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6. Genome-wide association study identifies inversion in the CTRB1-CTRB2 locus to modify risk for alcoholic and non-alcoholic chronic pancreatitis

Author

Rosendahl, Jonas, primary, Kirsten, Holger, additional, Hegyi, Eszter, additional, Kovacs, Peter, additional, Weiss, Frank Ulrich, additional, Laumen, Helmut, additional, Lichtner, Peter, additional, Ruffert, Claudia, additional, Chen, Jian-Min, additional, Masson, Emmanuelle, additional, Beer, Sebastian, additional, Zimmer, Constantin, additional, Seltsam, Katharina, additional, Algül, Hana, additional, Bühler, Florence, additional, Bruno, Marco J, additional, Bugert, Peter, additional, Burkhardt, Ralph, additional, Cavestro, Giulia Martina, additional, Cichoz-Lach, Halina, additional, Farré, Antoni, additional, Frank, Josef, additional, Gambaro, Giovanni, additional, Gimpfl, Sebastian, additional, Grallert, Harald, additional, Griesmann, Heidi, additional, Grützmann, Robert, additional, Hellerbrand, Claus, additional, Hegyi, Péter, additional, Hollenbach, Marcus, additional, Iordache, Sevastitia, additional, Jurkowska, Grazyna, additional, Keim, Volker, additional, Kiefer, Falk, additional, Krug, Sebastian, additional, Landt, Olfert, additional, Leo, Milena Di, additional, Lerch, Markus M, additional, Lévy, Philippe, additional, Löffler, Markus, additional, Löhr, Matthias, additional, Ludwig, Maren, additional, Macek, Milan, additional, Malats, Nuria, additional, Malecka-Panas, Ewa, additional, Malerba, Giovanni, additional, Mann, Karl, additional, Mayerle, Julia, additional, Mohr, Sonja, additional, te Morsche, Rene H M, additional, Motyka, Marie, additional, Mueller, Sebastian, additional, Müller, Thomas, additional, Nöthen, Markus M, additional, Pedrazzoli, Sergio, additional, Pereira, Stephen P, additional, Peters, Annette, additional, Pfützer, Roland, additional, Real, Francisco X, additional, Rebours, Vinciane, additional, Ridinger, Monika, additional, Rietschel, Marcella, additional, Rösmann, Eva, additional, Saftoiu, Adrian, additional, Schneider, Alexander, additional, Schulz, Hans-Ulrich, additional, Soranzo, Nicole, additional, Soyka, Michael, additional, Simon, Peter, additional, Skipworth, James, additional, Stickel, Felix, additional, Strauch, Konstantin, additional, Stumvoll, Michael, additional, Testoni, Pier Alberto, additional, Tönjes, Anke, additional, Werner, Lena, additional, Werner, Jens, additional, Wodarz, Norbert, additional, Ziegler, Martin, additional, Masamune, Atsushi, additional, Mössner, Joachim, additional, Férec, Claude, additional, Michl, Patrick, additional, P H Drenth, Joost, additional, Witt, Heiko, additional, Scholz, Markus, additional, and Sahin-Tóth, Miklós, additional

Published
2017
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9. Genome-wide association study identifies inversion in the CTRB1-CTRB2locus to modify risk for alcoholic and non-alcoholic chronic pancreatitis

Author

Rosendahl, Jonas, Kirsten, Holger, Hegyi, Eszter, Kovacs, Peter, Weiss, Frank Ulrich, Laumen, Helmut, Lichtner, Peter, Ruffert, Claudia, Chen, Jian-Min, Masson, Emmanuelle, Beer, Sebastian, Zimmer, Constantin, Seltsam, Katharina, Algul, Hana, Buhler, Florence, Bruno, Marco J, Bugert, Peter, Burkhardt, Ralph, Cavestro, Giulia Martina, Cichoz-Lach, Halina, Farré, Antoni, Frank, Josef, Gambaro, Giovanni, Gimpfl, Sebastian, Grallert, Harald, Griesmann, Heidi, Grutzmann, Robert, Hellerbrand, Claus, Hegyi, Pééter, Hollenbach, Marcus, Iordache, Sevastitia, Jurkowska, Grazyna, Keim, Volker, Kiefer, Falk, Krug, Sebastian, Landt, Olfert, Leo, Milena Di, Lerch, Markus M, Lééévy, Philippe, Loffler, Markus, Lohr, Matthias, Ludwig, Maren, Macek, Milan, Malats, Nuria, Malecka-Panas, Ewa, Malerba, Giovanni, Mann, Karl, Mayerle, Julia, Mohr, Sonja, te Morsche, Rene H M, Motyka, Marie, Mueller, Sebastian, Muller, Thomas, Nothen, Markus M, Pedrazzoli, Sergio, Pereira, Stephen P, Peters, Annette, Pfutzer, Roland, Real, Francisco X, Rebours, Vinciane, Ridinger, Monika, Rietschel, Marcella, Rosmann, Eva, Saftoiu, Adrian, Schneider, Alexander, Schulz, Hans-Ulrich, Soranzo, Nicole, Soyka, Michael, Simon, Peter, Skipworth, James, Stickel, Felix, Strauch, Konstantin, Stumvoll, Michael, Testoni, Pier Alberto, Tonjes, Anke, Werner, Lena, Werner, Jens, Wodarz, Norbert, Ziegler, Martin, Masamune, Atsushi, Mossner, Joachim, Féééérec, Claude, Michl, Patrick, P H Drenth, Joost, Witt, Heiko, Scholz, Markus, and Sahin-Tééééóóth, Miklééééós

Abstract

ObjectiveAlcohol-related pancreatitis is associated with a disproportionately large number of hospitalisations among GI disorders. Despite its clinical importance, genetic susceptibility to alcoholic chronic pancreatitis (CP) is poorly characterised. To identify risk genes for alcoholic CP and to evaluate their relevance in non-alcoholic CP, we performed a genome-wide association study and functional characterisation of a new pancreatitis locus.Design1959 European alcoholic CP patients and population-based controls from the KORA, LIFE and INCIPE studies (n=4708) as well as chronic alcoholics from the GESGA consortium (n=1332) were screened with Illumina technology. For replication, three European cohorts comprising 1650 patients with non-alcoholic CP and 6695 controls originating from the same countries were used.ResultsWe replicated previously reported risk loci CLDN2-MORC4, CTRC, PRSS1-PRSS2and SPINK1in alcoholic CP patients. We identified CTRB1-CTRB2(chymotrypsin B1 and B2) as a new risk locus with lead single-nucleotide polymorphism (SNP) rs8055167(OR 1.35, 95% CI 1.23 to 1.6). We found that a 16.6 kb inversion in the CTRB1-CTRB2locus was in linkage disequilibrium with the CP-associated SNPs and was best tagged by rs8048956. The association was replicated in three independent European non-alcoholic CP cohorts of 1650 patients and 6695 controls (OR 1.62, 95% CI 1.42 to 1.86). The inversion changes the expression ratio of the CTRB1 and CTRB2 isoforms and thereby affects protective trypsinogen degradation and ultimately pancreatitis risk.ConclusionAn inversion in the CTRB1-CTRB2locus modifies risk for alcoholic and non-alcoholic CP indicating that common pathomechanisms are involved in these inflammatory disorders.

Published
2018
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10. Insulin resistance and response to telaprevir plus peginterferon &agr; and ribavirin in treatment-naïve patients infected with HCV genotype 1.

Author

Serfaty, Lawrence, Forns, Xavier, Goeser, Tobias, Ferenci, Peter, Nevens, Frederik, Carosi, Giampiero, Drenth, Joost P., Lonjon-Domanec, Isabelle, DeMasi, Ralph, Picchio, Gaston, Beumont, Maria, and Marcellin, Patrick

Subjects
CHRONIC hepatitis C, INSULIN resistance, RIBAVIRIN, VIROLOGY, ANTIVIRAL agents, MULTIPLE regression analysis, DATA analysis, THERAPEUTICS
Abstract

Objective Insulin resistance is a predictor of poor response to peginterferon/ribavirin in patients infected with the chronic hepatitis C virus (HCV). There are no data on direct-acting antivirals. This exploratory analysis assessed the effect of metabolic factors and insulin resistance, measured by homoeostatic model assessment (HOMA), on virological response to telaprevir in Study C208. Design Overall, 161 HCV genotype 1-infected, treatment-nai &vumle patients received 12 weeks of telaprevir plus peginterferon/ribavirin, then 12/36 weeks of peginterferon/ribavirin depending on on-treatment response criteria. The prognostic significance of several factors, including HOMA-insulin resistance (HOMA-IR), on virological response at weeks 4 and 12, end of treatment and 24 weeks after treatment was explored by multiple regression analysis. Results Baseline HOMA-IR data were available for 147 patients; baseline characteristics were consistent with the overall population. Baseline HOMA-IR <2, 2e4 and >4 was seen in 54%, 30% and 16% of patients, respectively. Neither response rates (any time point) nor week 4 viral load decline were significantly influenced by baseline HOMA-IR. In multivariate analyses, fibrosis stage and low-density lipoprotein cholesterol level were predictive of sustained virological response (OR 0.47 and 1.02, respectively). After the end of treatment, HOMA-IR was significantly lower in patients with sustained virological response than in those without (0.61 vs 1.34 for relapsers and 1.15 for non-responders; p<0.05). Conclusion In this study, baseline HOMA-IR was not predictive of virological response to telaprevir in HCV genotype 1-infected, treatment-nai &vuml;e patients, while sustained virological response was associated with improved HOMA-IR. These results suggest that metabolic factors and insulin resistance do not have a significant effect on telaprevir-based treatment efficacy. [ABSTRACT FROM AUTHOR]

Published
2012
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11. Genome-wide association study identifies inversion in the CTRB1-CTRB2 locus to modify risk for alcoholic and non-alcoholic chronic pancreatitis.

Author

Rosendahl J, Kirsten H, Hegyi E, Kovacs P, Weiss FU, Laumen H, Lichtner P, Ruffert C, Chen JM, Masson E, Beer S, Zimmer C, Seltsam K, Algül H, Bühler F, Bruno MJ, Bugert P, Burkhardt R, Cavestro GM, Cichoz-Lach H, Farré A, Frank J, Gambaro G, Gimpfl S, Grallert H, Griesmann H, Grützmann R, Hellerbrand C, Hegyi P, Hollenbach M, Iordache S, Jurkowska G, Keim V, Kiefer F, Krug S, Landt O, Leo MD, Lerch MM, Lévy P, Löffler M, Löhr M, Ludwig M, Macek M, Malats N, Malecka-Panas E, Malerba G, Mann K, Mayerle J, Mohr S, Te Morsche RHM, Motyka M, Mueller S, Müller T, Nöthen MM, Pedrazzoli S, Pereira SP, Peters A, Pfützer R, Real FX, Rebours V, Ridinger M, Rietschel M, Rösmann E, Saftoiu A, Schneider A, Schulz HU, Soranzo N, Soyka M, Simon P, Skipworth J, Stickel F, Strauch K, Stumvoll M, Testoni PA, Tönjes A, Werner L, Werner J, Wodarz N, Ziegler M, Masamune A, Mössner J, Férec C, Michl P, P H Drenth J, Witt H, Scholz M, and Sahin-Tóth M

Subjects
Adult, Aged, Europe epidemiology, Female, Genetic Predisposition to Disease, Humans, Male, Middle Aged, Polymorphism, Single Nucleotide, Chymotrypsin genetics, Pancreatitis, Alcoholic epidemiology, Pancreatitis, Alcoholic genetics
Abstract

Objective: Alcohol-related pancreatitis is associated with a disproportionately large number of hospitalisations among GI disorders. Despite its clinical importance, genetic susceptibility to alcoholic chronic pancreatitis (CP) is poorly characterised. To identify risk genes for alcoholic CP and to evaluate their relevance in non-alcoholic CP, we performed a genome-wide association study and functional characterisation of a new pancreatitis locus., Design: 1959 European alcoholic CP patients and population-based controls from the KORA, LIFE and INCIPE studies (n=4708) as well as chronic alcoholics from the GESGA consortium (n=1332) were screened with Illumina technology. For replication, three European cohorts comprising 1650 patients with non-alcoholic CP and 6695 controls originating from the same countries were used., Results: We replicated previously reported risk loci CLDN2-MORC4 , CTRC , PRSS1-PRSS2 and SPINK1 in alcoholic CP patients. We identified CTRB1-CTRB2 (chymotrypsin B1 and B2) as a new risk locus with lead single-nucleotide polymorphism (SNP) rs8055167 (OR 1.35, 95% CI 1.23 to 1.6). We found that a 16.6 kb inversion in the CTRB1-CTRB2 locus was in linkage disequilibrium with the CP-associated SNPs and was best tagged by rs8048956 . The association was replicated in three independent European non-alcoholic CP cohorts of 1650 patients and 6695 controls (OR 1.62, 95% CI 1.42 to 1.86). The inversion changes the expression ratio of the CTRB1 and CTRB2 isoforms and thereby affects protective trypsinogen degradation and ultimately pancreatitis risk., Conclusion: An inversion in the CTRB1-CTRB2 locus modifies risk for alcoholic and non-alcoholic CP indicating that common pathomechanisms are involved in these inflammatory disorders., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Published
2018
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