{"title":"Traitements à long terme de l’hépatite chronique B chez le patient co-infecté par le VIH","authors":"R. Pais, Y. Benhamou","doi":"10.1016/S0399-8320(10)70033-6","DOIUrl":"10.1016/S0399-8320(10)70033-6","url":null,"abstract":"<div><p>As human immunodeficiency virus (HIV) and hepatitis B virus (HBV) are acquired through the same routes of contamination, the prevalence of HBV serological markers found in the HIV-infected population is approximately 7%. Liver-related mortality and morbidity is higher in HIV/HBV co-infected patients than in HBV mono-infected patients. Both viruses must be considered before a treatment decision is made. According to the European consensus conference on the treatment of chronic hepatitis B and C in HIV coinfected patients, treatment is based on whether there is an existing indication of anti- HIV therapy or not. In patients with no indication of anti-HIV therapy, drugs with dual anti-viral activity (lamivudine, entecavir, tenofovir disoproxil fumarate) should not be used due to the risk of developing HIV-resistance. Interferon or adefovir in combination with telbivudine are recommended. In patients with an indication of anti-HIV therapy, a backbone of highly active anti-retroviral therapy should include tenofovir in combination with lamivudine or emtricitabine. The same regimen is recommended in patients who develop lamivudine resistance.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S136-S141"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0399-8320(10)70033-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29484213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gut microbiota and IBD","authors":"P. Seksik","doi":"10.1016/S0399-8320(10)70020-8","DOIUrl":"10.1016/S0399-8320(10)70020-8","url":null,"abstract":"<div><p>Gut microbiota contains about 10<sup>14</sup> bacterial cells classified within 4 bacterial phyla, namely Firmicutes, Bacteroidetes, Actinobacteria, and Proteobacteria. Much of the information has been generated through the application of nucleic acid-based methodologies (16S rRNA) which provide a cornerstone of microbial taxonomy. Inflammatory bowel disease (IBD) involves a dysregulated immune response to the gut microbiota in genetically predisposed hosts. Experimental animal models of colitis provide the best evidence that bacteria present in the bowel of the animals have an essential role in the pathogenesis of colitis since in most models, germ-free animals do not develop disease. Moreover, in the immunodeficient mouse model of colitis called TRUC (T-bet-/- x RAG2-/-), a colitogenic gut microbiota is selected and can be transmitted to mice with intact immunity and induce colitis. Current interest therefore focuses on the bacterial community as the source of antigens that fuel the chronic inflammation seen in IBD. Dysbiosis, an imbalance between harmful and protective bacteria, has been evoked and investigated in IBD. Thus, besides the classical pathogens, gut microbiota can drive pathogenicity via two mechanisms: an expansion of ‘pro-inflammatory'species or a restriction in the protective compounds of the microbiota. Complexity of the microbiota suggests that both mechanisms may contribute to chronic gut inflammation in IBD.</p></div><div><p>Le microbiote intestinal contient environ 10<sup>14</sup> bactéries classées en 4 phyla bactériens: <em>Firmicutes</em>, <em>Bacteroidetes</em>, <em>Actinobacteria</em>, et <em>Proteobacteria</em>. Une grande partie des informations concernant cet écosystème a été générée par l’application de méthodes moléculaires visant la reconnaisance des acides nucléiques (16S ARNr) motifs moléculaires clefs de la taxonomie microbienne. Les maladies inflammatoires de l’intestin (MICI) résultent d’une réponse immunitaire dérégulée vis-à-vis du microbiote intestinal chez des sujets génétiquement prédisposés. Les modèles murins de colite expérimentale fournissent des arguments expérimentaux solides pour incriminer la microflore intestinale dans la pathogenèse d’une colite. En effet, dans la plupart des modèles, la colite ne se développe pas en absence de microbiote (situation axénique). Récemment, avec le modèle de souris immunodéficientes de colite appelée TRUC (T-bet<sup>– /–</sup> x RAG2<sup>– /–</sup> , ulcerative colitis), un nouveau paradigme a emergé puisque le microbiote intestinal semble pouvoir transmettre la colite suggérant ainsi l’existence d’un microbiote ‘colitogénique’. Un intérêt grandissant centré sur l’étude des communautés bactériennes comme source antigénique alimentant l’inflammation chronique au cours des MICI a vu le jour. Une dysbiose, i.e. un déséquilibre entre des bactéries ‘délétères’et ‘bénéfiques’, a été évoquée et recherchée dans les MICI. A côté des agents pathogènes classiques, l","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S44-S51"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0399-8320(10)70020-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29326526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Body mass index and risk of liver cirrhosis in middle aged UK women: Prospective study","authors":"S. Naveau","doi":"10.1016/j.gcb.2010.05.003","DOIUrl":"10.1016/j.gcb.2010.05.003","url":null,"abstract":"","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 429-430"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.05.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29077071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Antiangiogenic therapies in portal hypertension: A breakthrough in hepatology","authors":"O. Rosmorduc","doi":"10.1016/j.gcb.2010.05.007","DOIUrl":"10.1016/j.gcb.2010.05.007","url":null,"abstract":"<div><p>Portal hypertension is the most important complication that develops in patients with cirrhosis. Several studies have shown that angiogenesis (i.e. splanchnic neovascularization) driven by VEGF and other proangiogenic molecules, like PDGF, may be a major mechanism involved in portal hypertension, hyperdynamic splanchnic circulation and portosystemic collateralization. According with this, antiangiogenic therapies, like sorafenib or sunitinib, have been recently shown to reduce portosystemic collateral circulation, improve splanchnic hyperdynamics and decrease portal pressure in experimental model of portal hypertension. This effect was associated to a decrease in VEGF, PDGF expression and splanchnic neovascularization. In addition, these therapies were associated with a decrease in both splanchnic and intrahepatic inflammatory infiltrates, in hepatic stellate cell activation and in intrahepatic fibrosis. These data suggest that antiangiogenic therapies may therefore, by limiting liver fibrosis and inflammation in cirrhosis, prevent the occurrence of severe complications, such as portal hypertension and potentially liver cancer.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 446-449"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.05.007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29121826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
E. Gruden , E. Ragot , R. Arienzo , A. Revaux , M. Magri , M. Grossin , C. Leroy , S. Msika , R. Kianmanesh
{"title":"Massive rectal bleeding distant from a blunt car trauma","authors":"E. Gruden , E. Ragot , R. Arienzo , A. Revaux , M. Magri , M. Grossin , C. Leroy , S. Msika , R. Kianmanesh","doi":"10.1016/j.gcb.2010.05.008","DOIUrl":"10.1016/j.gcb.2010.05.008","url":null,"abstract":"<div><p>Mesenteric trauma is one of the possible injuries caused by the use of seat belts in case of motor vehicle crash. We report here a rare case of rectal bleeding by rupture of a mesosigmoid haematoma. An emergent laparotomy revealed a mesosigmoid haematoma with a centimetric rectal perforation. The wearing of safety belts added some specific blunt abdominal trauma, which directly depends on lap-and-sash belts. Mesenteric injuries are found out up to 5% of blunt abdominal traumas. “Seat belt mark” leads the surgical team to strongly suspect an intra-abdominal trauma. When “seat belt mark” sign is found, in patients with mild to severe blunt car injuries, CT-scan has to be realised to eliminate intra-abdominal complications, including mesenteric and mesosigmoid ones. In case of proved mesenteric haematoma associated to intestinal bleeding, a surgical treatment must be considered as first choice. Conservative approach remains possible in stable patients but surgical exploration remains necessary in unstable patients with active bleeding.</p></div><div><p>Le traumatisme du mésentère est un des dommages causés par l’utilisation de la ceinture de sécurité en cas d’accident de véhicule. Nous reportons ici un rare cas de rectorragie dû à la rupture d’un hématome du mésosigmoïde. Une laparotomie en urgence a révélé un hématome du mésosigmoïde avec perforation rectale centimétrique. L’utilisation de la ceinture de sécurité a rajouté des caractéristiques spécifiques aux traumatismes abdominaux dépendant directement du système des ceintures à trois points. Les plaies du mésentère sont constatées jusqu’à 5 % des traumatismes contusifs abdominaux. Le « signe de la ceinture de sécurité » conduit l’équipe chirurgicale à suspecter fortement un traumatisme intra-abdominal. Lors que le « signe de la ceinture de sécurité » est retrouvé chez les patients qui présentent des contusions suite à un accident de voiture, une TDM devrait être réalisée afin d’exclure la présence de complications intra-abdominales, y compris celles du mésosigmoïde. En cas d’hématome du mésentère prouvé, avec rectorragie, le traitement chirurgical devrait être le traitement de choix. Un traitement conservatif est envisageable chez les patients stables mais l’exploration chirurgicale demeure nécessaire chez les patients instables avec saignement actif.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 499-501"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.05.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29129550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Microsporidiosis: Epidemiology, clinical data and therapy","authors":"S. Anane, H. Attouchi","doi":"10.1016/j.gcb.2010.07.003","DOIUrl":"10.1016/j.gcb.2010.07.003","url":null,"abstract":"<div><p>Microsporidiosis is an emerging and opportunistic infection in AIDS patients, organ transplant recipients, children, travelers, contact lens wearers and the elderly. It is associated with a wide range of clinical syndromes of microsporidiosis in humans. The disease is caused by microsporidia, obligate intracellular microorganisms that were recently reclassified from protozoa to fungi. The 14 species of microsporidia currently known to infect humans, <em>Enterocytozoon bieneusi</em> and <em>Encephalitozoon intestinalis</em>, are the most common causes of human infections and are associated with diarrhea and systemic disease. Species of microsporidia infecting humans have been identified in water sources as well as in wild, domestic and food-producing farm animals, raising concerns of water-borne, food-borne and zoonotic transmission. Various molecules have been tested for treating microsporidiosis in humans with variable success. Albendazole is effective against <em>Encephalitozoon</em> species such us <em>Encephalitozoon intestinalis</em> but not against <em>Enterocytozoon bieneusi</em>. This species has shown excellent clinical therapeutic response to direct action with fumagillin, but this drug is toxic when administered systematically to mammals. Its analog, TNP 470, could be promising alternative. Further work is necessary to identify other drugs, which are both effective and devoid of adverse effects.</p></div><div><p>La microsporidiose est une infection opportuniste émergente chez les personnes atteintes du sida, les greffés d’organes, les enfants, les voyageurs, les porteurs de lentilles de contact et les personnes âgées. Elle est caractérisée par un spectre clinique varié chez l’homme. Elle est causée par des microsporidies, des microorganismes intracellulaires obligatoires, récemment classées parmi les champignons. Actuellement, 14 espèces sont incriminées en pathologie humaine dont <em>Enterocytozoon bieneusi</em> et <em>Encephalitozoon intestinalis</em> sont les espèces les plus fréquentes. Elles sont associées surtout à des manifestations intestinales ou disséminées. Les espèces de microsporidies infectant l’homme ont été identifiées aussi bien dans des sources d’eau que des aliments ou des animaux de ferme ou domestiques suggérant une transmission hydrique, alimentaire et zoonotique. Différentes molécules ont été testées pour le traitement de la microsporidiose humaine avec un succès variable. L’albendazole est le traitement de choix pour <em>Encephalitozoon</em> dont <em>Encephalitozoon intestinalis</em> mais non contre <em>Enterocytozoon bieneusi</em>. Cette espèce a montré une excellente réponse avec la fumagilline qui est toxique lorsqu’elle est administrée chez les mammifères par voie systémique. Un autre traitement employant le TNP-470, un analogue de la fumagilline, semble assez promoteur. Les efforts doivent continuer afin de développer d’autres molécules efficaces et dénuées d’effets indésirables.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 450-464"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.07.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29181964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}