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High prevalence of cholestasis, with increased conjugated bile acids in inflammatory bowel diseases patients

World Journal of Clinical Cases 2018年第4期6卷 44-53页

作者： Marc Girardin antoine hadengue Jean-Louis Frossard Service of Gastroenterology and Hepatology Geneva University Hospital

AIM To investigate the prevalence and causes of cholestasis in patients with inflammatory bowel diseases in the Swiss Inflammatory Bowel Diseases Cohort. METHODS A retrospective cohort study was performed of all the patients in the Swiss Inflammatory bowel disease Cohort. Total bile acid was measured for all patients and cholestasis was defined as a concentration > 8 μmol/L. The characteristics of patients with or without cholestasis were compared. Bile acid profiles were then determined for 80 patients with high total bile acid and 80 matched patients with low total bile acid. Bile acid profiles were compared for smokers vs nonsmokers, ileal vs colonic disease, and inflammatory vs non inflammatory diseases.RESULTS Ninety-six patients had more than 8 μmol/L total bile acid, giving a prevalence of 7.15%. Patients with an obvious cause of cholestasis, such as primary sclerosing cholangitis, were then excluded, leaving 1190 participants with total bile acid 8 μmol/L. In multivariate analysis, calcium supplementation was significantly associated with cholestasis(odds ratio, 2.36, 95%CI: 1.00-5.21, P = 0.040) whereas current smoking significantly reduced the risk of cholestasis(odds ratio, 0.42, 95%CI: 0.17-0.91, P = 0.041). Levels of all conjugated bile acids were higher in the cholestasis group than in the control group. When we compared patients with ileal vs colonic disease, the former had higher levels of primary, secondary, and tertiary bile acids whereas patients with colonic disease had higher levels of conjugated bile acids.CONCLUSION Prevalence of cholestasis is high. Smoking appears to reduce cholestasis. Conjugated bile acids are higher in cholestasis and in colonic disease whereas unconjugated in ileal disease.

关键词： Lipid Liver Crohn’s disease Ulcerative colitis Cholestasis

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Age,smoking and overweight contribute to the development of intestinal metaplasia of the cardia

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World Journal of Gastroenterology 2012年第17期18卷 2076-2083页

作者： Christian Felley Hanifa Bouzourene Marianne Bründler G VanMelle antoine hadengue Pierre Michetti Gian Dorta Laurent Spahr Emiliano Giostra Jean Louis Frossard Service of Gastroenterology University Hospital1000 LausanneSwitzerland Institute of Pathology University Hospital1000 LausanneSwitzerland Institute of Social and Preventive Medicine University of Lausanne1000 LausanneSwitzerland Service of Gastroenterology Geneva University Hospital1211 GenevaSwitzerland

AIM:To assess the role of Helicobacter pylori(H.pylori),gastroesophageal reflux disease(GERD),age,smoking and body weight on the development of intestinal metaplasia of the gastric cardia(IMC).METHODS:Two hundred and seventeen patients scheduled for esophagogastroduodenoscopy were enrolled in this study.Endoscopic biopsies from the esophagus,gastroesophageal junction and stomach were evaluated for inflammation,the presence of H.pylori and intestinal metaplasia.The correlation of these factors with the presence of IMC was assessed using logistic regression.RESULTS:IMC was observed in 42% of the patients.Patient age,smoking habit and body mass index(BMI) were found as potential contributors to IMC.The risk of developing IMC can be predicted in theory by combining these factors according to the following formula:Risk of IMC = a + s-2B where a = 2,…6 decade of age,s = 0 for non-smokers or ex-smokers,1 for 10 cigarettes/d and B = 0 for BMI 25 kg/m2(BMI > 27 kg/m2 in females).Among potential factors associated with IMC,H.pylori had borderline signif icance(P = 0.07),while GERD showed no signif icance.CONCLUSION:Age,smoking and BMI are potential factors associated with IMC,while H.pylori and GERD show no significant association.IMC can be predicted in theory by logistic regression analysis.

关键词：吸烟者肠上皮年龄 Logistic回归分析 logistic回归幽门螺旋杆菌幽门螺杆菌超重

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Endothelial nitric oxide synthase regulation is altered in pancreas from cirrhotic rats

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World Journal of Gastroenterology 2006年第2期12卷 228-233页

作者： Jean-Louis Frossard Rafael Quadri antoine hadengue Philippe Morel Catherine M Pastor Division de Gastroenterologie Hpitaux Universitaires de Geneve Departement de Chirurgie Hopitaux Universitaires de Geneve Laboratoire de Physiopathologie Hepatique et Imagerie Moleculaire Hpitaux Universitaires de Geneve

瞄准：决定胆汁性肝硬变是否能在内皮的氮的氧化物 synthase (eNOS ) 导致象修正那样的胰腺的机能障碍表达式并且 eNOS 的规定是否能被规章的蛋白质 caveolin 改变并且加热吃惊蛋白质 90 (Hsp90 ) ，以及由对 eNOS 有约束力的 calmodul... 详细信息

瞄准：决定胆汁性肝硬变是否能在内皮的氮的氧化物 synthase (eNOS ) 导致象修正那样的胰腺的机能障碍表达式并且 eNOS 的规定是否能被规章的蛋白质 caveolin 改变并且加热吃惊蛋白质 90 (Hsp90 ) ，以及由对 eNOS 有约束力的 calmodulin 的修正。方法：Immunoprecipitations 和西方的弄污分析在从假冒、肝脏硬化症的老鼠孤立的胰被执行。结果：胰腺的损害在肝脏硬化症的老鼠是次要的，但是 eNOS 表示重要地与长度减少了(并且严厉) 疾病。因为有 Hsp90 和 caveolin 的 eNOS 的 co-immunoprecipitation 同样在肝脏硬化症的老鼠减少了， eNOS 活动没被这机制修改。相反，肝硬化减少了 calmodulin 绑定到有在 eNOS 的伴随物减少的 eNOS 活动。结论：在胆汁性肝硬变，胰腺的损害是次要的但是胰腺的氮的氧化物(没有) 生产被二机制显著地减少：酶和到 eNOS 的 calmodulin 的减少的绑定的减少的表情。

关键词：胰腺胆汁性肝硬变内皮NO合酶热休克蛋白大鼠

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Concomitant autoimmune and genetic pancreatitis leads to severe inflammatory conditions

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World Journal of Gastroenterology 2008年第16期14卷 2596-2598页

作者： Jean Louis Frossard Jean Marc Dumonceau Catherine Pastor Laurent Spahr antoine hadengue Division de Gastroentérologie et Hépatologie Geneva University Hospital

Chronic pancreatitis characterized by an early onset should be extensively investigated including the search for a mutation of the PRSS1, SPINK-1 or CFTR genes and potential features of autoimmune pancreatitis. We here describe a case of chronic pancreatitis with an onset at a very young age in which a mutation of the PRSS1 and several features of autoimmune pancreatitis were identified.

关键词：慢性胰腺炎遗传学 SPINK-1 CFTR PRSS1

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Neutrophil depletion-but not prevention of Kupffer cell activation-decreases the severity of cerulein-induced acute pancreatitis

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World Journal of Gastroenterology 2006年第8期12卷 1219-1224页

作者： Catherine M Pastor Alain Vonlaufen Fabianna Georgi antoine hadengue Philippe Morel Jean-Louis Frossard Laboratoire de Physiopathologie Hépatique et Imagerie Moléculaire H■pitaux Universitaires de GenèveB■timent CRoom 6-79524 Rue Micheli-du-Crest1205 GenevaSwitzerland Division of Gastroentérologie et Hépatologie H■pitaux Universitaires de Genève24 Rue Micheli-du-Crest1205 GenevaSwitzerland Département APSI H■pitaux Universitaires de Genève24 Rue Micheli-du-Crest1205 GenevaSwitzerland Département de Chirurgie H■pitaux Universitaires de Genève24 Rue Micheli-du-Crest1205 GenevaSwitzerland

瞄准：为了决定嗜中性的弄空和 Kupffer 房间抑制是否可能联合，他们的 protective 完成尖锐胰腺炎的严厉到减少。方法：老鼠有 cerulein 管理导致尖锐胰腺炎并且是有任何一个反老鼠 neutrophil 浆液或金轧氯化物(GdCl3 ) 的 pretreated... 详细信息

瞄准：为了决定嗜中性的弄空和 Kupffer 房间抑制是否可能联合，他们的 protective 完成尖锐胰腺炎的严厉到减少。方法：老鼠有 cerulein 管理导致尖锐胰腺炎并且是有任何一个反老鼠 neutrophil 浆液或金轧氯化物(GdCl3 ) 的 pretreated 阻止 Kupffer 房间激活，或两个处理。损害在胰和肺被估计。Myeloperoxidases (军邮局) 估计了嗜中性的渗入。Interleukin-6 (IL-6 ) 和 IL-10 在浆液，胰，肺和肝被测量。结果：在有尖锐胰腺炎的老鼠，嗜中性的弄空减少了胰腺炎和联系胰腺炎的肺损害的严厉。在由 GdCl3 的激活的 Kupffer 房间有更少的保护的效果，尽管 IL-6 和 IL-10 集中显著地被减少。嗜中性的弄空带的普雷茨氏疗法没被 Kupffer 房间在激活提高，两个处理没联合他们的保护的效果。结论：当 Kupffer 房间激活的角色是不太明显的时，我们的结果在在尖锐胰腺炎加重机关损害证实激活的 neutrophils 的角色。

关键词：中性白细胞疾病预防蛙皮缩胆囊肽胰腺炎

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