, Creteil, France.
    Marinho, R. T.
    Ctr Hosp Lisboa Norte, Dept Gastroenterol, Hosp Santa Maria,Lisbon, Portugal.
    Sherman, M.
    Toronto Gen Hosp, Univ Hlth Network, Univ Toronto, Toronto, Canada.
    Ryder, S. D.
    Nottingham Univ Hosp NHS Trust, Nottingham, England; Biomed Res Unit, Nottingham, England.
    Sperl, J.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Akarca, U.
    Ege Univ, Izmir, Turkey.
    Balik, I.
    Ankara Univ, Ankara, Turkey.
    Bihl, F.
    Dept Gastroenterol, Osped Cantonale, Bellinzona, Switzerland.
    Bilodeau, M.
    Dept Med, Liver Unit, Univ Montreal, Montreal, Canada.
    Blasco, A. J.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Buti, M.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Valle De Hebron, Barcelona, Spain.
    Calinas, F.
    Dept Gastroenterol, Ctr Hosp Lisboa Cent, Hosp Santo Antonio Capuchos, Lisbon, Portugal.
    Calleja, J. L.
    Hosp Puerta Hierro, Madrid, Spain.
    Cheinquer, H.
    Hosp Clin, Univ Fed Rio Grande do Sul, Porto Alegre RS, Brazil.
    Christensen, P. B.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Clausen, M.
    Region Hosp Hovedstaden, Region Hovedstaden, Hillerød, Denmark.
    Coelho, H. S. M.
    Dept Clin Med, Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
    Cornberg, M.
    Dept Gastroenterol Hepatol & Endocrinol,Hannover Med Sch, Hannover, Germany; German Liver Fdn, Hannover, Germany.
    Cramp, M. E.
    Peninsula Schools Med & Dent, Univ Plymouth, Plymouth, England.
    Dore, G. J.
    Kirby Inst, Univ New S Wales, Sydney NSW, Australia.
    Doss, W.
    Cairo Univ, Cairo, Egypt.
    Duberg, Ann-Sofi
    Örebro University, School of Medicine, Örebro University, Sweden. Örebro University Hospital. Dept Infect Dis, Örebro University Hospital, Örebro, Sweden.
    El-Sayed, M. H.
    Ain Shams Univ, Cairo, Egypt.
    Ergor, G.
    Dokuz Eylul Univ, Izmir, Turkey.
    Esmat, G.
    Cairo Univ, Cairo, Egypt.
    Estes, C.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Falconer, K.
    Infect Dis Unit, Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden.
    Felix, J.
    Exigo Consultores, Alhos Vedros, Portugal.
    Ferraz, M. L. G.
    Div Gastroenterol, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Ferreira, P. R.
    Div Infect Dis, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Frankova, S.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Garcia-Samaniego, J.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Carlos III, Madrid, Spain.
    Gerstoft, J.
    Univ Copenhagen, Copenhagen, Denmark.
    Giria, J. A.
    Direccao Geral Saude, Lisbon, Portugal.
    Goncales, F. L., Jr.
    Fac Ciencias Med, UNICAMP,Dept Clin Med, Grp Estudo Hepatites,Disciplina Doencas Infeccios, Univ Estadual Campinas, Sao Paulo, Brazil.
    Gower, E.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Gschwantler, M.
    Dept Internal Med 4, Wilhelminenspital Stadt Wien, Vienna, Austria.
    Guimaraes Pessoa, M.
    Sch Med, Div Gastroenterol & Hepatol, Univ Sao Paulo, Sao Paulo, Brazil.
    Hezode, C.
    Serv Hepatogastroenterol, Hop Henri Mondor, Creteil, France.
    Hofer, H.
    Dept Internal Med 3, Div Gastroenterol & Hepatol, Med Univ Vienna, Vienna, Austria.
    Husa, P.
    Clin Infect Dis, Univ Hosp Brno, Masaryk Univ, Brno, Czech Republic.
    Idilman, R.
    Dept Gastroenterol, Sch Med, Ankara Univ, Ankara, Turkey.
    Kåberg, M.
    Infect Dis Unit, Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden.
    Kaita, K. D. E.
    Dept Internal Med, Sect Hepatol, Univ Manitoba, Winnipeg MB, Canada; Viral Hepatitis Invest Unit, Hlth Sci Ctr, Winnipeg MB, Canada.
    Kautz, A.
    European Liver Patients Assoc, St Truiden, Belgium.
    Kaymakoglu, S.
    Istanbul Univ, Istanbul, Turkey.
    Krajden, M.
    British Columbia Ctr Dis Control, Univ British Columbia, Vancouver, Canada.
    Krarup, H.
    Dept Med Gastroenterol, Aalborg Univ Hosp, Aalborg, Denmark; Sect Mol Diagnost, Aalborg Univ Hosp, Aalborg, Denmark.
    Laleman, W.
    Univ Hosp Leuven, Katholieke Univ Leuven, Louvain, Belgium.
    Lavanchy, D.
    Lazaro, P.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Marotta, P.
    Div Gastroenterol, Univ Western Ontario, London ON, Canada.
    Mauss, S.
    Univ Dusseldorf, Dusseldorf, Germany.
    Mendes Correa, M. C.
    Sch Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Muellhaupt, B.
    Swiss HPB Hepatopancreatobiliary Ctr, Univ Zurich Hosp, Zurich, Switzerland; Dept Gastroenterol & Hepatol, Univ Zurich Hosp, Zurich, Switzerland.
    Myers, R. P.
    Liver Unit, Div Gastroenterol & Hepatol, Univ Calgary, Calgary AB, Canada.
    Negro, F.
    Div Gastroenterol & Hepatol, Univ Hosp, Geneva, Switzerland; Div Clin Pathol,Univ Hosp, Geneva, Switzerland.
    Nemecek, V.
    Natl Reference Lab Hepatitis, Natl Inst Publ Hlth, Prague, Czech Republic.
    Ormeci, N.
    Ankara Univ, Ankara, Turkey.
    Parkes, J.
    Univ Southhampton, Southampton, England.
    Peltekian, K. M.
    Dept Med, Halifax, NS, Canada; Dept Surg, Dalhousie Univ, Halifax, Canada; Serv Hepatol, Queen Elizabeth II Hlth Sci Ctr, Capital Dist Hlth Author, Halifax NS, Canada.
    Ramji, A.
    Dept Gastroenterol, Univ British Columbia, Vancouver, Canada.
    Razavi, H.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Reis, N.
    Assembleia Republ, Lisbon, Portugal.
    Roberts, S. K.
    Alfred Hosp, Melbourne Vic, Australia; Monash Univ, Melbourne, Australia.
    Rosenberg, W. M.
    Inst Liver & Digest Hlth, Div Med, University College London (UCL), London, England.
    Sarmento-Castro, R.
    Dept Infect Dis, Ctr Hosp Porto, Oporto, Portugal.
    Sarrazin, C.
    JW Goethe Univ Hosp, Frankfurt, Germany.
    Semela, D.
    Div Gastroenterol & Hepatol, Cantonal Hosp St Gallen, St Gallen, Switzerland.
    Shiha, G. E.
    Egyptian Liver Res Inst & Hosp ELRIAH, Dakahliah, Egypt.
    Sievert, W.
    Monash Univ, Melbourne, Australia; Monash Hlth, Melbourne Vic, Australia.
    Starkel, P.
    Clin Univ St Luc, Catholic Univ Louvain, Brussels, Belgium.
    Stauber, R. E.
    Dept Internal Med, Div Gastroenterol & Hepatol, Med Univ Graz, Graz, Austria.
    Thompson, A. J.
    Dept Gastroenterol, St Vincents Hosp, Melbourne Vic, Australia; Univ Melbourne, Melbourne Vic, Australia.
    Urbanek, P.
    Dept Internal Med, Fac Med 1, Charles Univ Prague, Prague, Czech Republic; Cent Mil Hosp, Prague, Czech Republic.
    van Thiel, I.
    St Truiden, Belgium; Deutsch Leberhilfe eV, European Liver Patients Assoc, Cologne, Germany.
    Van Vlierberghe, H.
    Ghent Univ Hosp, Ghent, Belgium.
    Vandijck, D.
    Ghent Univ Hosp, Ghent, Belgium; Univ Ghent, Ghent, Belgium; Dept Hlth Econ & Patient Safety, Hasselt Univ, Diepenbeek, Belgium.
    Vogel, W.
    Med Univ Innsbruck, Innsbruck, Austria.
    Waked, I.
    Natl Liver Inst, Menoufia, Egypt.
    Wedemeyer, H.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany; German Liver Fdn, Hannover, Germany.
    Weis, N.
    Copenhagen Univ Hosp, Hvidovre, Denmark.
    Wiegand, J.
    Univ Leipzig, Leipzig, Germany.
    Yosry, A.
    Cairo Univ, Cairo, Egypt.
    Zekry, A.
    St George Hosp Clin Sch Med, Univ New S Wales, Sydney NSW, Australia; Sch Med Sci, Univ New S Wales, Sydney NSW, Australia.
    Van Damme, P.
    Univ Antwerp, Antwerp, Belgium.
    Aleman, S.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Dept Gastroenterol & Hepatol Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden.
    Hindman, S. J.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Historical epidemiology of hepatitis C virus (HCV) in selected countries2014In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 21, p. 5-33Article in journal (Refereed)
    Abstract [en]

    Chronic infection with hepatitis C virus (HCV) is a leading indicator for liver disease. New treatment options are becoming available, and there is a need to characterize the epidemiology and disease burden of HCV. Data for prevalence, viremia, genotype, diagnosis and treatment were obtained through literature searches and expert consensus for 16 countries. For some countries, data from centralized registries were used to estimate diagnosis and treatment rates. Data for the number of liver transplants and the proportion attributable to HCV were obtained from centralized databases. Viremic prevalence estimates varied widely between countries, ranging from 0.3% in Austria, England and Germany to 8.5% in Egypt. The largest viremic populations were in Egypt, with 6358000 cases in 2008 and Brazil with 2106000 cases in 2007. The age distribution of cases differed between countries. In most countries, prevalence rates were higher among males, reflecting higher rates of injection drug use. Diagnosis, treatment and transplant levels also differed considerably between countries. Reliable estimates characterizing HCV-infected populations are critical for addressing HCV-related morbidity and mortality. There is a need to quantify the burden of chronic HCV infection at the national level.

  • 2.
    Büsch, Katharina
    et al.
    AbbVie AB, Stockholm, Sweden; Department of Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Waldenström, Jesper
    Department of Infectious Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Lagging, Martin
    Department of Infectious Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Aleman, Soo
    Department of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Weiland, Ola
    Department of Medicine Huddinge, Division of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Kövamees, Jan
    AbbVie AB, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Health Sciences. Department of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Söderholm, Jonas
    AbbVie AB, Stockholm, Sweden; Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Prevalence and comorbidities of chronic hepatitis C: a nationwide population-based register study in Sweden2017In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 52, no 1, p. 61-68Article in journal (Refereed)
    Abstract [en]

    Purpose: The aim of this study was to estimate the prevalence of physician-diagnosed and registered chronic hepatitis C (CHC), and to estimate the reported frequencies of Charlson comorbidities compared with matched comparators from the general population.

    Materials and methods: Patients were identified according to ICD codes for CHC in the Swedish National Patient Register (1997-2013). Prevalence was estimated according to different patient identification algorithms and for different subgroups. Charlson comorbidities were ascertained from the same register and compared with age/sex/county of residence matched general population comparators.

    Results: A total of 34,633 individuals with physician-diagnosed CHC were alive in Sweden in 2013 (mean age, 49 years; 64% men), corresponding to a physician-diagnosed prevalence of 0.36%. The prevalence varied by case definition (0.22%-0.36%). The estimate dropped to 0.14% for monitored CHC disease (defined as ≥1 CHC-related visit in 2013). Overall, 41.3% of the CHC patients had ≥1 physician-registered Charlson comorbidity; the most common was liver diseases (22.1%). Compared with matched comparators from the general population (n = 171,338), patients with CHC had more physician-diagnosed and registered diseases such as chronic pulmonary disease (10.2% vs. 4.0%), diabetes (10.6% vs. 5.5%) and liver-related cancer (1.3% vs. 0.2%; all p < .01). No information on behavioural factors, such as smoking, alcohol consumption or on-going illicit drug use, was available.

    Conclusion: The physician-diagnosed prevalence of CHC was slightly lower than previously reported estimates, and varied by case definition. The additional comorbidities observed in the CHC group should be taken into consideration, as these comorbidities add to the disease burden.

  • 3.
    Davídsdóttir, Lóa
    et al.
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Duberg, Ann-Sofi
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden .
    Törner, Anna
    Department of Epidemiology, Swedish Institute for Infectious Disease Control, Solna, Sweden .
    Aleman, Soo
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Bäck, Erik
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden .
    Ekdahl, Karl
    European Centre for Disease Prevention and Control (ECDC), Stockholm, Sweden.
    Blaxhult, Anders
    Department of Epidemiology, Swedish Institute for Infectious Disease Control, Solna, Sweden .
    Ekbom, Anders
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Solna, Sweden .
    Hultcrantz, Rolf
    Department of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden .
    Hepatocellular carcinoma in individuals with HBV infection or HBV-HCV co-infection in a low endemic country2010In: Scandinavian journal of gastroenterology, ISSN 1502-7708, Vol. 45, no 7-8, p. 944-952Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: The aim of this nationwide cohort study was to assess the risk for hepatocellular carcinoma (HCC) in patients with chronic hepatitis B virus (HBV) infection or HBV and hepatitis C virus (HCV) co-infection in Sweden, a low endemic country.

    MATERIAL AND METHODS: A total of 12,080 patients with HBV and 3238 patients with HBV-HCV co-infection were notified to the Swedish institute for Infectious Disease Control between 1990 and 2004. After excluding 1850 patients with acute HBV and 584 patients infected in adult life, we analyzed the cohort of 9646 subjects with chronic HBV infection. In the co-infection cohort, 1697 patients were analyzed after excluding 1541 cases with acute HBV. The Swedish national cancer registry was used for follow-up. The HCC incidence rate in the cohorts was compared with the HCC incidence rate in the general population and the standardized incidence ratio (SIR) was calculated for different strata according to estimated infection period.

    RESULTS: HCC was found in 45 patients in the HBV cohort. In the stratum of 40-49 years of infection we found a SIR of 47 and in stratum 50-59 years the SIR was 54. In the co-infected cohort 10 HCCs were found. The SIR in the stratum 20-29 years of infection was 34 and the SIR in the stratum 30 years and over was 91.

    CONCLUSIONS: This national cohort study of HBV infected and HBV-HCV co-infected subjects in a low endemic country confirms a highly increased risk of liver cancer compared to the general population.

  • 4.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Universitetssjukhuset i Örebro, Örebro, Sweden.
    Bakterie- och parasitorsakade leversjukdomar2016In: Gastroenterologi och Hepatologi / [ed] Greger Lindberg, Henry Nyhlin, Lund: Studentlitteratur AB, 2016, 1, p. 253-256Chapter in book (Other academic)
  • 5.
    Duberg, Ann-Sofi
    Örebro University, School of Health and Medical Sciences.
    Hepatitis C virus infection: a nationwide study of associated morbidity and mortality2009Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    The hepatitis C virus (HCV) was characterised in 1989. HCV was transmitted through transfusion of blood/blood products, but injection drug use is now the most common route of transmission. The infection is usually asymptomatic but becomes chronic in about 75%, and in 20 years 15-25% develops liver cirrhosis, with a risk for liver failure and liver cancer. HCV has also been associated with lymphoproliferative disorders. The aim of this thesis was to study morbidity and mortality in a national, population-based cohort of HCV-infected individuals. The study population consisted of all persons with a diagnosed HCV-infection recorded in the national surveillance database. This file was linked to other national registers to obtain information of emigration, deaths, cancers, and inpatient care. All personal identifiers were removed before analysis.

    In Paper I the standardized incidence ratios (SIR) for Hodgkin’s and non-Hodgkin’s lymphoma (NHL), multiple myeloma, acute and chronic lymphatic leukaemia, and thyroid cancer were studied. In the HCV-cohort (n: 27,150) there was a doubled risk for NHL and multiple myeloma in patients infected for more than 15 years, compared with the general population (age-, sex- and calendar-year specific incidence rates). The results strengthened these earlier controversial associations.

    The SIR and also the absolute risk for primary liver cancer were estimated in Paper II. In the HCV-cohort (n: 36,126) the individuals infected for more than 25 years had a more than 40 times increased risk for liver cancer compared with the general population. The absolute risk of primary liver cancer was 7% within 40 years of HCV-infection.

    Mortality and cause of death were studied in Paper III. The standardized mortality ratio (SMR) demonstrated a 5.8 times excess mortality in the HCV-cohort (n: 34,235) compared with the general population, and a 35.5 times excess mortality from liver disease. Deaths from illicit drugs and external reasons were common in young adults.

    Paper IV presents a study of inpatient care. The HCV-cohort (n: 43,000) was compared with a matched reference population (n: 215,000). Cox regression was used to estimate the likelihood, a hazard ratio, for admission to hospital, and frequencies and rates to estimate the total burden. In the HCV-cohort inpatient care was high and about 50% was psychiatric, often drug-related care. The likelihood for liver-related admissions was very high, and serious liver complications increased in the 2000s, indicating that HCV-associated liver disease will increase the next decade. In the 2000s, about 1000 individuals per year were treated with HCV-combination therapy.

    To conclude, the risk for NHL and multiple myeloma was doubled, and liver- and drug-related morbidity and mortality was very high in the HCV-cohort. Serious liver complications increased in the 2000s and will probably increase the coming decade.

    List of papers
    1. Non-Hodgkin's lymphoma and other nonhepatic malignancies in Swedish patients with hepatitis C virus infection
    Open this publication in new window or tab >>Non-Hodgkin's lymphoma and other nonhepatic malignancies in Swedish patients with hepatitis C virus infection
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    2005 (English)In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 41, no 3, p. 652-659Article in journal (Refereed) Published
    Abstract [en]

    The aim of this study was to evaluate the association between hepatitis C virus (HCV) infection and non-Hodgkin's lymphoma (NHL), multiple myeloma (MM), thyroid cancer (TC), chronic lymphatic leukemia (CLL), acute lymphatic leukemia (ALL), and Hodgkin's lymphoma (HL). A Swedish cohort of 27,150 HCV-infected persons notified during 1990-2000 was included in the study. The database was linked to other national registers to calculate the observation time, expressed as person-years, and to identify all incident malignancies in the cohort. The patients were stratified according to assumed time of previous HCV infection. The relative risk of malignancy was expressed as a standardized incidence ratio (SIR)-the observed number compared to the expected number. During 1990-2000 there were 50 NHL, 15 MM, 14 ALL, 8 TC, 6 CLL, and 4 HL diagnoses in the cohort. Altogether, 20 NHL, 7 MM, 5 TC, 4 CLL, 1 ALL, and 1 HL patient fulfilled the criteria to be included in the statistical analysis. The observation time was 122,272 person-years. The risk of NHL and MM was significantly increased in the stratum with more than 15 years of infection (SIR 1.89 [95% CI, 1.10-3.03] and 2.54 [95% CI, 1.11-5.69], respectively). The association was not significant in TC or CLL. In conclusion, we report the incidence of several malignancies in a nationwide cohort of HCV-infected persons. Although the delayed diagnosis of HCV probably has resulted in an underestimation of the risk, this study showed a significantly increased risk of NHL and MM.

    Keywords
    Hepatitis C/*complications, Humans, Leukemia; Lymphocytic; Chronic; B-Cell/etiology, Lymphoma; Non-Hodgkin/*etiology, Male, Middle Aged, Multiple Myeloma/etiology, Neoplasms, Precursor Cell Lymphoblastic Leukemia-Lymphoma/etiology, RNA; Viral/analysis, Risk Factors, Thyroid Neoplasms/etiology
    National Category
    Medical and Health Sciences
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-4743 (URN)10.1002/hep.20608 (DOI)15723449 (PubMedID)
    Available from: 2008-11-24 Created: 2008-11-24 Last updated: 2017-12-14Bibliographically approved
    2. Hepatocellular carcinoma and other primary liver cancers in hepatitis C patients in Sweden: a low endemic country
    Open this publication in new window or tab >>Hepatocellular carcinoma and other primary liver cancers in hepatitis C patients in Sweden: a low endemic country
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    2008 (English)In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 15, no 7, p. 531-537Article in journal (Refereed) Published
    Abstract [en]

    The aim of this study was to assess the risk of hepatocellular carcinoma (HCC) and other primary liver cancers (PLC) in the nationwide cohort of hepatitis C virus (HCV) infected patients in Sweden. The basis was the total HCV-cohort notified in 1990-2004, after excluding 3238 people also reported with hepatitis B, the study cohort consisted of 36 126 people contributing an observation time of 246 105 person-years. The most common route of transmission was intravenous drug use (57%). The national Cancer Registry was used for follow-up, and 354 developed PLC (mainly HCC), of whom 234 were eligible for statistical analysis. The PLC incidence in the HCV cohort was compared with the incidence in the general population, and a standardized incidence ratio (SIR) was calculated for six different strata according to estimated duration of infection. The highest relative risk, SIR: 46 (95% CI: 36-56) was found in the stratum 25-30 years with HCV infection and SIR: 40 (95% CI: 31-51) in the stratum 30-35 years with infection. In the entire community-based HCV cohort in Sweden we found a highly increased risk of liver cancer compared to the general population. The highest relative risk was among people who had been infected for more than 25 years.

    PMID: 18397224 [PubMed - indexed for MEDLINE]

    Keywords
    Carcinoma; Hepatocellular/*epidemiology/etiology/virology, Cohort Studies, Female, Hepatitis C/*complications, Humans, Liver Neoplasms/epidemiology/*etiology/virology, Male, Substance Abuse; Intravenous, Sweden/epidemiology
    National Category
    Medical and Health Sciences Infectious Medicine Microbiology in the medical area
    Research subject
    Medicine
    Identifiers
    urn:nbn:se:oru:diva-4745 (URN)10.1111/j.1365-2893.2008.00979.x (DOI)18397224 (PubMedID)
    Note
    Delat 1:e författarskap Strauss, Törner, Duberg. Part of thesis: http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-7835Available from: 2008-11-24 Created: 2008-11-24 Last updated: 2018-01-13Bibliographically approved
    3. Cause of death in individuals with chronic HBV and/or HCV infection, a nationwide community-based register study
    Open this publication in new window or tab >>Cause of death in individuals with chronic HBV and/or HCV infection, a nationwide community-based register study
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    2008 (English)In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 15, no 7, p. 538-550Article in journal (Refereed) Published
    Abstract [en]

    Studies on chronic viral hepatitis and mortality have often been made on selected populations or in high-endemic countries. The aim of this study was to investigate the causes of death and the mortality rates in the nationwide cohorts of people chronically infected with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) in Sweden, a low-endemic country. All notifications on chronic HBV infection and HCV infection 1990-2003 were linked to the Cause of Death Register. A total of 9517 people with chronic HBV infection, 34 235 people with HCV infection and 1601 with chronic HBV-HCV co-infection were included, and the mean observation times were 6.4, 6.3 and 7.9 years, respectively. The mortality in the cohorts was compared with age- and gender-specific mortality in the general population and standardized mortality ratios (SMR) were calculated. All-cause mortality was significantly increased, SMR 2.3 (HBV), 5.8 (HCV) and 8.5 (HBV-HCV), with a great excess liver-related mortality in all cohorts, SMR 21.7, 35.5 and 46.2, respectively. In HCV and HBV-HCV infected there was an increased mortality due to drug-related psychiatric diagnoses (SMR: 20.7 and 27.6) and external causes (SMR: 12.4 and 11.4), predominantly at younger age. To conclude, this study demonstrated an increased all-cause mortality, with a great excess mortality from liver disease, in all cohorts. In people with HCV infection the highest excess mortality in younger ages was from drug-related and external reasons.

    PMID: 18397223 [PubMed - indexed for MEDLINE]

    Keywords
    Carcinoma; Hepatocellular/*mortality, Cohort Studies, Female, Hepatitis B; Chronic/epidemiology/*mortality, Hepatitis C; Chronic/epidemiology/*mortality, Humans, Liver Neoplasms/etiology/*mortality, Male, Medical Record Linkage, Population Surveillance/methods, Registries
    National Category
    Medical and Health Sciences Infectious Medicine
    Research subject
    Infectious Diseases
    Identifiers
    urn:nbn:se:oru:diva-4744 (URN)10.1111/j.1365-2893.2008.00982.x (DOI)18397223 (PubMedID)
    Note
    Part of thesis: http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-7835Available from: 2008-11-24 Created: 2008-11-24 Last updated: 2017-12-14Bibliographically approved
    4. The burden of hepatitis C in Sweden: a national study of inpatient care
    Open this publication in new window or tab >>The burden of hepatitis C in Sweden: a national study of inpatient care
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    (English)Manuscript (preprint) (Other academic)
    Keywords
    Hepatitis C, hepatocellular carcinoma, psychiatric disease, epidemiology, hospitalization
    National Category
    Medical and Health Sciences Microbiology in the medical area Infectious Medicine
    Research subject
    Infectious Diseases; Medicine
    Identifiers
    urn:nbn:se:oru:diva-7869 (URN)
    Available from: 2009-09-09 Created: 2009-09-09 Last updated: 2018-01-13Bibliographically approved
  • 6.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Universitetssjukhuset i Örebro, Örebro, Sweden.
    Virushepatiter2016In: Gastroenterologi och Hepatologi / [ed] Greger Lindberg, Henry Nyhlin, Lund: Studentlitteratur AB, 2016, 1, p. 247-252Chapter in book (Other academic)
  • 7.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden. Örebro University Hospital. Department of Infectious Diseases, , Örebro University Hospital, Örebro, Sweden.
    Blach, Sarah
    Center for Disease Analysis (CDA), Louisville CO, USA.
    Falconer, Karolin
    Department of Medicine Huddinge, Division of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Kåberg, Martin
    Department of Medicine Huddinge, Division of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, , Stockholm, Sweden.
    Razavi, Homie
    Center for Disease Analysis (CDA), Louisville CO, USA.
    Aleman, Soo
    Department of Medicine Huddinge, Division of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Medicine Huddinge, Division of Gastroenterology and Hepatology, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    The future disease burden of hepatitis C virus infection in Sweden and the impact of different treatment strategies2015In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 50, no 2, p. 233-244Article in journal (Refereed)
    Abstract [en]

    Objective: Recently, new highly effective direct-acting antivirals (DAAs) against hepatitis C virus (HCV) were introduced. Whether these will alleviate the anticipated increase of liver disease burden in Sweden is unknown, partly because high costs may restrict the use. The objectives were to model the HCV epidemic in Sweden, the burden of disease, and the potential impact of different treatment strategies.

    Material and methods: HCV disease progression was modeled to 2030. Scenarios were simulated using new DAAs with sustained annual treatment rate (n = 1130), reduced treatment rate (n = 380) to maintain budget, and increased treatment rates (n = 1430 or 2260) to reduce HCV infections.

    Results: With today's triple therapies, the estimated number of serious liver complications and death are expected to peak in 2021. Using new DAAs among F0-F4 patients, an unchanged annual treatment rate can reduce the number of HCV infections by 10% by 2030; however, hepatocellular carcinoma (HCC) and mortality will remain unchanged. By reducing to 380 treatments annually and focusing on patients with advanced fibrosis (F3-F4), serious complications will remain constant but the total number of HCV infections will increase. By doubling the number of DAA treatments, HCC-incidence and liver-related deaths would decrease by 65-70% by 2030.

    Conclusion: Mortality and HCC can be reduced with new DAAs and sustained treatment uptake when restricted to F2-F4 patients, or with increased uptake in F0-F4 patients. Treatment restrictions to limit cost may reduce the positive effects and increase the burden of HCV infection. These results may be important for the future strategies of HCV management.

  • 8.
    Duberg, Ann-Sofi
    et al.
    Örebro University Hospital.
    Hansdotter, F.
    How, A. -L
    Holmström, A.
    Lesko, B.
    Angeläget med generösare provtagning för hepatit C efter blodtransfusion Socialstyrelsens nya rekommendation för riskgrupper2013In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, no 34-35, p. 1477-Article in journal (Refereed)
  • 9.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences.
    Hultcrantz, Rolf
    Misleading figures on trends in mortality from hepatocellular carcinoma in Europe2009In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 49, no 1, p. 336-336Article in journal (Refereed)
  • 10.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences.
    Janzon, R.
    Bäck, Erik
    Örebro University, School of Health and Medical Sciences.
    Ekdahl, Karl
    Blaxhult, A.
    The epidemiology of hepatitis C virus infection in Sweden2008In: Eurosurveillance, ISSN 1560-7917, Vol. 13, no 21Article in journal (Refereed)
    Abstract [en]

    In Sweden, infection with hepatitis C virus (HCV) has been a notifiable disease since 1990, when diagnostic methods became available. Blood donor screening indicated that about 0.5% of the Swedish population (9 millions) had been HCV infected. Here we present the Swedish hepatitis C epidemic based on data from all the HCV notifications 1990-2006. During this time about 42,000 individuals (70% men) were diagnosed and reported as HCV infected. The majority (80%) were born in 1950 or later, with a high percentage (60%) born in the 1950s and 1960s. Younger people, 15-24 years old at notification, were reported on the same level each year. The main reported routes of HCV transmission were intravenous drug use in 65%, blood transfusions/products in 6%, and sexual in 2%, though unknown or not stated in 26%. Approximately 6,000 of all notified individuals have died during the study period. To conclude, the Swedish HCV epidemic is highly related to the increase of intravenous drug use in the late 1960s and 1970s, with a high proportion of people now chronically infected for more than 25 years, resulting in an increase of severe liver complications in form of cirrhosis and hepatocellular carcinoma. Furthermore the unchanged number of notifications of newly infected younger people indicates an ongoing HCV epidemic.

    PMID: 18761966 [PubMed - indexed for MEDLINE]

  • 11.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Medical Sciences.
    Lybeck, Charlotte
    Örebro University, School of Medical Sciences.
    Fält, A.
    Department of Clinical Epidemiology and Biostatistics, Örebro University, Örebro, Sweden.
    Wedemeyer, H.
    Department of Gastroenterology and Hepatology, Hannover Medical School, Hannover, Germany.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Clinical Epidemiology Unit, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, United Kingdom.
    Aleman, S.
    Department of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden.
    The incidence of hepatocellular carcinoma in hepatitis B virus infected persons of different origins, living in Sweden2018In: Journal of Hepatology, ISSN 0168-8278, E-ISSN 1600-0641, Vol. 68, no Suppl. 1, p. S488-S488Article in journal (Other academic)
    Abstract [en]

    Background and Aims: Chronic hepatitis B (CHB) is associated with an increased risk of hepatocellular carcinoma (HCC) in both cirrhotic and non-cirrhotic persons. CHB patients with high risk for HCC are therefore recommended to undergo surveillance for HCC, with an estimated cut-off for surveillance in non-cirrhotic patients at incidence rate (IR) of 0.2% per year. People originating from Asia and men from Africa are estimated to have particularly high risks, but the IR for HCC when living in the Western world has not been fully estimated. Therefore, our aim was to study the incidence of HCC by age and origin in persons with CHB who are living in Sweden.

    Method: In this national population-based study all persons diagnosed with CHB in Sweden during 1990–2015, their country of birth, co-infections, antiviral therapy, liver cancer or death/emigration were identified retrospectively, using the national HBV-surveil-lance register and other national registers. Those co-infected with hepatitis C were excluded. Observation time started at date of reported CHB diagnosis. The IR was calculated for different age groups and by region of birth.

    Results: In total 16,410 persons (47% women) with CHB were studied. The number of persons and observation time (person-years) by origin were: Western Europe 2,316 (25,415); Eastern Europe 2,349 (26,237); Middle East/North Africa 4,402 (47,320); Sub-Saharan Africa 3,677 (30,565), Asia 3,537 (35,358) and other 129 (1,277). Those from Sub-Saharan Africa were youngest and had the shortest mean time in Sweden, 11.6 years. There were in total 232 diagnosed HCCs (82% in men); 23, 54 and 58 in people from Sub-Saharan Africa ,Asia and Middle East/North Africa, respectively. The corresponding mean ages at HCC diagnoses were 45, 51 and 59 years, respectively. The IRexceeded 0.2% for men from Asia from age-group≥40–49 years (IR 0.63, 95%CI 0.39–1.00), and for men of all other origins from age-group≥50–59 years. Among African men aged <40 yearstherewere 7 HCC, with incidence rate 0.05 and 0.11 in age groups 20–29 and 30–39 years, respectively. In women, HCC was rare but exceeded 0.2% among those aged≥60 years with origins from East Europe, Asia and Middle East/North Africa.

    Conclusion: In this study only men of Asian origin exceeded the cut-off for HCC surveillance by ages 40–49 years. African men had a few HCCs at youngerages, but did not exceed the cut-off before age 50–59 years. This study confirms the high risk for HCC in especially Asian men living in the Western world, but questions the benefit of surveillance at younger ages for men with African origin who live in a Northern European country

  • 12.
    Duberg, Ann-Sofi
    et al.
    Örebro University, Department of Clinical Medicine.
    Nordström, Marie
    Törner, Anna
    Reichard, Olle
    Strauss, Reinhild
    Janzon, Ragnhild
    Bäck, Erik
    Örebro University, Department of Clinical Medicine.
    Ekdahl, Karl
    Non-Hodgkin's lymphoma and other nonhepatic malignancies in Swedish patients with hepatitis C virus infection2005In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 41, no 3, p. 652-659Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to evaluate the association between hepatitis C virus (HCV) infection and non-Hodgkin's lymphoma (NHL), multiple myeloma (MM), thyroid cancer (TC), chronic lymphatic leukemia (CLL), acute lymphatic leukemia (ALL), and Hodgkin's lymphoma (HL). A Swedish cohort of 27,150 HCV-infected persons notified during 1990-2000 was included in the study. The database was linked to other national registers to calculate the observation time, expressed as person-years, and to identify all incident malignancies in the cohort. The patients were stratified according to assumed time of previous HCV infection. The relative risk of malignancy was expressed as a standardized incidence ratio (SIR)-the observed number compared to the expected number. During 1990-2000 there were 50 NHL, 15 MM, 14 ALL, 8 TC, 6 CLL, and 4 HL diagnoses in the cohort. Altogether, 20 NHL, 7 MM, 5 TC, 4 CLL, 1 ALL, and 1 HL patient fulfilled the criteria to be included in the statistical analysis. The observation time was 122,272 person-years. The risk of NHL and MM was significantly increased in the stratum with more than 15 years of infection (SIR 1.89 [95% CI, 1.10-3.03] and 2.54 [95% CI, 1.11-5.69], respectively). The association was not significant in TC or CLL. In conclusion, we report the incidence of several malignancies in a nationwide cohort of HCV-infected persons. Although the delayed diagnosis of HCV probably has resulted in an underestimation of the risk, this study showed a significantly increased risk of NHL and MM.

  • 13.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences.
    Pettersson, Helena
    Smittskyddsinstitutet.
    Aleman, Soo
    Karolinska Sjukhuset.
    Blaxhult, Anders
    Smittskyddsinstitutet.
    Davidsdottir, Loa
    Karolinska sjukhuset.
    Hultcrantz, Rolf
    Karolinska Institutet.
    Bäck, Erik
    Örebro University, School of Health and Medical Sciences.
    Ekdahl, Karl
    Karolinska Institutet.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences.
    The burden of hepatitis C in Sweden: a national study of inpatient careManuscript (preprint) (Other academic)
  • 14.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Pettersson, Helena
    Department of Epidemiology, Swedish Institute for Infectious Disease Control Solna, Stockholm, Sweden.
    Aleman, Soo
    Department of Gastroenterology and Hepatology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Blaxhult, Anders
    Department of Epidemiology, Swedish Institute for Infectious Disease Control Solna, Stockholm, Sweden.
    Davidsdottir, Loa
    Department of Gastroenterology and Hepatology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Hultcrantz, Rolf
    Department of Gastroenterology and Hepatology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Bäck, Erik
    Örebro University, School of Health and Medical Sciences. Department of Clinical Medicine, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Ekdahl, Karl
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute, Stockholm, Sweden; European Centre for Disease Prevention and Control (ECDC), Stockholm, Sweden.
    Montgomery, Scott M.
    Örebro University, School of Health and Medical Sciences. Department of Clinical Medicine, Örebro University, Örebro, Sweden; Department of Medicine, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    The burden of hepatitis C in Sweden: a national study of inpatient care2011In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 18, no 2, p. 106-118Article in journal (Refereed)
    Abstract [en]

    The spread of hepatitis C virus (HCV) in Sweden in the 1970s indicated that serious liver complications (SLC) would increase in the 2000s. The aim of this study was to analyse the burden of HCV-associated inpatient care in Sweden, to demonstrate the changes over time and to compare the findings with a noninfected population. The HCV-cohort (n: 43 000) was identified from the national surveillance database 1990-2006, and then linked to national registers to produce an age-, sex-, and region-matched noninfected comparison population (n: 215 000) and to obtain information on demographics, cancers, inpatient care and prescriptions. Cox regression was used to estimate the likelihood (hazard ratios) for admission to hospital in the HCV compared with the noninfected cohort. The hazard ratios were 4.03 (95% CI: 3.98-4.08) for all care, 77.52 (71.02-84.60) for liver-related care and 40.74 (30.58-54.27) for liver cancer care. The admission rate in the HCV-cohort compared with the noninfected cohort, the rate ratio (age- and sex-adjusted) for all inpatient care was 5.91 (95% CI: 5.87-5.94), and the rate ratio for liver-related care was 70.05 (66.06-74.28). In the HCV-cohort, 45% of all episodes were for psychiatric, mostly drug-related, care. Inpatient care for SLC increased in the 2000s. To conclude, drug-related care was common in the HCV-infected cohort, the demand for liver-related care was very high, and SLC increased notably in the 2000s, indicating that the burden of inpatient care from serious liver disease in HCV-infected individuals in Sweden is an increasing problem.

  • 15.
    Duberg, Ann-Sofi
    et al.
    Örebro University, School of Health and Medical Sciences.
    Törner, Anna
    Davidsdóttir, Lóa
    Aleman, Soo
    Blaxhult, Anders
    Svensson, Åke
    Hultcrantz, Rolf
    Bäck, Erik
    Örebro University, School of Health and Medical Sciences.
    Ekdahl, Karl
    Cause of death in individuals with chronic HBV and/or HCV infection, a nationwide community-based register study2008In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 15, no 7, p. 538-550Article in journal (Refereed)
    Abstract [en]

    Studies on chronic viral hepatitis and mortality have often been made on selected populations or in high-endemic countries. The aim of this study was to investigate the causes of death and the mortality rates in the nationwide cohorts of people chronically infected with hepatitis B virus (HBV) and/or hepatitis C virus (HCV) in Sweden, a low-endemic country. All notifications on chronic HBV infection and HCV infection 1990-2003 were linked to the Cause of Death Register. A total of 9517 people with chronic HBV infection, 34 235 people with HCV infection and 1601 with chronic HBV-HCV co-infection were included, and the mean observation times were 6.4, 6.3 and 7.9 years, respectively. The mortality in the cohorts was compared with age- and gender-specific mortality in the general population and standardized mortality ratios (SMR) were calculated. All-cause mortality was significantly increased, SMR 2.3 (HBV), 5.8 (HCV) and 8.5 (HBV-HCV), with a great excess liver-related mortality in all cohorts, SMR 21.7, 35.5 and 46.2, respectively. In HCV and HBV-HCV infected there was an increased mortality due to drug-related psychiatric diagnoses (SMR: 20.7 and 27.6) and external causes (SMR: 12.4 and 11.4), predominantly at younger age. To conclude, this study demonstrated an increased all-cause mortality, with a great excess mortality from liver disease, in all cohorts. In people with HCV infection the highest excess mortality in younger ages was from drug-related and external reasons.

    PMID: 18397223 [PubMed - indexed for MEDLINE]

  • 16.
    Einberg, Afrodite Psaros
    et al.
    Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Karolinska University Hospital, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Filipovich, Olga
    North-Western State Medical University of I.I.Mechnikov, Saint Petersburg, Russia.
    Nyström, Jessica
    Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden.
    Zhirkov, Anton
    Science Research Institute of Children's Infections, Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia.
    Brenndörfer, Erwin Daniel
    Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden.
    Frelin, Lars
    Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden.
    Rukoiatkina, Elena
    Maternity Hospital No. 16, Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia; Department of Pediatrics, Gynecology and Female Reproductology, Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia.
    Lobzin, Yuriy
    Science Research Institute of Children's Infections, Saint Petersburg State Pediatric Medical University, Saint Petersburg, Russia.
    Sällberg, Matti
    Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden.
    Fischler, Björn
    Department of Clinical Science, Intervention and Technology (CLINTEC), Karolinska Institutet, Stockholm, Sweden; Department of Pediatrics, Karolinska University Hospital, Stockholm, Sweden.
    Lutckii, Anton
    Department of Laboratory Medicine, Division of Clinical Microbiology, Karolinska Institutet, Stockholm, Sweden; Science Research Institute of Children's Infections.
    Lack of association between interleukin 28B polymorphism and vertical transmission of hepatitis C2017In: Journal of Pediatric Gastroenterology and Nutrition - JPGN, ISSN 0277-2116, E-ISSN 1536-4801, Vol. 65, no 6, p. 608-612Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Single genetic nucleotide polymorphism (rs12979860) near the gene for Interleukin 28B (IL28B), is known to be of importance for frequency of spontaneous clearance and treatment outcome in interferon based therapies in patients with hepatitis C virus (HCV) infection. The aim of this study was to investigate if IL28B polymorphism in children and/or their mothers plays a role in vertical transmission of HCV (HCV-VT).

    METHODS: Plasma samples from 59 infected women, 76 uninfected children born to infected mothers, and 47 children with known vertically transmitted HCV infection, were analysed for IL28B polymorphism and classified by the IL28B genotype (C/C, C/T and T/T) as well as by viral genotype.

    RESULTS: The proportion of children with genotype C/C was the same in the vertically infected (36%, 17/47) and the exposed uninfected children (38%, 29/76). No difference was seen when stratifying for viral genotype. There was no association between mothers' IL28B genotype and the risk of vertical transmission.

    CONCLUSION: Regardless of viral genotype we found no association between IL28B genotype and the risk of HCV-VT. The IL28B genotype CC, which has been shown to be favourable in other settings, was not protective of HCV-VT. Thus, other factors possibly associated with the risk of HCV-VT need to be explored.

  • 17.
    Gahrton, Caroline
    et al.
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Lindahl, K.
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Westman, G.
    Department of Medical Sciences, Section of Infectious Diseases, Uppsala University, Uppsala, Sweden.
    Öhrn, F.
    Center for Innovation, Karolinska University Hospital, Stockholm, Sweden.
    Dalgard, O.
    Department of Infectious Diseases, Akershus University Hospital, Lørenskog, Norway; Division of Medicine and Laboratory Sciences, University of Oslo, Oslo, Norway.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Lidman, C.
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Said, K.
    Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden; Department of Upper Gastrointestinal Diseases, Karolinska University Hospital, Stockholm, Sweden.
    Aleman, S.
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden.
    Prevalence of viremic hepatitis C virus, hepatitis B virus, or HIV infection and vaccination status among Swedish prisoners2018Conference paper (Other academic)
  • 18.
    Hofmann, Jonathan N.
    et al.
    Div Canc Epidemiol & Genet, National Cancer Institute, Bethesda MD, USA.
    Törner, Anna
    Dept Epidemiol, Swedish Inst Infect Dis Control, Solna, Sweden.
    Chow, Wong-Ho
    Div Canc Epidemiol & Genet, National Cancer Institute, Bethesda MD, USA.
    Ye, Weimin
    Dept Med Epidemiol & Biostat, Karolinska Institute, Stockholm, Sweden.
    Purdue, Mark P
    Div Canc Epidemiol & Genet, National Cancer Institute, Bethesda MD, USA.
    Duberg, Ann-Sofi
    Dept Infect Dis, Örebro University Hosp, Örebro, Sweden.
    Risk of kidney cancer and chronic kidney disease in relation to hepatitis C virus infection: a nationwide register-based cohort study in Sweden2011In: European Journal of Cancer Prevention, ISSN 0959-8278, E-ISSN 1473-5709, Vol. 20, no 4, p. 326-30Article in journal (Refereed)
    Abstract [en]

    Chronic hepatitis C virus (HCV) infection is an established cause of liver cancer, and recent studies have suggested a link with kidney cancer. The aim of this study was to evaluate risk of kidney cancer in relation to HCV infection in a nationwide registry-based study of Swedish residents diagnosed with HCV between 1990 and 2006. A total of 43 000 individuals with chronic HCV infection were included, and the mean follow-up time was 9.3 years. Observed kidney cancer incidence and mortality in the cohort were compared with expected values based on the age-adjusted and sex-adjusted rates in the general population. Risk of hospitalization for other chronic kidney disease was also evaluated using Cox proportional hazards regression. No association between HCV infection and risk of kidney cancer was observed [standardized incidence ratio with 1-year lag=1.2; 95% confidence interval (CI): 0.8-1.7]. Risk of hospitalization for noncancer kidney disease was significantly elevated in the HCV cohort, with significantly stronger associations observed among women than among men [hazard ratio=5.8 (95% CI: 4.2-7.9) and 3.9 (95% CI: 3.2-4.8) for women and men, respectively]. Results of this study do not support the hypothesis that chronic HCV infection confers an increased risk of kidney cancer. However, we did find an association between HCV infection and chronic kidney disease, particularly among women. Given inconsistent findings in the literature, it is premature to consider HCV infection to be a risk factor for kidney cancer.

  • 19.
    Holmström, M.
    et al.
    Coagulation Unit, Department of Medicine Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Nangarhari, A.
    Department of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Öhman, J.
    Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Majeed, A.
    Coagulation Unit, Department of Medicine Solna, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; Department of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Aleman, S.
    Department of Infectious Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
    Long-term liver-related morbidity and mortality related to chronic hepatitis C virus infection in Swedish patients with inherited bleeding disorders2016In: Haemophilia, ISSN 1351-8216, E-ISSN 1365-2516, Vol. 22, no 6, p. e494-e501Article in journal (Refereed)
    Abstract [en]

    Introduction: Hepatitis C virus (HCV) infection is common in patients with inherited bleeding disorders treated with clotting factor concentrates prior to the introduction of viral inactivation of these products. The long-term consequences of hepatitis C infection in Swedish patients are not fully understood.

    Aim: To examine the impact of HCV infection on liver-related morbidity and mortality in Swedish patients with inherited bleeding disorders.

    Methods: We retrospectively collected data on 183 patients with inherited bleeding disorders infected with HCV who attended the Coagulation Unit at Karolinska University Hospital, Sweden. Data regarding end-stage liver disease (ESLD), defined as presence of ascites, encephalopathy, variceal bleeding, hepatocellular carcinoma or liver-related death, were collected from the patient records and the national registers.

    Results: The median follow-up time was 35.9 years (IQR 29.0-41.2). A total of 41% had achieved sustained virological response (SVR) after treatment. In total, 14.2% developed ESLD at the median age of 52.6 years (IQR 46.5-64.7). Nineteen (35.8%) of all deaths were due to liver-related causes. Co-infection with human immunodeficiency virus (HIV), older age at time of infection and severe form of bleeding disorder was associated with higher risk of developing ESLD, while SVR was a strong protective factor.

    Conclusions: This study demonstrated that liver-related morbidity and mortality was significant in patients with bleeding disorders and HCV infection in Sweden. Patients with HCV-infection should be candidates for treatment with the new highly effective antiviral drugs, since SVR proved to be a strong protective factor.

  • 20.
    Huang, Jiaqi
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Magnusson, Måns
    Department of Analysis and Prevention, Swedish Institute for Communicable Disease Control, Solna, Sweden .
    Törner, Anna
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Ye, Weimin
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden .
    Duberg, Ann-Sofi
    Örebro University Hospital. Department of Infectious Diseases.
    Risk of pancreatic cancer among individuals with hepatitis C or hepatitis B virus infection: a nationwide study in Sweden2013In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 109, no 11, p. 2917-2923Article in journal (Refereed)
    Abstract [en]

    Background: A few studies indicated that hepatitis C and hepatitis B virus (HCV/HBV) might be associated with pancreatic cancer risk. The aim of this nationwide cohort study was to examine this possible association.

    Methods: Hepatitis C virus- and hepatitis B virus-infected individuals were identified from the national surveillance database from 1990 to 2006, and followed to the end of 2008. The pancreatic cancer risk in the study population was compared with the general population by calculation of Standardized Incidence Ratios (SIRs), and with a matched reference population using a Cox proportional hazards regression model to calculate hazard ratios (HRs).

    Results: In total 340 819 person-years in the HCV cohort and 102 295 in the HBV cohort were accumulated, with 34 and 5 pancreatic cancers identified, respectively. The SIRHCV was 2.1 (95% confidence interval, CI: 1.4, 2.9) and the SIRHBV was 1.4 (0.5, 3.3). In the Cox model analysis, the HR for HCV infection was 1.9 (95% CI: 1.3, 2.7), diminishing to 1.6 (1.04, 2.4) after adjustment for potential confounders.

    Conclusion: Our results indicated that HCV infection might be associated with an increased risk of pancreatic cancer but further studies are needed to verify such association. The results in the HBV cohort indicated an excess risk, however, without statistical significance due to lack of power.

  • 21.
    Kamal, Habiba
    et al.
    Department of Infectious Diseases, Karolinska University Hospital, Solna, Sweden; Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Falconer, Karolin
    Department of Infectious Diseases, Karolinska University Hospital, Solna, Sweden; Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Westman, Gabriel
    Medical Sciences, Uppsala University, Uppsala, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Weiland, Ola R. H. J.
    Department of Infectious Diseases, Karolinska University Hospital, Solna, Sweden; Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Wejstal, Rune
    Department of Infectious Diseases, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Carlssson, Tony
    Department of Infectious Diseases, Danderyd University Hospital, Danderyd, Sweden.
    Kampmann, Christian
    Department of Infectious Diseases, Skåne University Hospital, Lund, Sweden.
    Björkman, Per
    Department of Infectious Diseases, Lund University, Lund, Sweden.
    Nystedt, Anders
    Department of Infectious Diseases, Sunderby Hospital, Södra Sunderbyn, Sweden.
    Cardell, Kristina
    Department of Infectious Diseases and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Svensson, Stefan
    Department of Infectious Diseases and Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden.
    Stenmark, Stephan
    Department of Infectious Diseases, University Hospital of Umeå, Umeå, Sweden; Department of Translational Medicine, Lund University, Lund, Sweden.
    Wedemeyer, Heiner
    Klinik für Gastroenterologie und Hepatologie, University Hospital, Essen, Germany.
    Aleman, Soo
    Department of Infectious Diseases, Karolinska University Hospital, Solna, Sweden; Department of Medicine, Karolinska Institutet, Solna, Sweden.
    Long-Term Liver-Related Outcomes in Hepatitis B and D Co-Infected Patients in Sweden2018In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 68, no Suppl.1, p. 1190A-1191AArticle in journal (Refereed)
  • 22.
    Kileng, Hege
    et al.
    Department of Clinical Medicine, Gastroenterology and Nutrition Research Group, UiT The Arctic University of Norway, Tromsø, Norway; Department of Medicine, University Hospital of North Norway, Tromsø, Norway.
    Kjellin, Midori
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Akaberi, Dario
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Bergfors, Assar
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Wesslén, Lars
    Gävle Hospital, Gävle, Sweden.
    Danielsson, Astrid
    Falun Hospital, Falun, Sweden.
    Gangsøy Kristiansen, Magnhild
    Nordlandssykehuset Bodø, Department of Clinical Medicine (IKM), UiT The Artic University of Tromsø, Bodø, Norway.
    Gutteberg, Tore
    Department of Medical Biology, Research Group for Host-Microbe Interactions, UiT The Arctic University of Norway, Tromsø, Norway; Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway.
    Goll, Rasmus
    Department of Clinical Medicine, Gastroenterology and Nutrition Research Group, UiT The Arctic University of Norway, Tromsø, Norway; Department of Medicine, University Hospital of North Norway, Tromsø, Norway.
    Lannergård, Anders
    Department of Medical Sciences, Section of Infectious Diseases, Uppsala University Hospital, Uppsala, Sweden.
    Lennerstrand, Johan
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Personalized treatment of hepatitis C genotype 1a in Norway and Sweden 2014-2016: a study of treatment outcome in patients with or without resistance-based DAA-therapy2018In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708, Vol. 53, no 10-11, p. 1347-1353Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Resistance-associated substitutions (RASs) may impair treatment response to direct-acting antivirals (DAA) in hepatitis C virus (HCV) treatment. We investigated the effects of baseline NS3-RASs (Q80K and R155K) and clinically relevant NS5A-RASs in patients with HCV genotype (GT) 1a infection on treatment outcome, with or without resistance-based DAA-treatment. This multi-center study was carried out between 2014 and 2016.

    PATIENTS/METHODS: Treatment in the intervention group (n = 92) was tailored to baseline resistance. Detection of NS3-RAS led to an NS5A-inhibitor-based regimen and detection of NS5A-RAS to a protease-inhibitor regimen. Patients without baseline RAS in the intervention group and all patients in the control group (n = 101) received recommended standard DAA-treatment.

    RESULTS: The sustained virologic response rates (SVR) in the intervention and control groups were 97.8% (90/92) and 93.1% (94/101), respectively (p = .174). A trend toward higher SVR-rate in cirrhotic patients (p = .058) was noticed in the intervention group compared to the control group with SVR-rates 97.5% (39/40) and 83.3% (35/42), respectively. All patients with baseline NS3 (Q80K/R155K) or NS5A-RASs in the intervention group achieved SVR with personalized resistance-based treatment. In the control group, five patients with Q80K or R155K at baseline were treated with simeprevir + sofosbuvir and treatment failed in two of them. Furthermore, one of three patients who failed ledipasvir + sofosbuvir treatment had NS5A-RASs at baseline.

    CONCLUSIONS: In line with the findings of the OPTIMIST-2 trial for Q80K and the EASL-guidelines 2016 for NS5A-RASs, baseline RASs appeared to have an impact on treatment outcome albeit a statistical significance was not observed in this low-prevalence population.

  • 23.
    Kileng, Hege
    et al.
    Tromsø University Hospital, Tromsø, Norway.
    Kjellin, Midori
    Medical Science, Uppsala University, Uppsala, Sweden.
    Bergfors, Assar
    Medical Science, Uppsala University, Uppsala, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Öebro University Hospital, Örebro, Sweden.
    Wesslen, Lars
    Gävle Hospital, Gävle, Sweden.
    Danielsson, Astrid
    Falun Hospital, Falun, Sweden.
    Kristiansen, Magnhild G.
    Bodø Hospital, Bodø, Norway.
    Gutteberg, Tore
    Tromsø University Hospital, Tromsø, Norway.
    Lannergard, Anders
    Medical Science, Uppsala University, Uppsala, Sweden.
    Lennerstrand, Johan
    Medical Science, Uppsala University, Uppsala, Sweden.
    Effect of pre-existing Hepatitis C NS3 Q80K variant in Genotype la and NS5A Y93H variant in Genotype 3 for interferon-free treatment combinations with direct antiviral agents (DAAs): Real-life experience from a multicenter study in Sweden and Norway2016In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 64, no Suppl. S1, p. 1001A-1001A, article id 2014Article in journal (Other academic)
  • 24.
    Kjellin, Midori
    et al.
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Kileng, Hege
    Gastroenterology and Nutrition Research Group, Department of Clinical Medicine, UiT the Arctic University of Norway, Tromsø, Norway; Department of Medicine, University Hospital of North Norway, Tromsø, Norway.
    Akaberi, Dario
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Palanisamy, Navaneethan
    Institute of Biology II, University of Freiburg, Freiburg, Germany; Institute of Biology II, University of Freiburg, Freiburg, Germany.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Danielsson, Astrid
    Department of Infectious Diseases, Falun Hospital, Falun, Sweden.
    Kristiansen, Magnhild Gangsøy
    Nordlandssykehuset Bodø, Department of Clinical Medicine (IKM), UiT the Artic University of Tromsø, Tromsø, Norway.
    Nöjd, Johan
    Nordlandssykehuset Bodø, Department of Clinical Medicine (IKM), UiT the Artic University of Tromsø, Tromsø, Norway.
    Aleman, Soo
    Department of Infectious Diseases, Karolinska University Hospital/Karolinska Institutet, Stockholm, Sweden.
    Gutteberg, Tore
    Research Group for Host-Microbe Interactions, Department of Medical Biology, UiT the Arctic University of Norway, Tromsø, Norway; Department of Microbiology and Infection Control, University Hospital of North Norway, Tromsø, Norway.
    Goll, Rasmus
    Gastroenterology and Nutrition Research Group, Department of Clinical Medicine, UiT the Arctic University of Norway, Tromsø, Norway; Department of Medicine, University Hospital of North Norway, Tromsø, Norway.
    Lannergård, Anders
    Department of Medical Sciences, Section of Infectious Diseases, Uppsala University Hospital, Uppsala, Sweden.
    Lennerstrand, Johan
    Department of Medical Sciences, Section of Clinical Microbiology, Uppsala University, Uppsala, Sweden.
    Effect of the baseline Y93H resistance-associated substitution in HCV genotype 3 for direct-acting antiviral treatment: real-life experience from a multicenter study in Sweden and Norway2019In: Scandinavian Journal of Gastroenterology, ISSN 0036-5521, E-ISSN 1502-7708Article in journal (Refereed)
    Abstract [en]

    Background: The NS5A resistance-associated substitution (RAS) Y93H is found quite frequently (5-10%) at baseline in direct-acting antiviral agents (DAA) treatment-naive genotype (GT) 3a patients when studied by the population-sequencing method (cut-off 20%). This RAS may impair HCV DAA treatment response, since it possesses a high fold in vitro resistance to daclatasvir (DCV) and velpatasvir (VEL) in GT 3. We investigated the effect of baseline Y93H in patients with GT 3a infection on treatment outcome, with or without resistance-based DAA-treatment during 2014-2017.

    Patients/Methods: Treatment in the intervention group (n = 130) was tailored to baseline resistance-findings by population-sequencing method. Detection of baseline Y93H above 20% prompted a prolonged treatment duration of NS5A-inhibitor and sofosbuvir (SOF) and/or addition of ribavirin (RBV). Patients without baseline Y93H in the intervention group and all patients in the control group (n = 78) received recommended standard DAA-treatment.

    Results: A higher sustained virologic response rate (SVR) in the intervention group was shown compared to the control group at 95.4% (124/130) and 88.5% (69/78), respectively (p = .06). All five patients with baseline Y93H in the intervention group achieved SVR with personalised treatment based on results from resistance testing; either with the addition of RBV or prolonged treatment duration (24w). In the control group, 2/4 patients with Y93H at baseline treated with ledipasvir/SOF/RBV or DCV/SOF without RBV, failed treatment.

    Conclusion: The results from this real-life study are in accordance with the findings of the randomised controlled trials in 2015 and the EASL-guidelines of 2016, thus, baseline Y93H impacts on DCV and VEL treatment outcome.

  • 25.
    Lagging, Martin
    et al.
    Dept Infect Dis, Inst Biomed, Univ Gothenburg, Gothenburg, Sweden.
    Duberg, Ann-Sofi
    Dept Infect Dis, Örebro Univ Hosp, Örebro, Sweden.
    Wejstål, Rune
    Dept Infect Dis, Inst Biomed, Univ Gothenburg, Gothenburg, Sweden; Swedish Reference Grp Antiviral Therapy RAV, Karolinska Univ Hosp, Stockholm, Sweden.
    Weiland, Ola
    Dept Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden.
    Lindh, Magnus
    Dept Infect Dis, Inst Biomed, Univ Gothenburg, Gothenburg, Sweden.
    Aleman, Soo
    Dept Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden.
    Josephson, Filip
    Medical Products Agency (Läkemedelsverket), Uppsala, Sweden.
    Treatment of hepatitis C virus infection in adults and children: updated Swedish consensus recommendations2012In: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, E-ISSN 1651-1980, Vol. 44, no 7, p. 502-521Article in journal (Refereed)
    Abstract [en]

    Swedish recommendations for the treatment of hepatitis C virus (HCV) infection were updated at a recent expert meeting. Therapy for acute HCV infection should be initiated if spontaneous resolution does not occur within 12 weeks. The recommended standard-of-care therapy for chronic HCV genotype 1 infection is an HCV protease inhibitor in combination with peginterferon (peg-IFN) and ribavirin. Treatment is strongly recommended in patients with bridging fibrosis and cirrhosis, whereas in patients with less advanced fibrosis, deferring therapy may be preferential in light of likely therapeutic improvements in the near future. Patients with chronic genotype 2/3 infection should generally be treated with peg-IFN and ribavirin for 24 weeks. In patients with a very rapid viral response (i.e. HCV RNA below 1000 IU/ml on day 7), or favourable baseline characteristics and undetectable HCV RNA week 4, treatment can be shortened to 12-16 weeks, provided that no dose reductions are needed.

  • 26.
    Lagging, Martin
    et al.
    Department of Infectious Diseases, Institute of Biomedicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Wejstål, Rune
    Department of Infectious Diseases, Institute of Biomedicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Aleman, Soo
    Department of Medicine, Division of Infectious Diseases, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Weiland, Ola
    Department of Medicine, Division of Infectious Diseases, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Westin, Johan
    Department of Infectious Diseases, Institute of Biomedicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; Swedish Reference Group for Antiviral Therapy (RAV), Stockholm, Sweden.
    Treatment of hepatitis C virus infection for adults and children: updated Swedish consensus guidelines 20172018In: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243, Vol. 50, no 8, p. 569-583Article, review/survey (Refereed)
    Abstract [en]

    Aim: Following the approval of two new therapeutic combinations within the European Union in 2017, the former Swedish recommendations for the treatment of hepatitis C virus (HCV) infection from 2016 were deemed in need of updating.

    Materials and methods: An expert meeting to this end was held in Stockholm, Sweden in October 2017.

    Results and conclusions: An interferon-free combination of direct-acting antiviral agents is now recommended for all patients with chronic HCV infection, regardless of liver fibrosis stage, in order to limit morbidity and spread of the disease. An extended discussion of treatment for people who inject drugs in order to diminish transmission is included.

  • 27.
    Leblebicioglu, Hakan
    et al.
    Department of Infectious Diseases and Clinical Microbiology, Ondokuz Mayis University, Medical School, Samsun, Turkey.
    Arends, Joop E.
    Internal Medicine and Infectious Diseases, Universitair Medisch Centrum Utrecht, Utrecht, The Netherlands.
    Ozaras, Resat
    Department of Infectious Diseases and Clinical Microbiology, Istanbul University Cerrahpasa Medical School, Istanbul, Turkey.
    Corti, Giampaolo
    Infectious Disease Unit, University of Florence School of Medicine, Florence, Italy.
    Santos, Lurdes
    Infectious Diseases Service C Hospitalar São João, Faculty of Medicine, Alameda Professor Hernani Monteiro, Porto, Portugal.
    Boesecke, Christoph
    Department of Medicine I, Bonn University, Bonn, Germany.
    Ustianowski, Andrew
    Infectious Diseases & Tropical Medicine and Research Lead, North Western Infectious Diseases Unit, Pennine Acute Hospitals NHS Trust, North Manchester General Hospital, Manchester, UK.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Ruta, Simona
    Stefan S. Nicolau Institute of Virology, Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
    Salkic, Nermin N.
    Department of Gastroenterology and Hepatology, University Clinical Center Tuzla, Tuzla, Bosnia and Herzegovina.
    Husa, Petr
    Infectious Diseases, Masaryk University, Brno, Czech Republic; Infectious Diseases, University Hospital Brno, Brno, Czech Republic.
    Lazarevic, Ivana
    Institute of Microbiology and Immunology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia.
    Pineda, Juan A.
    Unidad de Enfermedades Infecciosas y Microbiología, Hospital Universitario de Valme, Sevilla, Spain.
    Pshenichnaya, Natalia Yurievna
    Rostov State Medical University, Rostov-on-Don, Russia.
    Tsertswadze, Tengiz
    Infectious Diseases, AIDS and Clinical Immunology Research Center, Tbilisi, Georgia; Faculty of Medicine, Ivane Javakhishvili Tbilisi State University, Tbilisi, Georgia.
    Matičič, Mojca
    Clinic for Infectious Diseases and Febrile Illnesses, University Medical Centre, Ljubljana, Slovenia.
    Puca, Edmond
    Department of Infection Diseases, University Hospital Center, Tirane, Albania.
    Abuova, Gulzhan
    Infectious Diseases Department, South - Kazakhstan State Pharmaceutical Academy, Shymkent, Kazakhstan.
    Gervain, Judit
    Division Hepato-Pancreatology, 1st Department of Gastroenterology and Molecular Diagnostic Laboratory, "Szent György" Teaching Hospital Székesfehérvár, Székesfehérvár, HungaryDivision Hepato-Pancreatology, 1st Department of Gastroenterology and Molecular Diagnostic Laboratory, "Szent György" Teaching Hospital Székesfehérvár, Székesfehérvár, Hungary.
    Bayramli, Ramin
    Department of Microbiology and Immunology, Azerbaijan Medical University, Educational Therapeutic Hospital, Baku, Azerbaijan.
    Ahmeti, Salih
    Infectious Disease Clinic, University Clinical Centre of Kosova, Faculty of Medicine, Prishtina University, Pristina, Kosovo.
    Koulentaki, Mairi
    Department of Gastroenterology, University Hospital of Heraklion, Heraklion, Crete, Greece.
    Kilani, Badreddine
    Service des Maladies Infectieuses, Faculté de Médecine de Tunis, Université Tunis EL Manar, Hôpital la Rabta, Tunis, Tunisia.
    Vince, Adriana
    University Hospital of Infectious Diseases, Zagreb School of Medicine, Zagreb, Croatia.
    Negro, Francesco
    Divisions of Gastroenterology and Hepatology of Clinical Pathology, University Hospital of Geneva, Geneva, Switzerland.
    Sunbul, Mustafa
    Department of Infectious Diseases and Clinical Microbiology, Ondokuz Mayis University, Medical School, Samsun, Turkey.
    Salmon, Dominique
    Infectious Diseases, Hôpitaux Universitaires Paris Centre, Université Paris Descartes, Paris, France.
    Availability of hepatitis C diagnostics and therapeutics in European and Eurasia countries2018In: Antiviral Research, ISSN 0166-3542, E-ISSN 1872-9096, Vol. 150, p. 9-14Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Treatment with direct acting antiviral agents (DAAs) has provided sustained virological response rates in >95% of patients with chronic hepatitis C virus (HCV) infection. However treatment is costly and market access, reimbursement and governmental restrictions differ among countries. We aimed to analyze these differences among European and Eurasian countries.

    METHODS: A survey including 20-item questionnaire was sent to experts in viral hepatitis. Countries were evaluated according to their income categories by the World Bank stratification.

    RESULTS: Experts from 26 countries responded to the survey. As of May 2016, HCV prevalence was reported as low (≤1%) in Croatia, Czech Republic, Denmark, France, Germany, Hungary, the Netherlands, Portugal, Slovenia, Spain, Sweden, UK; intermediate (1-4%) in Azerbaijan, Bosnia and Herzegovina, Italy, Kosovo, Greece, Kazakhstan, Romania, Russia, Serbia and high in Georgia (6.7%). All countries had national guidelines except Albania, Kosovo, Serbia, Tunisia, and UK. Transient elastography was available in all countries, but reimbursed in 61%. HCV-RNA was reimbursed in 81%. PegIFN/RBV was reimbursed in 54% of the countries. No DAAs were available in four countries: Kazakhstan, Kosovo, Serbia, and Tunisia. In others, at least one DAA combination with either PegIFN/RBV or another DAA was available. In Germany and the Netherlands all DAAs were reimbursed without restrictions: Sofosbuvir and sofosbuvir/ledipasvir were free of charge in Georgia.

    CONCLUSION: Prevalence of HCV is relatively higher in lower-middle and upper-middle income countries. DAAs are not available or reimbursed in many Eurasia and European countries. Effective screening and access to care are essential for reducing liver-related morbidity and mortality.

  • 28. Lindh, Magnus
    et al.
    Uhnoo, Ingrid
    Bläckberg, Joans
    Duberg, Ann-Sofi
    Örebro University, School of Health and Medical Sciences.
    Friman, Stybjörn
    Fischler, Björn
    Karlström, Olof
    Norkrans, Gunnar
    Reichard, Olle
    Sangfeldt, Per
    Söderström, Ann
    Sönnerborg, Anders
    Weiland, Ola
    Wejstål, Rune
    Wiström, Johan
    Treatment of chronic hepatitis B infection: an update of Swedish recommendations2008In: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, E-ISSN 1651-1980, Vol. 40, no 6-7, p. 436-450Article in journal (Refereed)
    Abstract [en]

    The main goal for treatment of chronic hepatitis B is to prevent complications such as liver cirrhosis or hepatocellular carcinoma. Knowledge from population studies of the long-term risk of chronic HBV infection, as well as the recent introduction of pegylated interferon and additional nucleoside analogues has changed the therapeutic situation. Recently, a Swedish expert panel convened to update the national recommendations for treatment. The panel recommends treatment for patients with active HBV infection causing protracted liver inflammation or significant liver fibrosis, verified by liver histology. In general, pegylated interferon alpha-2a is recommended as first-line treatment, in particular for HBeAg-positive patients with HBV genotypes A or B. Among nucleoside analogues, entecavir is the first choice and adefovir or tenofovir can be used as alternatives. Lamivudine monotherapy is not recommended due to the high risk of resistance development. Combinations of nucleoside analogues such as tenofovir and lamivudine or emtricitabine are alternatives for patients with non-response or infection with resistant variants, or as first choice for patients with advanced liver disease. Nucleoside analogue treatment should be monitored to detect primary non-response and virological breakthrough. Special recommendations are given for HBV/HIV coinfected patients, immunosuppressed patients, children, and for treatment before and after liver transplantation. The present guideline is translated from Swedish, where it is published on the MPA and RAV websites (www.mpa.se and www.rav.nu.se) including 7 separate papers based on thorough literature search. The complete reference list can be received from the Medical Products Agency upon request.

  • 29.
    Lybeck, Charlotte
    et al.
    Department of Infectious Diseases, Faculty of Medicine and Health.
    Brenndörfer, Erwin D
    Department of Laboratory Medicine, Division of Clinical Microbiology.
    Sällberg, Matti
    Department of Laboratory Medicine, Division of Clinical Microbiology.
    Montgomery, Scott
    Örebro University, School of Medical Sciences. Clinical Epidemiology Unit; Department of Epidemiology and Public Health, University College London, London, UK.
    Aleman, Soo
    Department of Gastroenterology and Hepatology; Department of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Department of Infectious Diseases, Faculty of Medicine and Health.
    Long-term follow-up after cure from chronic hepatitis C virus infection shows occult hepatitis and a risk of hepatocellular carcinoma in noncirrhotic patients2019In: European Journal of Gastroenterology and Hepathology, ISSN 0954-691X, E-ISSN 1473-5687, Vol. 31, no 4, p. 506-513Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: Curing hepatitis C virus (HCV) infection primarily aims to prevent severe liver complications. Our objectives were to investigate the long-term presence and impact of occult HCV infection (OCI) and to study the outcomes in terms of liver disease after virological cure.

    PATIENTS AND METHODS: A total of 97 patients with achieved sustained virological response (SVR) during 1990-2005 were followed either by a clinical follow-up (FU) visit with blood sampling and liver elastography (n=54) or through national registries for outcomes (n=43). To diagnose OCI among patients with SVR, a highly sensitive method was used to detect HCV-RNA traces in whole blood. The FU duration was a median of 10.5 years, with samples up to 21.5 years after the end of treatment (EOT).

    RESULTS: The majority of patients [52 (96%)] were HCV-RNA negative at FU, and regression of fibrosis was statistically significant. OCI was found in two (4%) of them at 8 and 9 years after EOT. These patients had F1 and F2 fibrosis before treatment and F2 at FU, but no other abnormal findings. Three previously noncirrhotic men were diagnosed with hepatocellular carcinoma 8-11 years after EOT.

    CONCLUSION: Occult infection could be detected many years after the achievement of SVR but was not associated with the serious liver disease. The majority had persistent viral eradication and regression of fibrosis after SVR. However, an increased risk of hepatocellular carcinoma may persist in the long term after SVR even in noncirrhotic patients. Further studies with FU after direct-acting antiviral therapy and on the long-term impact after cure are needed.

  • 30.
    Lybeck, Charlotte
    et al.
    Örebro University, School of Medical Sciences. Department of Infectous diseases.
    Bruce, D.
    Department of Statistics, Scandinavian Development Services, Danderyd, Sweden.
    Montgomery, Scott
    Örebro University, School of Medical Sciences.
    Aleman, S.
    Department of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectous diseases.
    A national study of risk for non-liver cancer in people with hepatitis C treated with direct acting antivirals or an interferon-based regimen2018In: Journal of Hepatology, ISSN 0168-8278, E-ISSN 1600-0641, Vol. 68, no Suppl. 1, p. S263-S264Article in journal (Other academic)
    Abstract [en]

    Background and Aims: Direct acting antivirals (DAA) against hepatitis C virus (HCV) have been shown to have an immune modulatory effect, with a possibly decreased tumour specific CD8 T cell response. Reports indicative of a high risk for hepatocellular carcinoma or advanced tumours early after DAA treatment, have raised concerns about whether the risk for non-liver cancer could be increased. Therefore, our aim was to study the early incidence of non-liver cancer after initiation of DAA or interferon (IFN-based) therapy in a national HCV cohort.

    Method: All diagnosed HCV-infected persons in Sweden, their antiviral treatments, non-liver cancer or death/emigration were identified retrospectively, using the national HCV-surveillance register and other national registers. Cox regression was used to compare persons treated with DAAs (n = 1,920), IFN-based therapy(n = 2,586) or no HCV therapy (n = 13,872) between 2009 and 2015. Persons with a previous cancer diagnosis (5.7%) were studied separately. Age was used as the time-scale, and the analyses were stratified by sex and adjusted for the Charlson comorbidity index.

    Results: In total 492 non-liver cancers were diagnosed, with 222 among persons with no previous cancer and 270 new cancer diagnoses among those with previous cancer. Among persons with no previous cancer, 21, 24 and 177 developed non-liver cancer following DAA, IFN-based and no treatment, respectively. The corresponding numbers for those with previous cancer were 25, 20 and 225, respectively. The hazard ratios (and 95% confidence intervals) for non-liver cancer in the no previous cancer group are 1.35 (0.66–2.76; p = 0.41) for men and 1.75 (0.59–5.18; p = 0.31) for women with DAA treatment, compared with IFN treatment. For those with previous cancer, the corresponding hazard ratios are 1.03 (0.41–2.57; p = 0.95) for men and 0.86 (0.35–2.13; p = 0.75) for women with DAA treatment.

    Conclusion: This study did not demonstrate any significantly increased risk for non-liver cancer early after DAA therapy initiation. The hazard ratio was slightly increased among those with outprevious cancer, but the cancers were few and the results were not statistically significant. Further studies with higher numbers of DAA treated patients and longer follow-up are needed to fully explore thisissue.

  • 31.
    Malm, Kerstin
    et al.
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medicine, Örebro University, Sweden.
    Sundqvist, Martin
    Fredlund, Hans
    Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
    Andersson, Sören
    Evaluation of a hepatitis C virus core antigen assay to monitor viral load in patients on antiviral therapy and in untreated patientsManuscript (preprint) (Other academic)
  • 32.
    Millbourn, C.
    et al.
    Department of Medicine Huddinge, Unit of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden; Dept of Infectious Diseases, I73, Karolinska University Hospital, Stockholm, Sweden.
    Lybeck, Charlotte
    Örebro University, School of Medical Sciences. Dept of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Fadl, Helena
    Örebro University, School of Medical Sciences. Örebro University Hospital. Dept of Obstetrics and Gynecology, Örebro University Hospital, Örebro, Sweden.
    Fredlund, Hans
    Dept Clin Microbiology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
    Lindahl, K.
    Department of Medicine Huddinge, Unit of Infectious Diseases, Karolinska Institutet, Stockholm, Sweden; Dept of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Dept of Infectious Diseases, Faculty of Health and Medical Sciences, Örebro University, Örebro, Sweden.
    Screening for HCV in pregnant women and their partners2017In: Journal of Hepatology, ISSN 0168-8278, E-ISSN 1600-0641, Vol. 66, no 1, p. S404-S405Article in journal (Refereed)
  • 33.
    Norda, Rut
    et al.
    Departments of Transfusion Medicine and Immunohemotherapy, Örebro Medical Center Hospital, Örebro, Sweden.
    Duberg, Ann-Sofi
    Departments of Infectious Diseases, Örebro Medical Center Hospital, Örebro, Sweden.
    Sönnerborg, Anders
    Departments of Clinical Microbiology and Immunology, Örebro Medical Center Hospital, Örebro, Sweden.
    Olcén, Per
    Departments of Division of Clinical Virology, Karolinska Institutet, Huddinge University Hospital, Huddinge, Sweden.
    Transmission of hepatitis C virus by transfusion in Orebro County, Sweden, 1990-19921995In: Scandinavian Journal of Infectious Diseases, ISSN 0036-5548, E-ISSN 1651-1980, Vol. 27, no 5, p. 449-452Article in journal (Refereed)
    Abstract [en]

    A retrospective study of hepatitis C virus (HCV) transmission by transfusion was conducted in Orebro county. Out of the 7,900 active, registered blood donors, 21 repeatedly anti-HCV reactive (RIVA 2 positive or indeterminate) donors were diagnosed. Their 84 recipients from January 1990 through June 1992 were identified and 41 (49%) were alive in December 1992. A total of 13 anti-HCV reactive (RIBA 2 positive or indeterminate) were diagnosed in 39 investigated recipients. Of these 11 were previously undiagnosed, and seven were HCV RNA-positive. In the donor population 1.03% were anti-HCV-positive by ELISA, but only 0.09% were RIBA and HCV RNA-positive. In 1990, 0.06% of the blood components came from the HCV RNA-positive donors, and none during the first 6 months of 1992. In order to identify transfusion-transmitted HCV infections that took place before the introduction of tests for anti-HCV antibodies, patients with a history of transfusion and symptoms and signs of liver dysfunction or damage should be thoroughly tested.

  • 34.
    Palanisamy, Navaneethan
    et al.
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Danielsson, Axel
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Kokkula, Chakradhar
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Yin, Hong
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Bondeson, Kåre
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Wesslén, Lars
    Dept Infect Dis, Gävle Cent Hosp, Gävle, Sweden.
    Duberg, Ann-Sofi
    Örebro University Hospital. Dept Infect Dis.
    Lennerstrand, Johan
    Dept Med Sci, Uppsala Univ, Uppsala, Sweden.
    Implications of baseline polymorphisms for potential resistance to NS3 protease inhibitors in Hepatitis C virus genotypes 1a, 2b and 3a.2013In: Antiviral Research, ISSN 0166-3542, E-ISSN 1872-9096, Vol. 99, no 1, p. 12-17Article in journal (Refereed)
    Abstract [en]

    The future interferon-free treatment of hepatitis C virus (HCV) infection could include NS3 protease inhibitors (PIs) for potent pan-genotypic effect. We studied the prevalence of pre-existing PI resistance associated amino acid variants (RAVs) in 126 treatment-naive patient samples of HCV genotypes 1a, 2b and 3a, the most common genotypes in Sweden. The NS3 genes were each amplified by nested PCR method with degenerated primers to enable a broad genotype analysis. Population sequencing method was used, and the sequences were aligned with the NS3 sequence from HCV genotype 1a H77 strain. Interpretation of fold-change resistance to NS3 candidate drugs were done from already published phenotypic resistance data. The prevalence of known PI RAVs at baseline in genotype 1a was 28% (15/53), either single (V36L or Q80K/R) or combinations (T54A/S and V55A/I) of mutation(s). In genotype 2b, specific mutations like V36L, Q80G and S122R of viral NS3 protease gene were found in 100% (11/11). These may be the natural polymorphisms unique to genotype 2b. Similarly, specific mutations like V36L and D168Q were found uniquely in all 3a samples (30/30). The natural PI RAVs found in genotype 1a, although with relatively weak resistance, could still render up to 10-fold-resistance to the approved (boceprevir and telaprevir) and the 2nd generation PIs (faldaprevir and simeprevir). Moreover, the natural polymorphisms in genotype 2b (i.e. S122R) and 3a (i.e. D168Q), with inherent PI drug resistance of up to 20 and 700 fold respectively, would explain why current PIs are primarily directed against genotype 1.

  • 35. Polaris Observatory, Collaborators
    Global prevalence, treatment, and prevention of hepatitis B virus infection in 2016: a modelling study2018In: The Lancet Gastroenterology & Hepatology, ISSN 2468-1253, Vol. 3, no 6, p. 383-403Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The 69th World Health Assembly approved the Global Health Sector Strategy to eliminate viral hepatitis by 2030. Although no virological cure exists for hepatitis B virus (HBV) infection, existing therapies to control viral replication and prophylaxis to minimise mother-to-child transmission make elimination of HBV feasible. We aimed to estimate the national, regional, and global prevalence of HBsAg in the general population and in the population aged 5 years in 2016, as well as coverage of prophylaxis, diagnosis, and treatment.

    METHODS: In this modelling study, we used a Delphi process that included a literature review in PubMed and Embase, followed by interviews with experts, to quantify the historical epidemiology of HBV infection. We then used a dynamic HBV transmission and progression model to estimate the country-level and regional-level prevalence of HBsAg in 2016 and the effect of prophylaxis and treatment on disease burden.

    FINDINGS: We developed models for 120 countries, 78 of which were populated with data approved by experts. Using these models, we estimated that the global prevalence of HBsAg in 2016 was 3·9% (95% uncertainty interval [UI] 3·4-4·6), corresponding to 291 992 000 (251 513 000-341 114 000) infections. Of these infections, around 29 million (10%) were diagnosed, and only 4·8 million (5%) of 94 million individuals eligible for treatment actually received antiviral therapy. Around 1·8 (1·6-2·2) million infections were in children aged 5 years, with a prevalence of 1·4% (1·2-1·6). We estimated that 87% of infants had received the three-dose HBV vaccination in the first year of life, 46% had received timely birth-dose vaccination, and 13% had received hepatitis B immunoglobulin along with the full vaccination regimen. Less than 1% of mothers with a high viral load had received antiviral therapy to reduce mother-to-child transmission.

    INTERPRETATION: Our estimate of HBV prevalence in 2016 differs from previous studies, potentially because we took into account the effect of infant prophylaxis and early childhood vaccination, as well as changing prevalence over time. Although some regions are well on their way to meeting prophylaxis and prevalence targets, all regions must substantially scale-up access to diagnosis and treatment to meet the global targets.

  • 36.
    Razavi, H.
    et al.
    Ctr Dis Anal, Louisville, USA.
    Waked, I.
    Natl Liver Inst, Menoufia, Egypt.
    Sarrazin, C.
    JW Goethe Univ Hosp, Frankfurt, Germany.
    Myers, R. P.
    Liver Unit, Div Gastroenterol & Hepatol, Univ Calgary, Calgary AB, Canada.
    Idilman, R.
    Dept Gastroenterol, Sch Med, Ankara Univ, Ankara, Turkey.
    Calinas, F.
    Dept Gastroenterol, Ctr Hosp Lisboa Cent, Hosp Santo Antonio Capuchos, Lisbon, Portugal.
    Vogel, W.
    Med Univ Innsbruck, Innsbruck, Austria.
    Mendes Correa, M. C.
    Sch Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Hezode, C.
    Serv Hepatogastroenterol, Hop Henri Mondor, Creteil, France.
    Lazaro, P.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Akarca, U.
    Ege Univ, Izmir, Turkey.
    Aleman, S.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Dept Gastroenterol & Hepatol Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden.
    Balik, I.
    Ankara Univ, Ankara, Turkey.
    Berg, T.
    Univ Leipzig, Leipzig, Germany.
    Bihl, F.
    Dept Gastroenterol, Osped Cantonale, Bellinzona, Switzerland.
    Bilodeau, M.
    Dept Med, Liver Unit, Univ Montreal, Montreal, Canada.
    Blasco, A. J.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Brandao Mello, C. E.
    Dept Gastroenterol, Fed Univ State Rio de Janeiro, Rio De Janeiro, Brazil.
    Bruggmann, P.
    Arud Ctr Addict Med, Zurich, Switzerland.
    Buti, M.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Valle De Hebron, Barcelona, Spain.
    Calleja, J. L.
    Hosp Puerta Hierro, Madrid, Spain.
    Cheinquer, H.
    Hosp Clin, Univ Fed Rio Grande do Sul, Porto Alegre RS, Brazil.
    Christensen, P. B.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Clausen, M.
    Reg Hosp Hovedstaden, Copenhagen, Denmark.
    Coelho, H. S. M.
    Dept Clin Med, Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
    Cramp, M. E.
    Peninsula Sch Med & Dent, Univ Plymouth, Plymouth, England.
    Dore, G. J.
    Kirby Inst, Univ New S Wales, Sydney NSW, Australia.
    Doss, W.
    Cairo Univ, Cairo, Egypt.
    Duberg, Ann-Sofi
    Örebro University, School of Medicine, Örebro University, Sweden. Örebro University Hospital. Dept Infect Dis, Örebro University Hospital, Örebro, Sweden.
    El-Sayed, M. H.
    Ain Shams Univ, Cairo, Egypt.
    Ergor, G.
    Dokuz Eylul Univ, Izmir, Turkey.
    Esmat, G.
    Cairo Univ, Cairo, Egypt.
    Falconer, K.
    Dept Med Huddinge, Infect Dis Unit, Karolinska Univ Hosp, Karolinska Inst,Stockholm, Sweden.
    Felix, J.
    Exigo Consultores, Alhos Vedros, Portugal.
    Ferraz, M. L. G.
    Div Gastroenterol, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Ferreira, P. R.
    Div Infect Dis, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Frankova, S.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Garcia-Samaniego, J.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases (CIBEREHD), Hosp Carlos III, Madrid, Spain.
    Gerstoft, J.
    Univ Copenhagen, Copenhagen, Denmark.
    Giria, J. A.
    Direccao Geral Saude, Lisbon, Portugal.
    Goncales, F. L., Jr.
    Disciplina Doencas Infecciosas, Dept Clin Med, Grp Estudo Hepatites,Fac Ciencias Med,UNICAMP, Univ Estadual Campinas, Sao Paulo, Brazil.
    Gower, E.
    Ctr Dis Anal, Louisville, USA.
    Gschwantler, M.
    Dept Internal Med 4, Wilhelminenspital Stadt Wien, Vienna, Austria.
    Guimaraes Pessoa, M.
    Sch Med, Div Gastroenterol & Hepatol, Univ Sao Paulo, Sao Paulo, Brazil.
    Hindman, S. J.
    Ctr Dis Anal, Louisville, USA.
    Hofer, H.
    Div Gastroenterol & Hepatol, Dept Internal Med 3, Med Univ Vienna, Vienna, Austria.
    Husa, P.
    Clin Infect Dis, Univ Hosp Brno, Masaryk Univ, Brno, Czech Republic.
    Kåberg, M.
    Dept Med Huddinge, Infect Dis Unit, Karolinska Univ Hosp, Karolinska Inst, Stockholm, Sweden.
    Kaita, K. D. E.
    Dept Internal Med, Sect Hepatol, Univ Manitoba, Winnipeg MB, Canada; Hlth Sci Ctr, Viral Hepatitis Invest Unit, Winnipeg MB, Canada.
    Kautz, A.
    European Liver Patients Assoc, St Truiden, Belgium.
    Kaymakoglu, S.
    Istanbul Univ, Istanbul, Turkey.
    Krajden, M.
    British Columbia Ctr Dis Control, Univ British Columbia, Vancouver, Canada.
    Krarup, H.
    Dept Med Gastroenterol, Aalborg Univ Hosp, Aalborg, Denmark; Sect Mol Diagnost, Aalborg Univ Hosp, Aalborg, Denmark.
    Laleman, W.
    Univ Hosp Leuven, Katholieke Univ Leuven, Louvain, Belgium.
    Lavanchy, D.
    Marinho, R. T.
    Dept Gastroenterol, Ctr Hosp Lisboa Norte, Hosp Santa Maria, Lisbon, Portugal.
    Marotta, P.
    Div Gastroenterol, Univ Western Ontario, London ON, Canada.
    Mauss, S.
    Univ Dusseldorf, Dusseldorf, Germany.
    Moreno, C.
    Erasme Univ Hosp, Univ Libre Brussels, Brussels, Belgium.
    Murphy, K.
    Ctr Dis Anal, Louisville, USA.
    Negro, F.
    Div Gastroenterol & Hepatol, Univ Hosp, Geneva, Switzerland;Div Clin Pathol, Univ Hosp, Geneva, Switzerland.
    Nemecek, V.
    Natl Inst Publ Hlth, Natl Reference Lab Hepatitis, Prague, Czech Republic.
    Ormeci, N.
    Ankara Univ, Ankara, Turkey.
    Ovrehus, A. L. H.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Parkes, J.
    Univ Southhampton, Southampton, England.
    Pasini, K.
    Ctr Dis Anal, Louisville, USA.
    Peltekian, K. M.
    Capital Dist Hlth Author, Queen Elizabeth II Hlth Sci Ctr, Dept Med,Dalhousie Univ & Hepatol Serv, Halifax NS, Canada; Capital Dist Hlth Author, Queen Elizabeth II Hlth Sci Ctr, Dept Surg, Dalhousie Univ & Hepatol Serv, Halifax NS, Canada.
    Ramji, A.
    Dept Gastroenterol, Univ British Columbia, Vancouver, Canada.
    Reis, N.
    Assembleia Republ, Lisbon, Portugal.
    Roberts, S. K.
    Alfred Hosp, Melbourne Vic, Australia; Monash Univ, Melbourne, Australia.
    Rosenberg, W. M.
    Div Med, UCL Inst Liver & Digest Hlth, University College London, London, England.
    Roudot-Thoraval, F.
    Dept Sante Publ, Hop Henri Mondor, Creteil, France.
    Ryder, S. D.
    Nottingham Univ Hosp NHS Trust, Nottingham, England; Biomed Res Unit, Nottingham, England.
    Sarmento-Castro, R.
    Dept Infect Dis, Ctr Hosp Porto, Oporto, Portugal.
    Semela, D.
    Div Gastroenterol & Hepatol, Cantonal Hosp St Gallen, St Gallen, Switzerland.
    Sherman, M.
    Univ Hlth Network, Toronto Gen Hosp, Univ Toronto, Toronto, Canada.
    Shiha, G. E.
    Egyptian Liver Res Inst & Hosp, Dakahliah, Egypt.
    Sievert, W.
    Monash Univ, Melbourne, Australia; Monash Hlth, Melbourne Vic, Australia.
    Sperl, J.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Starkel, P.
    Clin Univ St Luc, Catholic Univ Louvain, Brussels, Belgium.
    Stauber, R. E.
    Div Gastroenterol & Hepatol, Dept Internal Med, Med Univ Graz, Graz, Austria.
    Thompson, A. J.
    Dept Gastroenterol, St Vincents Hosp, Melbourne Vic, Australia; Univ Melbourne, Melbourne Vic, Australia.
    Urbanek, P.
    Dept Internal Med, Fac Med 1, Charles Univ Prague, Prague, Czech Republic; Cent Mil Hosp, Prague, Czech Republic.
    Van Damme, P.
    Univ Antwerp, Antwerp, Belgium.
    van Thiel, I.
    St Truiden, Belgium; Deutsch Leberhilfe eV, European Liver Patients Assoc, Cologne, Germany.
    Van Vlierberghe, H.
    Ghent Univ Hosp, Ghent, Belgium.
    Vandijck, D.
    Dept Hlth Econ & Patient Safety, Belgium Hasselt Univ, Univ Ghent, Diepenbeek, Belgium.
    Wedemeyer, H.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany.
    Weis, N.
    Copenhagen Univ Hosp, Hvidovre, Denmark.
    Wiegand, J.
    Ankara Univ, Ankara, Turkey.
    Yosry, A.
    Cairo Univ, Cairo, Egypt.
    Zekry, A.
    St George Hosp Clin Sch Med, Univ New S Wales, Sydney NSW, Australia; Sch Med Sci, Univ New S Wales, Sydney NSW, Australia.
    Cornberg, M.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany.
    Muellhaupt, B.
    Swiss HPB Hepatopancreatobiliary Ctr, Univ Zurich Hosp, Zurich, Switzerland; Dept Gastroenterol & Hepatol, Univ Zurich Hosp, Zurich, Switzerland.
    Estes, C.
    Ctr Dis Anal, Louisville, USA.
    The present and future disease burden of hepatitis C virus (HCV) infection with today's treatment paradigm2014In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 21, no Suppl. 1, p. 34-59Article in journal (Refereed)
    Abstract [en]

    The disease burden of hepatitis C virus (HCV) is expected to increase as the infected population ages. A modelling approach was used to estimate the total number of viremic infections, diagnosed, treated and new infections in 2013. In addition, the model was used to estimate the change in the total number of HCV infections, the disease progression and mortality in 2013-2030. Finally, expert panel consensus was used to capture current treatment practices in each country. Using today's treatment paradigm, the total number of HCV infections is projected to decline or remain flat in all countries studied. However, in the same time period, the number of individuals with late-stage liver disease is projected to increase. This study concluded that the current treatment rate and efficacy are not sufficient to manage the disease burden of HCV. Thus, alternative strategies are required to keep the number of HCV individuals with advanced liver disease and liver-related deaths from increasing.

  • 37.
    Razavi, Homie A.
    et al.
    Center for Disease Analysis (CDA), Louisville CO, USA.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences.
    Hatzakis, Angelos
    Department of Hygiene, Epidemiology & Medical Statistics at Athens University Medical School, Athens, Greece.
    Hepatitis C virus prevalence and level of intervention required to achieve the WHO targets for elimination in the European Union by 2030: a modelling study2017In: The Lancet Gastroenterology & Hepatology, ISSN 2468-1253, Vol. 2, no 5, p. 325-336Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Hepatitis C virus (HCV) is a leading cause of liver-related morbidity and mortality worldwide. In the European Union (EU), treatment and cure of HCV with direct-acting antiviral therapies began in 2014. WHO targets are to achieve a 65% reduction in liver-related deaths, a 90% reduction of new viral hepatitis infections, and 90% of patients with viral hepatitis infections being diagnosed by 2030. This study assessed the prevalence of HCV in the EU and the level of intervention required to achieve WHO targets for HCV elimination.

    METHODS: We populated country Markov models for the 28 EU countries through a literature search of PubMed and Embase between Jan 1, 2000, and March 31, 2016, and a Delphi process to gain expert consensus and validate inputs. We aggregated country models to create a regional EU model. We used the EU model to forecast HCV disease progression (considering the effect of immigration) and developed a strategy to acehive WHO targets. We used weighted average sustained viral response rates and fibrosis restrictions to model the effect of current therapeutic guidelines. We used the EU model to forecast HCV disease progression (considering the effect of immigration) under current screening and therapeutic guidelines. Additionally, we back-calculated the total number of patients needing to be screened and treated to achieve WHO targets.

    FINDINGS: We estimated the number of viraemic HCV infections in 2015 to be 3 238 000 (95% uncertainty interval [UI] 2 106 000-3 795 000) of a total population of 509 868 000 in the EU, equating to a prevalence of viraemic HCV of 0·64% (95% UI 0·41-0·74). We estimated that 1 180 000 (95% UI 1 003 000-1 357 000) people were diagnosed with viraemia (36·4%), 150 000 (12 000-180 000) were treated (4·6% of the total infected population or 12·7% of the diagnosed population), 133 000 (106 000-160 000) were cured (4·1%), and 57 900 (43 900-67 300) were newly infected (1·8%) in 2015. Additionally, 30 400 (26 600-42 500) HCV-positive immigrants entered the EU. To achieve WHO targets, unrestricted treatment needs to increase from 150 000 patients in 2015 to 187 000 patients in 2025 and diagnosis needs to increase from 88 800 new cases annually in 2015 to 180 000 in 2025.

    INTERPRETATION: Given its advanced health-care infrastructure, the EU is uniquely poised to eliminate HCV; however, expansion of screening programmes is essential to increase treatment to achieve the WHO targets. A united effort, grounded in sound epidemiological evidence, will also be necessary.

     

  • 38.
    Safreed-Harmon, Kelly
    et al.
    Barcelona Institute for Global Health (ISGlobal), Hospital Clínic, University of Barcelona, Barcelona, Spain.
    Blach, Sarah
    Center for Disease Analysis Foundation, Lafayette, Colorado, United States.
    Aleman, Soo
    Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden; Department of Medicine Huddinge, Karolinska Institutet, Sweden.
    Boe Kielland, Knut
    Norwegian National Advisory Unit on Concurrent Substance Abuse and Mental Health Disorders, Innlandet Hospital Trust, Brumunddal, Norway.
    Bollerup, Signe
    Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Copenhagen, Denmark.
    Cooke, Graham
    Faculty of Medicine, Imperial College London, United Kingdom.
    Dalgard, Olav
    Department of Infectious Diseases, Akershus University Hospital, Lørenskog, Norway; Institute of clinical medicine, University of Oslo, Oslo, Norway.
    Dillon, John F.
    Division of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, United Kingdom.
    Dore, Gregory J.
    The Kirby Institute, UNSW Sydney, Sydney, Australia.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Department of Infectious Diseases.
    Grebely, Jason
    The Kirby Institute, UNSW Sydney, Sydney, Australia.
    Midgard, Håvard
    Department of Gastroenterology, Oslo University Hospital, Oslo, Norway.
    Porter, Kholoud
    Institute for Global Health, University College London, London, United Kingdom.
    Razavi, Homie
    Center for Disease Analysis Foundation, Lafayette, Colorado, United States.
    Tyndall, Mark
    School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada.
    Weis, Nina
    Department of Infectious Diseases, Copenhagen University Hospital, Hvidovre, Copenhagen, Denmark; Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
    Lazarus, Jeffrey V.
    Barcelona Institute for Global Health (ISGlobal), Hospital Clínic, University of Barcelona, Barcelona, Spain; CHIP, WHO Collaborating Centre on HIV and Viral Hepatitis, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.
    The Consensus Hepatitis C Cascade of Care: standardized reporting to monitor progress toward elimination2019In: Clinical Infectious Diseases, ISSN 1058-4838, E-ISSN 1537-6591, article id ciz714Article in journal (Refereed)
    Abstract [en]

    Cascade-of-care (CoC) monitoring is an important component of the response to the global hepatitis C virus (HCV) epidemic. CoC metrics can be used to communicate in simple terms the extent to which national and subnational governments are advancing on key targets, and CoC findings can inform strategic decision-making regarding how to maximize the progression of HCV-infected individuals to diagnosis, treatment and cure. The value of reporting would be enhanced if reporting entities utilized a standardized approach for generating their CoCs. We have described the Consensus HCV CoC that we developed to address this need and have presented findings from Denmark, Norway and Sweden, where it was piloted. We encourage the uptake of the Consensus HCV CoC as a global instrument for facilitating clear and consistent reporting via the World Health Organization (WHO) viral hepatitis monitoring platform and ensuring the accurate monitoring of progress toward WHO's 2030 hepatitis C elimination targets.

  • 39.
    Simon, Tracey G.
    et al.
    Massachusetts General Hospital, Boston MA, USA.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences.
    Aleman, Soo
    Department of Infectious Diseases, Karolinska University Hospital, Solna, Sweden.
    Hagström, Hannes
    Center for Digestive Diseases, Division of Hepatology, Karolinska Institutet, Solna, Sweden.
    Chung, Raymond T.
    Liver Center and Gastrointestinal Division, Massachusetts General Hospital, Boston MA, USA; Harvard Medical School, Boston MA, USA.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Lipophilic Statins and Risk of Hepatocellular Carcinoma and Mortality: A Prospective, Nationwide Population with Chronic Viral Hepatitis2018In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 68, no Suppl.1, p. 59A-60AArticle in journal (Refereed)
  • 40.
    Simon, Tracey G.
    et al.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences.
    Aleman, Soo
    Karolinska University Hospital, Stockholm, Sweden.
    Hagström, Hannes
    Karolinska University Hospital and Karolinska Institutet, Stockholm, Sweden.
    Nguyen, Long H.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Khalili, Hamed
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA; Karolinska Institutet, Stockholm, Sweden.
    Chung, Raymond T.
    Massachusetts General Hospital and Harvard Medical School, Boston Massachusetts, USA.
    Ludvigsson, Jonas F.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Columbia University College of Physicians and Surgeons, New York, USA.
    Lipophilic Statins and Risk for Hepatocellular Carcinoma and Death in Patients With Chronic Viral Hepatitis: Results From a Nationwide Swedish Population2019In: Annals of Internal Medicine, ISSN 0003-4819, E-ISSN 1539-3704, Vol. 171, no 5, p. 318-327Article in journal (Refereed)
    Abstract [en]

    Background: Whether statin type influences hepatocellular carcinoma (HCC) incidence or mortality in chronic hepatitis B or C virus infection is unknown.

    Objective: To assess the relationship between lipophilic or hydrophilic statin use and HCC incidence and mortality in a nationwide population with viral hepatitis.

    Design: Prospective propensity score (PS)-matched cohort.

    Setting: Swedish registers, 2005 to 2013.

    Participants: A PS-matched cohort of 16 668 adults (8334 who initiated statin use [6554 lipophilic and 1780 hydrophilic] and 8334 nonusers) among 63 279 eligible adults.

    Measurements: Time to incident HCC, ascertained from validated registers. Statin use was defined from filled prescriptions as 30 or more cumulative defined daily doses (cDDDs).

    Results: Compared with matched nonusers, 10-year HCC risk was significantly lower among lipophilic statin users (8.1% vs. 3.3%; absolute risk difference [RD], -4.8 percentage points [95% CI, -6.2 to -3.3 percentage points]; adjusted subdistribution hazard ratio [aHR], 0.56 [CI, 0.41 to 0.79]) but not hydrophilic statin users (8.0% vs. 6.8%; RD, -1.2 percentage points [CI, -2.6 to 0.4 percentage points]; aHR, 0.95 [CI, 0.86 to 1.08]). The in- verse association between lipophilic statins and HCC risk seemed to be dose-dependent. Compared with nonusers, 10-year HCC risk was lowest with 600 or more lipophilic statin cDDDs (8.4% vs. 2.5%; RD, -5.9 percentage points [CI, -7.6 to -4.2 percentage points]; aHR, 0.41 [CI, 0.32 to 0.61]), and 10-year mortality was significantly lower among both lipophilic (15.2% vs. 7.3%; RD, -7.9 percentage points [CI, -9.6 to -62 percentage points]) and hydrophilic (16.0% vs. 11.5%; RD, -4.5 percentage points [CI, -6.0 to -3.0 percentage points]) statin users.

    Limitation: Lack of lipid, fibrosis, or HCC surveillance data.

    Conclusion: In a nationwide viral hepatitis cohort, lipophilic statins were associated with significantly reduced HCC incidence and mortality. An association between hydrophilic statins and reduced risk for HCC was not found. Further research is needed to determine whether lipophilic statin therapy is feasible for prevention of HCC.

  • 41.
    Sjöberg, Lennart
    et al.
    Department of Clinical Microbiology, Örebro Medical Center Hospital, Örebro, Sweden.
    Fredlund, Hans
    Department of Clinical Microbiology, Örebro Medical Center Hospital, Örebro, Sweden.
    Duberg, Ann-Sofie
    Department of Clinical Microbiology, Örebro Medical Center Hospital, Örebro, Sweden.
    A comparison between Bactec aerobic resin and hypertonic blood culture media.1988In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 96, no 8, p. 720-722Article in journal (Refereed)
    Abstract [en]

    The presence of antimicrobial agents in patients' blood is thought to represent an important source of false-negative blood cultures. This has led to the incorporation of agents with inhibitory effects on antimicrobial drugs into culture medium. In the present study, Bactec aerobic resin-containing blood culture medium was compared with Bactec hypertonic blood culture medium. 504 patients receiving cytostatic and/or antibiotic treatment were studied. Sensitivity calculations on detection of bacteremia in these patients gave 0.91 for the resin medium and 0.79 for the hypertonic blood culture system and showed a significant difference (p = 0.016). In addition, the resin-containing system more rapidly detected positive cultures than the hypertonic system.

  • 42. Strauss, Reinhild
    et al.
    Törner, Anna
    Duberg, Ann-Sofi
    Örebro University, School of Health and Medical Sciences.
    Hultcrantz, Rolf
    Ekdahl, Karl
    Hepatocellular carcinoma and other primary liver cancers in hepatitis C patients in Sweden: a low endemic country2008In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 15, no 7, p. 531-537Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to assess the risk of hepatocellular carcinoma (HCC) and other primary liver cancers (PLC) in the nationwide cohort of hepatitis C virus (HCV) infected patients in Sweden. The basis was the total HCV-cohort notified in 1990-2004, after excluding 3238 people also reported with hepatitis B, the study cohort consisted of 36 126 people contributing an observation time of 246 105 person-years. The most common route of transmission was intravenous drug use (57%). The national Cancer Registry was used for follow-up, and 354 developed PLC (mainly HCC), of whom 234 were eligible for statistical analysis. The PLC incidence in the HCV cohort was compared with the incidence in the general population, and a standardized incidence ratio (SIR) was calculated for six different strata according to estimated duration of infection. The highest relative risk, SIR: 46 (95% CI: 36-56) was found in the stratum 25-30 years with HCV infection and SIR: 40 (95% CI: 31-51) in the stratum 30-35 years with infection. In the entire community-based HCV cohort in Sweden we found a highly increased risk of liver cancer compared to the general population. The highest relative risk was among people who had been infected for more than 25 years.

    PMID: 18397224 [PubMed - indexed for MEDLINE]

  • 43.
    Särnblad, Stefan
    et al.
    Örebro University, School of Medical Sciences.
    Lidskog, Marie
    Örebro University, School of Medical Sciences.
    Walfridsson, Helena
    Örebro University, School of Medical Sciences.
    Hjelmqvist, Hans
    Örebro University, School of Medical Sciences.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences.
    Will Early Clinical Training improve the professional skills?: Experience from a New Medical Education in Sweden2018Conference paper (Refereed)
    Abstract [en]

    Background: The undergraduate medical education in Sweden is 5½ years long (11 semesters), followed by an 18 months internship before license. The university curriculum used to be 6 theoretical semesters followed by 5 “clinical” semesters. Today it is common with integrated curricula with an early introduction of clinical training.

    Method: School of Medicine at Örebro University started in January 2011 and now admits 70 students every semester. The first students graduated in June 2016. The educational approach is problem-based learning and the curriculum is integrated with six themes based on physiological processes. Biomedicine, clinical medicine and professional development are integrated throughout the entire programme.

    Results: In total, clinical placement constitutes 74 weeks of which 16 weeks are spread through the first six semesters. The remaining 58 weeks (semester 7-11) are divided into six longer periods related to the themes. The objective of clinical placement during the first 6 semesters is to practice general clinical skills like communication, history-taking and clinical examination, but also to understand the health care system and the tasks of other health care personnel. The clinical placement in semester 6 ends with a seminar for reflection around the professional development and the value of early clinical placement. The students appreciate the early clinical placements. They manage to acquire general professional skills at this early stage and have the possibility to reflect upon their choice of profession. This stimulates theoretical studies and makes them more comfortable when entering the long clinical placements related to the themes. This is beneficial also for the clinical tutors. The first Örebro students that graduated were satisfied with the preparation given “to work as doctors” and gave the University the highest rank in a national survey.

    Conclusion: Early clinical training is beneficial for the development of professional skills; it motivates and gives the student an early understanding of their future professional role. A challenge may be to find enough placements and the need for coaching adjusted for different stages of professional development.

    Take-home message: Early clinical training is beneficial for the development of professional skills.

  • 44. The Polaris Observatory HCV, collaborators
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences.
    Razavi, Homie
    Center for Disease Analysis, Denver CO, USA.
    Global prevalence and genotype distribution of hepatitis C virus infection in 2015: a modelling study2017In: The Lancet Gastroenterology & Hepatology, ISSN 2468-1253, Vol. 2, no 3, p. 161-176Article in journal (Refereed)
    Abstract [en]

    Background: The 69th World Health Assembly approved the Global Health Sector Strategy to eliminate hepatitis C virus (HCV) infection by 2030, which can become a reality with the recent launch of direct acting antiviral therapies. Reliable disease burden estimates are required for national strategies. This analysis estimates the global prevalence of viraemic HCV at the end of 2015, an update of—and expansion on—the 2014 analysis, which reported 80 million (95% CI 64–103) viraemic infections in 2013.

    Methods: We developed country-level disease burden models following a systematic review of HCV prevalence (number of studies, n=6754) and genotype (n=11 342) studies published after 2013. A Delphi process was used to gain country expert consensus and validate inputs. Published estimates alone were used for countries where expert panel meetings could not be scheduled. Global prevalence was estimated using regional averages for countries without data.

    Findings: Models were built for 100 countries, 59 of which were approved by country experts, with the remaining 41 estimated using published data alone. The remaining countries had insuffi cient data to create a model. The global prevalence of viraemic HCV is estimated to be 1·0% (95% uncertainty interval 0·8–1·1) in 2015, corresponding to 71·1 million (62·5–79·4) viraemic infections. Genotypes 1 and 3 were the most common cause of infections (44% and 25%, respectively).

    Interpretation: The global estimate of viraemic infections is lower than previous estimates, largely due to more recent (lower) prevalence estimates in Africa. Additionally, increased mortality due to liver-related causes and an ageing population may have contributed to a reduction in infections.

  • 45.
    Törner, Anna
    et al.
    Department of Epidemiology, Swedish Institute for Infectious Disease Control, Solna, Sweden.
    Dickman, Paul
    Department of Medical Epidemiology and Biosta- tistics, Karolinska Institutet, Solna, Sweden.
    Duberg, Ann-Sofi
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Kristinsson, Sigurdur
    Division of Hematology, Department of Medicine, Karolinska University Hospital, Solna, Sweden.
    Landgren, Ola
    National Cancer Institute, Bethesda MD, USA.
    Björkholm, Magnus
    Division of Hematology, Department of Medicine, Karolinska University Hospital, Solna, Sweden.
    Svensson, Åke
    Department for Mathematical Statistics, Stockholm University, Stockholm, Sweden.
    A method to visualize and adjust for selection bias in prevalent cohort studies2011In: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 174, no 8, p. 969-76Article in journal (Refereed)
    Abstract [en]

    Selection bias and confounding are concerns in cohort studies where the reason for inclusion of subjects in the cohort may be related to the outcome of interest. Selection bias in prevalent cohorts is often corrected by excluding observation time and events during the first time period after inclusion in the cohort. This time period must be chosen carefully-long enough to minimize selection bias but not too long so as to unnecessarily discard observation time and events. A novel method visualizing and estimating selection bias is described and exemplified by using 2 real cohort study examples: a study of hepatitis C virus infection and a study of monoclonal gammopathy of undetermined significance. The method is based on modeling the hazard for the outcome of interest as a function of time since inclusion in the cohort. The events studied were "hospitalizations for kidney-related disease" in the hepatitis C virus cohort and "death" in the monoclonal gammopathy of undetermined significance cohort. Both cohorts show signs of considerable selection bias as evidenced by increased hazard in the time period after inclusion in the cohort. The method was very useful in visualizing selection bias and in determining the initial time period to be excluded from the analyses.

  • 46.
    Törner, Anna
    et al.
    Department of Epidemiology, Swedish Institute for Infectious Disease Control, Solna, Sweden.
    Duberg, Ann-Sofi
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    Dickman, Paul
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Solna, Sweden.
    Svensson, Åke
    Department for Mathematical Statistics, Stockholm University, Stockholm, Sweden.
    A proposed method to adjust for selection bias in cohort studies2010In: American Journal of Epidemiology, ISSN 0002-9262, E-ISSN 1476-6256, Vol. 171, no 5, p. 602-608Article in journal (Refereed)
    Abstract [en]

    Selection bias is a concern in cohort studies in which selection into the cohort is related to the studied outcome. An example is chronic infection with hepatitis C virus, where the initial infection may be asymptomatic for decades. This problem leads to selection of more severely ill individuals into registers of such infections. Cohort studies often adjust for this bias by introducing a time window between entry into the cohort and entry into the study. This paper describes and assesses a novel method to improve adjustment for this type of selection bias. The size of the time window is decided by calculating a standardized incidence ratio as a continuous function of the size of the time window. The resulting graph is used to decide on an appropriate window size. The method is evaluated by using the Swedish register of hepatitis C virus infections for 1990-2006. The complications studied were non-Hodgkin lymphoma and liver cancer. Selection bias differed for the studied outcomes, and a time window of a minimum of 2 months and 12 months, respectively, was judged to be appropriate. The novel method may have advantages compared with an interval-based method, especially in cohort studies with small numbers of events.

  • 47.
    Törner, Anna
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Stokkeland, Knut
    Department of Medicine, Visby Hospital, Visby, Sweden; Department of Medicine, Gastroenterology and Hepatology Unit, Karolinska Institutet, Stockholm, Sweden.
    Svensson, Åke
    Department of Mathematics, Stockholm University, Stockholm, Sweden.
    Dickman, Paul W.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Hultcrantz, Rolf
    Department of Medicine, Gastroenterology and Hepatology Unit, Karolinska Institutet, Stockholm, Sweden.
    Montgomery, Scott M.
    Örebro University, School of Medical Sciences. Örebro University Hospital. Clinical Epidemiology Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden; Department of Epidemiology and Public Health, University College London, London, UK.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Örebro University Hospital. Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden.
    The underreporting of hepatocellular carcinoma to the Cancer Register and a log-linear model to estimate a more correct incidence2017In: Hepatology, ISSN 0270-9139, E-ISSN 1527-3350, Vol. 65, no 3, p. 885-892Article in journal (Refereed)
    Abstract [en]

    The Cancer Register (CR) in Sweden has reported that the incidence of primary liver cancer (PLC) has slowly declined over the last decades. Even though all cancers, irrespective of diagnostic method, should be reported to the CR, the PLC incidence may not reflect the true rate. Improved diagnostic tools have enabled diagnosis of hepatocellular carcinoma (HCC) based on non-invasive methods without histological verification, possibly associated with missed cancer-reports or misclassification in the CR. Our objective was to study the completeness and assess the underreporting of PLC to the CR, and to produce a more accurate estimate based on three registers. The CR, the Cause of Death and the Patient Register were investigated. Differences and overlap were examined, the incidence was estimated by merging data from the registers, and the number reported to none of the registers was estimated using a log-linear capture-recapture model. The results show that 98% of the PLCs reported to the CR were histologically verified; 80% were HCC and 20% intrahepatic cholangiocarcinoma. Unspecified liver cancer decreased over time and constituted <10% of all reported liver cancers. The CR may underestimate the liver cancer incidence by 37% - 45%, primarily due to missed cancer-reports. The estimated annual number of liver cancers increased over time, but the standardized incidence was stable around 11 per 100,000. Hepatitis C associated liver cancer increased and constituted 20% in 2010.

    Conclusion: There was an underreporting of PLC diagnosed by non-invasive methods. The incidence was considerably higher than estimated by the CR, with a stable incidence over time. Reporting needs to improve and combining registers is recommended when studying incidence. This article is protected by copyright. All rights reserved.

  • 48.
    Wedemeyer, H.
    et al.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany; German Liver Fdn, Hannover, Germany.
    Duberg, Ann-Sofi
    Örebro University, School of Medicine, Örebro University, Sweden. Örebro University Hospital. Dept Infect Dis, Örebro University Hospital, Örebro, Sweden.
    Buti, M.
    CIBERehd, Hosp Valle De Hebron, Barcelona, Spain.
    Rosenberg, W. M.
    Div Med, UCL Inst Liver & Digest Hlth, University College, London, London, England.
    Frankova, S.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Esmat, G.
    Cairo Univ, Cairo, Egypt.
    Ormeci, N.
    Ankara Univ, Ankara, Turkey.
    Van Vlierberghe, H.
    Ghent Univ Hosp, Ghent, Belgium.
    Gschwantler, M.
    Dept Internal Med 4, Wilhelminenspital Stadt Wien, Vienna, Austria.
    Akarca, U.
    Ege Univ, Izmir, Turkey.
    Aleman, S.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Dept Gastroenterol & Hepatol Infect Dis, Karolinska Univ Hosp, Stockholm, Sweden .
    Balik, I.
    Ankara Univ, Ankara, Turkey.
    Berg, T.
    Univ Leipzig, Leipzig, Germany.
    Bihl, F.
    Dept Gastroenterol, Osped Cantonale, Bellinzona, Switzerland.
    Bilodeau, M.
    Dept Med, Liver Unit, Univ Montreal, Montreal, Canada.
    Blasco, A. J.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Brandao Mello, C. E.
    Dept Gastroenterol, Fed Univ State Rio de Janeiro, Rio De Janeiro, Brazil.
    Bruggmann, P.
    Arud Ctr Addict Med, Zurich, Switzerland.
    Calinas, F.
    Ctr Hosp Lisboa Cent, Dept Gastroenterol, Hosp Santo Antonio Capuchos, Lisbon, Portugal.
    Calleja, J. L.
    Hosp Puerta Hierro, Madrid, Spain.
    Cheinquer, H.
    Hosp Clin, Univ Fed Rio Grande do Sul, Porto Alegre RS, Brazil.
    Christensen, P. B.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Clausen, M.
    Region Hosp Hovedstaden, Region Hovedstaden, Hillerød, Denmark.
    Coelho, H. S. M.
    Dept Clin Med, Univ Fed Rio de Janeiro, Rio De Janeiro, Brazil.
    Cornberg, M.
    Dept Gastroenterol Hepatol & Endocrinol, Hannover Med Sch, Hannover, Germany; German Liver Fdn, Hannover, Germany.
    Cramp, M. E.
    Peninsula Sch Med & Dent, Univ Plymouth, Plymouth, England.
    Dore, G. J.
    Kirby Inst, Univ New S Wales, Sydney NSW, Australia.
    Doss, W.
    Cairo Univ, Cairo, Egypt.
    El-Sayed, M. H.
    Ain Shams Univ, Cairo, Egypt.
    Ergor, G.
    Dokuz Eylul Univ, Izmir, Turkey.
    Estes, C.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Falconer, K.
    Dept Med, Karolinska Inst, Huddinge, Sweden; Infect Dis Unit, Karolinska Univ Hosp, Stockholm, Sweden.
    Felix, J.
    Exigo Consultores, Alhos Vedros, Portugal.
    Ferraz, M. L. G.
    Div Gastroenterol, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Ferreira, P. R.
    Div Infect Dis, Univ Fed Sao Paulo, Sao Paulo, Brazil.
    Garcia-Samaniego, J.
    Biomedical Research Networking Center in Hepatic and Digestive Diseases, Hosp Carlos III, Madrid, Spain.
    Gerstoft, J.
    Univ Copenhagen, Copenhagen, Denmark.
    Giria, J. A.
    Direccao Geral Saude, Lisbon, Portugal.
    Goncales, F. L., Jr.
    Fac Ciencias Med, Disciplina Doencas Infecciosas, Grp Estudo Hepatites,Dept Clin Med, Univ Estadual Campinas, Sao Paulo, Brazil.
    Guimaraes Pessoa, M.
    Sch Med, Div Gastroenterol & Hepatol, Univ Sao Paulo, Sao Paulo, Brazil.
    Hezode, C.
    Serv Hepatogastroenterol, Hop Henri Mondor, Creteil, France.
    Hindman, S. J.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Infect Dis Unit, Karolinska Univ Hosp, Stockholm, Sweden.
    Hofer, H.
    Div Gastroenterol & Hepatol, Dept Internal Med 3, Med Univ Vienna, Vienna, Austria.
    Husa, P.
    Clin Infect Dis, Univ Hosp Brno, Masaryk Univ, Brno, Czech Republic.
    Idilman, R.
    Dept Gastroenterol, Sch Med, Ankara Univ, Ankara, Turkey.
    Kåberg, M.
    Dept Med Huddinge, Karolinska Inst, Stockholm, Sweden; Infect Dis Unit, Karolinska Univ Hosp, Stockholm, Sweden.
    Kaita, K. D. E.
    Dept Internal Med, Sect Hepatol, Univ Manitoba, Winnipeg MB, Canada; Viral Hepatitis Invest Unit, Hlth Sci Ctr, Winnipeg MB, Canada .
    Kautz, A.
    European Liver Patients Assoc, St Truiden, Belgium.
    Kaymakoglu, S.
    Istanbul Univ, Istanbul, Turkey.
    Krajden, M.
    British Columbia Ctr Dis Control, Univ British Columbia, Vancouver, Canada.
    Krarup, H.
    Dept Med Gastroenterol, Aalborg Univ Hosp, Aalborg, Denmark; Sect Mol Diagnost, Aalborg Univ Hosp, Aalborg, Denmark .
    Laleman, W.
    Univ Hosp Leuven, Katholieke Univ Leuven, Louvain, Belgium.
    Lavanchy, D.
    Lazaro, P.
    Adv Tech Hlth Serv Res TAISS, Madrid, Spain.
    Marinho, R. T.
    Ctr Hosp Lisboa Cent, Dept Gastroenterol, Hosp Santo Antonio Capuchos, Lisbon, Portugal.
    Marotta, P.
    Div Gastroenterol, Univ Western Ontario, London ON, Canada.
    Mauss, S.
    Univ Dusseldorf, Dusseldorf, Germany.
    Mendes Correa, M. C.
    Sch Med, Univ Sao Paulo, Sao Paulo, Brazil.
    Moreno, C.
    Erasme Univ Hosp, Univ Libre Brussels, Brussels, Belgium.
    Muellhaupt, B.
    Swiss HPB Hepatopancreatobiliary Ctr, Univ Zurich Hosp, Zurich, Switzerland; Dept Gastroenterol & Hepatol, Univ Zurich Hosp, Zurich, Switzerland.
    Myers, R. P.
    Div Gastroenterol & Hepatol, Liver Unit, Univ Calgary, Calgary AB, Canada.
    Nemecek, V.
    Natl Reference Lab Hepatitis, Natl Inst Publ Hlth, Prague, Czech Republic.
    Ovrehus, A. L. H.
    Dept Infect Dis, Odense Univ Hosp, Odense, Denmark.
    Parkes, J.
    Univ Southhampton, Southampton, England.
    Peltekian, K. M.
    Queen Elizabeth II Hlth Sci Ctr, Capital Dist Hlth Author, Dept Med, Dalhousie Univ & Hepatol Serv, Halifax NS, Canada; Queen Elizabeth II Hlth Sci Ctr, Capital Dist Hlth Author, Dept Surg, Dalhousie Univ & Hepatol Serv, Halifax NS, Canada .
    Ramji, A.
    Dept Gastroenterol, Univ British Columbia, Vancouver, Canada.
    Razavi, H.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Reis, N.
    Assembleia Republ, Lisbon, Portugal.
    Roberts, S. K.
    Alfred Hosp, Melbourne Vic, Australia; Monash Univ, Melbourne, Australia.
    Roudot-Thoraval, F.
    Dept Sante Publ, Hop Henri Mondor, Creteil, France.
    Ryder, S. D.
    Nottingham Univ Hosp NHS Trust, Nottingham, England; Biomed Res Unit, Nottingham, England .
    Sarmento-Castro, R.
    Dept Infect Dis, Ctr Hosp Porto, Oporto, Portugal.
    Sarrazin, C.
    JW Goethe Univ Hosp, Frankfurt, Germany.
    Semela, D.
    Div Gastroenterol & Hepatol, Cantonal Hosp St Gallen, St Gallen, Switzerland.
    Sherman, M.
    Univ Hlth Network, Univ Toronto, Toronto Gen Hosp, Toronto, Canada.
    Shiha, G. E.
    Egyptian Liver Res Inst & Hosp ELRIAH, Dakahliah, Egypt.
    Sperl, J.
    Dept Hepatogastroenterol, Inst Clin & Expt Med, Prague, Czech Republic.
    Starkel, P.
    Clin Univ St Luc, Catholic Univ Louvain, Brussels, Belgium.
    Stauber, R. E.
    Med Univ Graz, Div Gastroenterol & Hepatol, Dept Internal Med, Graz, Austria.
    Thompson, A. J.
    St Vincents Hosp, Dept Gastroenterol, Melbourne Vic, Australia; Univ Melbourne, Melbourne Vic, Australia.
    Urbanek, P.
    Dept Internal Med, Fac Med 1, Charles Univ, Prague, Czech Republic; Cent Mil Hosp, Prague, Czech Republic.
    Van Damme, P.
    Univ Antwerp, Antwerp, Belgium.
    van Thiel, I.
    European Liver Patients Assoc, St Truiden, Belgium; Deutsch Leberhilfe eV, Cologne, Germany.
    Vandijck, D.
    Univ Ghent, Dept Hlth Econ & Patient Safety, Ghent, Belgium; Hasselt Univ, Diepenbeek, Belgium.
    Vogel, W.
    Med Univ Innsbruck, Innsbruck, Austria.
    Waked, I.
    Natl Liver Inst, Menoufia, Egypt.
    Weis, N.
    Copenhagen Univ Hosp, Hvidovre, Denmark.
    Wiegand, J.
    Univ Leipzig, Leipzig, Germany.
    Yosry, A.
    Cairo Univ, Cairo, Egypt.
    Zekry, A.
    Univ New S Wales, St George Hosp Clin Sch Med, Sydney, NSW, Australia; Univ New S Wales, Sch Med Sci, Sydney, NSW, Australia.
    Negro, F.
    Univ Hosp, Div Gastroenterol & Hepatol, Geneva, Switzerland; Monash Hlth, Melbourne Vic, Australia.
    Sievert, W.
    Monash Hlth, Melbourne Vic, Australia; Monash Univ, Melbourne, Australia.
    Gower, E.
    Ctr Dis Anal CDA, Louisville CO, USA.
    Strategies to manage hepatitis C virus (HCV) disease burden2014In: Journal of Viral Hepatitis, ISSN 1352-0504, E-ISSN 1365-2893, Vol. 21, p. 60-89Article in journal (Refereed)
    Abstract [en]

    The number of hepatitis C virus (HCV) infections is projected to decline while those with advanced liver disease will increase. A modeling approach was used to forecast two treatment scenarios: (i) the impact of increased treatment efficacy while keeping the number of treated patients constant and (ii) increasing efficacy and treatment rate. This analysis suggests that successful diagnosis and treatment of a small proportion of patients can contribute significantly to the reduction of disease burden in the countries studied. The largest reduction in HCV-related morbidity and mortality occurs when increased treatment is combined with higher efficacy therapies, generally in combination with increased diagnosis. With a treatment rate of approximately 10%, this analysis suggests it is possible to achieve elimination of HCV (defined as a >90% decline in total infections by 2030). However, for most countries presented, this will require a 3-5 fold increase in diagnosis and/or treatment. Thus, building the public health and clinical provider capacity for improved diagnosis and treatment will be critical.

  • 49.
    Westin, Johan
    et al.
    Deparment of Infectious Diseases, Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Aleman, Soo
    Deparment of Medicine, Division of Infectious Diseases, Karolinska Institutet and Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Castedal, Maria
    Department of Surgery, Institute of Clinical Sciences, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Duberg, Ann-Sofi
    Örebro University, School of Medical Sciences. Deparment of Infectious Diseases.
    Eilard, Anders
    Deparment of Infectious Diseases, Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Fischler, Björn
    Deparment of Pediatrics, CLINTEC, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Kampmann, Christian
    Deparment of Infectious Diseases, Skåne University Hospital Lund, Lund, Sweden.
    Lindahl, Karin
    Deparment of Medicine, Division of Infectious Diseases, Karolinska Institutet and Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Lindh, Magnus
    Deparment of Infectious Diseases, Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Norkrans, Gunnar
    Deparment of Infectious Diseases, Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Stenmark, Stephan
    Deparment of Clinical Microbiology and Infectious Diseases, Umeå University, Umeå, Sweden.
    Weiland, Ola
    Deparment of Medicine, Division of Infectious Diseases, Karolinska Institutet and Karolinska University Hospital Huddinge, Stockholm, Sweden.
    Wejstål, Rune
    Deparment of Infectious Diseases, Institute of Biomedicine at the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Management of hepatitis B virus infection, updated Swedish guidelines2019In: Infectious Diseases, ISSN 2374-4235, E-ISSN 2374-4243Article in journal (Refereed)
    Abstract [en]

    Despite access to effective antiviral drugs and vaccines, hepatitis B virus (HBV) infection remains a major health issue worldwide. HBV is highly infectious and may cause chronic infection, progressive liver damage, hepatocellular cancer (HCC) and death. Early diagnosis, proper management and timing of treatment are crucial. The Swedish Reference group for Antiviral Treatment (RAV) here provides updated evidence-based guidelines for treatment and management of HBV infection which may be applicable also in other countries. Tenofovir alafenamide (TAF) has been introduced as a novel treatment option and new principles regarding indication and duration of treatment and characterization of hepatitis B have been gradually introduced which justifies an update of the previous guidelines from 2007. Updated guidelines on HCC surveillance in HBV-infected patients, treatment and prophylaxis for patients undergoing liver transplantation as well as management of pregnant women and children with HBV infection are also provided.

  • 50.
    Widlund, Martin
    et al.
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden .
    Duberg, Ann-Sofi
    Department of Infectious Diseases, Örebro University Hospital, Örebro, Sweden .
    Hundbett gav kvarstående dövhet: Capnocytophaga canimorsus orsakade allvarlig infektion med sepsisCapnocytophaga canimorsus orsakade allvarlig infektion med sepsis[Permanent hearing loss following dog bite. Capnocytophaga canimorsus caused severe infection with sepsis]2010In: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 107, no 29-31, p. 1771-3Article in journal (Other academic)
    Abstract [sv]

    Vid misstänkt infektionssjukdom några dagar efter ett hundbett bör man överväga infektion orsakad av Capnocytophaga canimorsus. Denna långsamt växande gramnegativa stav förekommer normalt i munflora hos tamhund och är en välkänd humanpatogen. Infektion med C canimorsus har ofta ett stillsamt initialförlopp och riskerar därför att förbises. Med anledning av detta bör sjukdom efter hundbett även vid disk­ret lokalstatus föranleda uppmärksamhet på symtomutveckling, och antibiotikabehandling bör övervägas för att undvika sjukdomsprogress och komplikationer.

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