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Archambeaud I.,Institute Des Maladies Of Lappareil Digestif | Auble H.,Institute Des Maladies Of Lappareil Digestif | Nahon P.,University of Paris Descartes | Planche L.,Cellule de Promotion a la Recherche Clinique | And 6 more authors.
Liver International | Year: 2015

Background & Aims: In patients with cirrhosis, the risk of hepatocellular carcinoma (HCC) depends upon age, gender and the etiology of liver disease. Few studies are available in Caucasian patients with alcoholic or metabolic cirrhosis without viral hepatitis. Methods: Cross-sectional clinical data from 905 HCV- and HBV-negative Caucasian patients with alcoholic or metabolic cirrhosis were prospectively collected in four French centres. The risk factors for HCC were identified by logistic regression analysis in the whole population and in a nested case-control study. Results: The etiology of cirrhosis was alcoholic (48%), metabolic (7%) or mixed (45%). Patients were predominantly male (80%), mean age 62 years old and 31% had HCC. Mean body mass index (BMI) was 27 ± 5 and 30% were obese at inclusion. The maximum BMI reached throughout life was 31 ± 6 and 63% had been obese. Ninety percent of the population had daily alcohol consumption, 73% were smokers. Hepatocellular carcinoma was independently related to male gender (P < 0.0001), older age (P < 0.0001), past obesity (P = 0.007), diabetes (P = 0.037), abnormal levels of transaminases (P < 0.0001) and tobacco consumption (P = 0.007). The case-control study (200 HCC cases matched with 400 non-HCC cases for gender, age and Child-Pugh score) confirmed past obesity, tobacco and abnormal levels of transaminases. Conclusions: Beside diabetes, male gender and age, a past history of obesity, but not an existing overweight, as well as exposure to tobacco and elevated transaminases were three risk factors which could improve the strategy for HCC screening in Caucasian cirrhotic patients without hepatitis B or C. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Source

Guillouche P.,Institute Des Maladies Of Lappareil Digestif | Feray C.,Institute Des Maladies Of Lappareil Digestif
Alimentary Pharmacology and Therapeutics | Year: 2011

Background Hepatitis C virus (HCV) infection is the first cause of liver transplantation worldwide. Recurrence of infection is constant, and compromises patient and graft survival. Aim To provide an updated review of the main treatments of recurrent HCV. Methods MEDLINE (1990 to August 2010) and national meeting abstract search. Search terms included hepatitis C, liver transplantation, treatment, sustained virological response. An emphasis was placed on randomised trials. Results Anti-viral therapy based on pegylated interferon and ribavirin must be considered before liver transplantation, but is poorly tolerated and has poor results in patients with cirrhosis and end-stage liver disease or hepatocellular carcinoma. Anti-viral therapy can be administrated systematically early after liver transplantation, or in patients with established recurrent chronic hepatitis. Combination of pegylated interferon alpha plus ribavirin results in a sustained virological response of up to 30% in patients with histological HCV recurrence. The results of a small trial of polyclonal anti-HCV to prevent recurrence were disappointing. Conclusions Currently available anti-viral therapy is effective only in a minority of transplanted patients infected with HCV. Specifically targeted anti-viral therapies combining interferon alpha and ribavirin, or a combination of antiprotease and antipolymerase components, associated with a genetic prediction of anti-viral response and blocking HCV cell entry should improve the long-term prognosis of recurrent hepatitis C in the near future. © 2010 Blackwell Publishing Ltd. Source

Martin Agnoux A.,French National Institute for Agricultural Research | Martin Agnoux A.,University of Nantes | Martin Agnoux A.,Institute Des Maladies Of Lappareil Digestif | Alexandre-Gouabau M.-C.,French National Institute for Agricultural Research | And 9 more authors.
Acta Physiologica | Year: 2014

Aim: The aim of this study was to assess the contribution of both foetal and/or post-natal nutritional periods on feeding regulation in adult rats. Methods: Body weight gain, adipose tissue development, food preferences and feeding pattern under regular chow or Western diets were characterized on four experimental groups of rats: pups born from protein-restricted dams (R) and weaned by control (RC) or R dams (RR) and pups born from control dams weaned by C (CC) or R dams (CR). Results: Rats born with intrauterine growth restriction (IUGR) and fed a Western diet at adulthood appeared predisposed to body weight gain and more fat accretion, whereas CR rats, despite their preference for high-fat diet and their hyperphagia for Western diet, did not show significant increase in fat tissue. Daytime food intakes, as well as their speed of ingestion, were found modified in RC and RR. Alterations in the hypothalamic appetite regulatory mechanisms were investigated through neuropeptide expression analysis. IUGR rats showed altered expression of key elements of leptin and NPY signalling, while CR rats exhibited lesser expression of enterostatin, MC4r and HT-1Br mRNA. Conclusion: Altogether, these results indicate that peri-natal nutrition has different lasting effects on feeding pattern and hypothalamic appetite regulation, depending on the time window insult. © 2013 Scandinavian Physiological Society. Source

Le Loupp A.-G.,French Institute of Health and Medical Research | Le Loupp A.-G.,University of Nantes | Le Loupp A.-G.,Institute Des Maladies Of Lappareil Digestif | Le Loupp A.-G.,Nantes University Hospital Center | And 25 more authors.
BMC Gastroenterology | Year: 2015

Background: Recent works provide evidence of the importance of the prostaglandin D2 (PGD2) metabolic pathway in inflammatory bowel diseases. We investigated the expression of PGD2 metabolic pathway actors in Crohn's disease (CD) and the ability of the enteric nervous system (ENS) to produce PGD2 in inflammatory conditions. Methods: Expression of key actors involved in the PGD2 metabolic pathway and its receptors was analyzed using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in colonic mucosal biopsies of patients from three groups: controls, quiescent and active CD patients. To determine the ability of the ENS to secrete PGD2 in proinflammatory conditions, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyzed by immunostaining. PGD2 levels were determined in a medium of primary culture of ENS and neuro-glial coculture model treated by lipopolysaccharide (LPS). Results: In patients with active CD, inflamed colonic mucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 levels than healthy colonic mucosa. On the contrary, peroxysome proliferator-activated receptor Gamma (PPARG) expression was reduced in inflamed colonic mucosa of CD patients with active disease. Immunostaining showed that L-PGDS was expressed in the neurons of human myenteric and submucosal plexi. A rat ENS primary culture model confirmed this expression. PGD2 levels were significantly increased on primary culture of ENS treated with LPS. This production was abolished by AT-56, a specific competitive L-PGDS inhibitor. The neuro-glial coculture model revealed that each component of the ENS, ECG and neurons, could contribute to PGD2 production. Conclusions: Our results highlight the activation of the PGD2 metabolic pathway in Crohn's disease. This study supports the hypothesis that in Crohn's disease, enteric neurons and glial cells form a functional unit reacting to inflammation by producing PGD2. © 2015 Le Loupp et al. Source

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