27 oktober 2011: Bron: the European Prospective Investigation Into Cancer and Nutrition (EPIC)

Primaire leverkanker blijkt veelal veroorzaakt te worden door leefstijlgewoontes en hepatitus B en C. Dit blijkt uit een groot Europees bevolkingsonderzoek in 10 landen bij ca. 500.000 mensen gedurende 8 jaar. Vooral het effect van roken dat maar liefst 50 procent voor zijn rekening zou nemen is extreem hoog en veel hoger dan bv. door hepatitus B en C.

Resultaten Chronische hepatitis B virus (HBV) of hepatitis C virus (HCV) infection (OR = 9.10, 95% confidence interval = 2.10 tot 39.50 en OR = 13.36, 95% CI = 4.11 to 43.45, respectievelijk), zwaarlijvigheid (OR = 2.13, 95% CI = 1.06 tot 4.29), vroegere of nog steeds roken (OR = 1.98, 95% CI = 0.90 tot 4.39 and OR = 4.55, 95% CI = 1.90 to 10.91, respectievelijk), en veel gebruik van alcohol (OR = 1.77, 95% CI = 0.73 tot 4.27) werden gerelateerd aan primaire leverkanker - HCC - hepatocellular carcinoma. Roken  werd gerelateerd aan bijna de helft van de primaire leverkanker gevallen (47.6%), waar respectievelijk 13.2% en 20.9% werden gerelateerd aan chronische HBV en HCV infecties. Zwaarlijvigheid en veel alcohol was voor respectievelijk  16.1% en 10.2% verantwoordelijk. Bijna twee derde (65.7%, 95% CI = 50.6% to 79.3%) van de ontstane primaire leverkanker - hepatocellular carcinomas kan worden gerelateerd aan een van deze risico factoren.  

Hier het abstract van de studie welke u tegen betaling in kunt zien als u hier klikt op de website van The Journal of the National  Cancer Institute

Smoking contributed to more hepatocellular carcinomas in this Europe-wide cohort than chronic HBV and HCV infections. Heavy alcohol consumption and obesity also contributed to sizeable fractions of this disease burden

Source: JNCI

Hepatocellular Carcinoma Risk Factors and Disease Burden in a European Cohort: A Nested Case–Control Study

  1. Dimitrios Trichopoulos,
  2. Christina Bamia,
  3. Pagona Lagiou,
  4. Veronika Fedirko,
  5. Elisabeth Trepo,
  6. Mazda Jenab,
  7. Tobias Pischon,
  8. Ute Nöthlings,
  9. Kim Overved,
  10. Anne Tjønneland,
  11. Malene Outzen,
  12. Francoise Clavel-Chapelon,
  13. Rudolf Kaaks,
  14. Annekatrin Lukanova,
  15. Heiner Boeing,
  16. Krasimira Aleksandrova,
  17. Vassiliki Benetou,
  18. Dimosthenis Zylis,
  19. Domenico Palli,
  20. Valeria Pala,
  21. Salvatore Panico,
  22. Rosario Tumino,
  23. Carlotta Sacerdote,
  24. H. Bas Bueno-De-Mesquita,
  25. Henk J. Van Kranen,
  26. Petra H.M. Peeters,
  27. Eiliv Lund,
  28. J. Ramón Quirós,
  29. Carlos A. González,
  30. Maria-Jose Sanchez Perez,
  31. Carmen Navarro,
  32. Miren Dorronsoro,
  33. Aurelio Barricarte,
  34. Björn Lindkvist,
  35. Sara Regnér,
  36. Mårten Werner,
  37. Göran Hallmans,
  38. Kay-Tee Khaw,
  39. Nick Wareham,
  40. Timothy Key,
  41. Isabelle Romieu,
  42. Shu-Chun Chuang,
  43. Neil Murphy,
  44. Paolo Boffetta,
  45. Antonia Trichopoulou and
  46. Elio Riboli

+ Author Affiliations

  1. Affiliations of authors: Department of Epidemiology, Harvard School of Public Health, Boston, MA (DT, PL); Bureau of Epidemiologic Research, Academy of Athens, Athens, Greece (DT, PL, ATr); WHO Collaborating Center for Food and Nutrition Policies, Department of Hygiene, Epidemiology, and Medical Statistics, University of Athens Medical School, Athens, Greece (PL, CB, VB, DZ, ATr); International Agency for Research on Cancer, Lyon, France (VF, MJ, IR, S-CC); Centre de Biologie République, Lyon, France (ET); Molecular Epidemiology Group, Max Delbrück Center for Molecular Medicine (MDC), Berlin-Buch, Germany (TP); Department of Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal, Germany (TP, HB, KA); Epidemiology Section, Institute for Experimental Medicine, Christian-Albrechts-University Kiel, Kiel, Germany (UN); Department of Epidemiology, School of Public Health, Aarhus University, Aarhus, Denmark (KO); Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark (ATj); Danish Cancer Society, Institute of Cancer Epidemiology, Copenhagen, Denmark (ATj, MO); INSERM, Center for Research in Epidemiology and Population Health, Paris, France (FC-C); Paris South University, Paris, France (FC-C); Division of Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany (RK, AL); Molecular and Nutritional Epidemiology Unit, Cancer Research and Prevention Institute, ISPO, Florence, Italy (DP); Nutritional Epidemiology Unit, Fondazione IRCCS Istituto Nazionale Tumori, Milan, Italy (VP); Department of Clinical and Experimental Medicine, Federico II University, Naples, Italy (SP); Cancer Registry and Histopathology Unit, “Civile M.P.Arezzo” Hospital, Ragusa, Italy (RT); Unit of of Cancer Epidemiology, ASOU S Giovanni Battista Hospital, Center for Cancer Prevention (CPO-Piemonte), Torino, Italy (CS); Molecular and genetic epidemiology Unit, Human Genetic Foundation (HuGeF), Torino, Italy (CS); National Institute for Public Health and the Environment (RIVM), Bilthoven, the Netherlands (HBBDEM, HJVK); Department of Gastroenterology and Hepatology, University Medical Center Utrecht (UMCU), Utrecht, the Netherlands (HBBDEM); Julius Center, University Medical Center Utrecht, Utrecht, the Netherlands (PHMP); Department of Epidemiology and Biostatistics, School of Public Health, Faculty of Medicine, Imperial College, London, UK (PHMP, S-CC, NM, ER); Institute for Community Medicine, University of Tromsø, Tromsø, Norway (EL); Public Health and Health Planning Directorate, Asturias, Spain (JRQ); Unit of Nutrition, Environment, and Cancer, Cancer Epidemiology Research Programme, Catalan Institute of Oncology (ICO), Barcelona, Spain (CAG); Andalusian School of Public Health, Granada, Spain (M-JSP); Consortium for Biomedical Research in Epidemiology and Public Health (CIBER Epidemiología y Salud Pública-CIBERESP), Madrid, Spain (M-JSP, CN, AB); Department of Epidemiology, Murcia Regional Health Authority, Murcia, Spain (CN); Public Health Division of Gipuzkoa, Basque Regional Health Department, San Sebastian, Spain (MD); Ciberesp-Biodonostia, San Sebastian, Spain (MD); Navarre Public Health Institute, Pamplona, Spain (AB); Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden (BL); Surgical Clinic, Malmö, SUS, Department of Clinical Sciences, Lund University, Malmö, Sweden (SR); Department of Public Health and Clinical Medicine, Medicine, Umeå University, Umeå, Sweden (MW, GH); University of Cambridge, Cambridge, UK (K-TK); Medical Research Council (MRC), Epidemiology Unit, Cambridge, UK (NW); Cancer Epidemiology Unit, Nuffield Department of Clinical Medicine, Oxford University, Oxford, UK (TK); International Prevention Research Institute, Lyon, France (PB); The Tisch Cancer Institute and Institute for Translational Epidemiology, Mount Sinai School of Medicine, New York, NY (PB); Hellenic Health Foundation, Athens, Greece (PB, ATr)
  1. Correspondence to:
    Dimitrios Trichopoulos, MD, PhD, Department of Epidemiology, Harvard School of Public Health, 677 Huntington Ave, Kresge Bldg, Boston, MA 02115 (e-mail: dtrichop@hsph.harvard.edu).
  • Received February 28, 2011.
  • Revision received September 2, 2011.
  • Accepted September 6, 2011.

Abstract

Background To date, no attempt has been made to systematically determine the apportionment of the hepatocellular carcinoma burden in Europe or North America among established risk factors.

Methods Using data collected from 1992 to 2006, which included 4 409 809 person-years in the European Prospective Investigation into Cancer and nutrition (EPIC), we identified 125 case patients with hepatocellular carcinoma, of whom 115 were matched to 229 control subjects. We calculated odds ratios (ORs) for the association of documented risk factors for hepatocellular carcinoma with incidence of this disease and estimated their importance in this European cohort.

Results Chronic hepatitis B virus (HBV) or hepatitis C virus (HCV) infection (OR = 9.10, 95% confidence interval = 2.10 to 39.50 and OR = 13.36, 95% CI = 4.11 to 43.45, respectively), obesity (OR = 2.13, 95% CI = 1.06 to 4.29), former or current smoking (OR = 1.98, 95% CI = 0.90 to 4.39 and OR = 4.55, 95% CI = 1.90 to 10.91, respectively), and heavy alcohol intake (OR = 1.77, 95% CI = 0.73 to 4.27) were associated with hepatocellular carcinoma. Smoking contributed to almost half of all hepatocellular carcinomas (47.6%), whereas 13.2% and 20.9% were attributable to chronic HBV and HCV infection, respectively. Obesity and heavy alcohol intake contributed 16.1% and 10.2%, respectively. Almost two-thirds (65.7%, 95% CI = 50.6% to 79.3%) of hepatocellular carcinomas can be accounted for by exposure to at least one of these documented risk factors.

Conclusions Smoking contributed to more hepatocellular carcinomas in this Europe-wide cohort than chronic HBV and HCV infections. Heavy alcohol consumption and obesity also contributed to sizeable fractions of this disease burden. These contributions may be underestimates because EPIC volunteers are likely to be more health conscious than the general population.


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