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Title: | Exposure to bacterial products lipopolysaccharide and flagellin and hepatocellular carcinoma: a nested case-control study |
Author: | Fedirko, Veronika Tran, Hao Quang Gewirtz, Andrew T. Stepien, Magdalena Trichopoulou, Antonia Aleksandrova, Krasimira Olsen, Anja Tjønneland, Anne Overvad, Kim Carbonnel, Franck Boutron-Ruault, Marie-Christine Severi, Gianluca Kühn, Tilman Kaaks, Rudolf Boeing, Heiner Bamia, Christina Lagiou, Pagona Grioni, Sara Panico, Salvatore Palli, Domenico Tumino, Rosario Naccarati, Alessio Peeters, Petra H. M. Bueno de Mesquita, H. Bas Weiderpass, Elisabete Huerta Castaño, José María Barricarte, Aurelio Sánchez, María José Dorronsoro, Miren Quirós, J. Ramón Agudo, Antonio Sjöberg, Klas Ohlsson, Bodil Hemmingsson, Oskar Werner, Mårten Bradbury, Kathryn E. Khaw, Kay-Tee Wareham, Nicholas J. Tsilidis, Konstantinos K. Aune, Dagfinn Scalbert, Augustin Romieu, Isabelle Riboli, Elio Jenab, Mazda |
Keywords: | Càncer de fetge Liver cancer |
Issue Date: | 4-Apr-2017 |
Publisher: | Biomed Central |
Abstract: | Background: Leakage of bacterial products across the gut barrier may play a role in liver diseases which often precede the development of liver cancer. However, human studies, particularly from prospective settings, are lacking. Methods: We used a case-control study design nested within a large prospective cohort to assess the association between circulating levels of anti-lipopolysaccharide (LPS) and anti-flagellin immunoglobulin A (IgA) and G (IgG) (reflecting long-term exposures to LPS and flagellin, respectively) and risk of hepatocellular carcinoma. A total of 139 men and women diagnosed with hepatocellular carcinoma between 1992 and 2010 were matched to 139 control subjects. Multivariable rate ratios (RRs), including adjustment for potential confounders, hepatitis B/C positivity, and degree of liver dysfunction, were calculated with conditional logistic regression. Results: Antibody response to LPS and flagellin was associated with a statistically significant increase in the risk of hepatocellular carcinoma (highest vs. lowest quartile: RR = 11.76, 95% confidence interval = 1.70-81.40; P-trend = 0.021). This finding did not vary substantially by time from enrollment to diagnosis, and did not change after adjustment for chronic infection with hepatitis B and C viruses. Conclusions: These novel findings, based on exposures up to several years prior to diagnosis, support a role for gut-derived bacterial products in hepatocellular carcinoma development. Further study into the role of gut barrier failure and exposure to bacterial products in liver diseases is warranted. |
Note: | Reproducció del document publicat a: https://doi.org/10.1186/s12916-017-0830-8 |
It is part of: | BMC Medicine, 2017, vol. 15, num. 72 |
URI: | http://hdl.handle.net/2445/124409 |
Related resource: | https://doi.org/10.1186/s12916-017-0830-8 |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
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