Gastroenterologie Clinique Et Biologique最新文献

{"title":"Microbiota and irritable bowel syndrome","authors":"P. Ducrotté","doi":"10.1016/S0399-8320(10)70021-X","DOIUrl":"10.1016/S0399-8320(10)70021-X","url":null,"abstract":"<div><p>Irritable bowel syndrome (IBS) is a multifactorial disease during which the pathophysiological role of the gut microbiota has been recently highlighted. In almost 20% of the patients, IBS is clearly a post-infectious IBS as a consequence of an acute bacterial gastroenteritis. Some papers have reported an abnormal colonic fermentation in IBS patients that could explain symptoms such as bloating and be one of the factors triggering visceral hypersensitivity. More recently, significant differences in the composition of both the luminal and mucosa-associated microbiota have been reported between both IBS patients and healthy controls and IBS subgroups while some arguments exist for a small intestinal overgrowth in a subset of IBS patients. All these arguments for a deleterious role of the gut microbiota lead to the actual discuss to consider new therapeutic options, including mainly pre- and probiotics and maybe antibiotics.</p></div><div><p>D’un point de vue physiopathologique, le syndrome de l’intestin irritable (SII) est une affection multifactorielle. Cependant, l’accent est mis actuellement sur le rôle probablement important joué par les anomalies de la flore, en particulier dans la sensibilisation des terminaisons sensitives et l’activation des cellules immunitaires dans la paroi digestive. Epidémiologiquement, un SII, surtout à forme diarrhéique, peut apparaitre au décours d’une gastroentérite aiguë, essentiellement d’origine bactérienne. L’action métabolique de la flore parait être excessive, pouvant contribuer à certain symptômes comme le ballonnement et peut-être favoriser la survenue d’une hypersensibilité viscérale. Des anomalies qualitatives de la flore à la fois endoluminale et adhérente au biofilm présent au contact de l’épithélium ont été décrites. Enfin, une pullulation bactérienne endo-luminale parait une réalité dans un sous-groupe de patients souffrant de SII, sans que l’on sache actuellement si cette anomalie est primitive ou secondaire aux troubles moteurs, notamment grêliques, qui s’observent au cours du SII. Ce rôle délétère de la flore ouvre des perspectives thérapeutiques avec un recours possible aux pré- ou probiotiques et peut-être aux antibiotiques.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S52-S56"},"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)70021-X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29326527","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":"Microbiote intestinal et MICI","authors":"P. Seksik","doi":"10.1016/S0399-8320(10)70007-5","DOIUrl":"10.1016/S0399-8320(10)70007-5","url":null,"abstract":"<div><p>Le microbiote intestinal contient environ 10¹⁴ bactéries classées en 4 phyla bactériens : Firmicutes, Bacteroidetes, Actinobacteria, et Proteobacteria. 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^-/- × RAG2^-/-, 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, le microbiote intestinal pourrait porter une pathogénicité de deux façons : par l’expansion d’espèces « pro-inflammatoires » ou par la diminution de bactéries protectrices « anti-inflammatoires ». La complexité du microbiote suggère que ces deux mécanismes pourraient contribuer à l’inflammation intestinale chronique rencontrée au cours des MICI.</p></div><div><p>Gut microbiota contains about 10¹⁴ bacterial cells 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 diseases (IBD) involve a dysregulated immune response to the gut microbiota in genetically predisposed host. Experimental animal models of colitis provide the best evidence that bacteria resident in the bowel of the animals have an essential role in the pathogenesis of colitis because, when maintained germfree, the animals do not develop disease. Moreover, in an immunodeficient mice model of colitis called TRUC (T-bet^-/- × RAG2^-/-), a colitogenic gut microbiota is selected and can be transmitted to an immune sufficient mice and induce colitis. Current interest therefore focuses on the bowel 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 searched in IBD","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 4","pages":"Pages 48-55"},"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)70007-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132948504","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":"Flore et syndrome de l’intestin irritable","authors":"P. Ducrotté","doi":"10.1016/S0399-8320(10)70008-7","DOIUrl":"10.1016/S0399-8320(10)70008-7","url":null,"abstract":"<div><p>D’un point de vue physiopathologique, le syndrome de l’intestin irritable (SII) est une affection multifactorielle. Cependant, l’accent est mis actuellement sur le rôle probablement important joué par les anomalies de la flore, en particulier dans la sensibilisation des terminaisons sensitives et l’activation des cellules immunitaires dans la paroi digestive. Epidémiologiquement, un SII, surtout à forme diarrhéique, peut apparaitre au décours d’une gastroentérite aiguë, essentiellement d’origine bactérienne. L’action métabolique de la flore parait excessive, pouvant contribuer à certain symptômes comme le ballonnement et peut-être favoriser la survenue d’une hypersensibilité viscérale. Des anomalies qualitatives de la flore à la fois endoluminale et adhérente au biofilm présent au contact de l’épithélium ont été décrites. Enfin, une pullulation bactérienne endo-luminale parait être une réalité dans un sous groupe de patients souffrant de SII, sans que l’on sache actuellement si cette anomalie est primitive ou secondaire aux troubles moteurs, notamment grêliques, qui s’observent au cours du SII. Ce rôle délétère de la flore ouvre des perspectives thérapeutiques avec un recours possible aux pré- ou probiotiques et peut-être aux antibiotiques.</p></div><div><p>Irritable bowel syndrome (IBS) is a multifactorial disease. The pathophysiological focus has recently been on the likely significant role played by anomalies of gut microbiota, particularly in the sensitisation of sensory nerve endings and the activation of immune cells in the digestive tract walls. Epidemiologically, IBS, especially the diarrhoeapredominant form, can appear following an acute episode of gastroenteritis, mainly of bacterial origin. The metabolic action of the microbiota appears to be overly responsive and can result in certain symptoms, such as bloating, and might facilitate the occurrence of visceral hypersensitivity. Qualitative anomalies of the microbiota have been described at both the endoluminal level and the thin layer in contact with the epithelium. Lastly, endoluminal bacterial overgrowth seems to be present in a subgroup of patients with IBS, although it is not currently known whether this anomaly is primary or secondary to motor disorders, especially in the small bowel, which are seen during IBS. Knowledge of this deleterious role of the microbiota opens the way to new therapeutic options, with a possible use of prebiotics or probiotics, as well as antibiotics.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 4","pages":"Pages 56-60"},"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)70008-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132697366","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":"Influence du traitement sur l’évolution à long terme de l’hépatite chronique B","authors":"J.-P. Zarski","doi":"10.1016/S0399-8320(10)70029-4","DOIUrl":"10.1016/S0399-8320(10)70029-4","url":null,"abstract":"<div><p>Le traitement de l’hépatite virale chronique B qui repose actuellement surtout sur l’utilisation des analogues de nucléoside et de nucléotide, permet une viro-suppression efficace dans la majorité des cas. En cas de viro-suppression efficace on assiste à une normalisation des transaminases et une amélioration histologique progressive avec réduction de la fibrose. La régression de la cirrhose est également possible si elle est récemment constituée. De plus avec les analogues de nouvelles générations, le risque de mutation de résistance est rare ou nul. Enfin, on commence à observer à moyen terme une négativation de l’antigène HBs voire une séroconversion HBs ce qui diminue le risque de survenue de complications et améliore la morbi-mortalité.</p></div><div><p>The treatment of chronic hepatitis B is essentially based on the use of nucleoside or nucleotide analogues, which lead to viral suppression in the majority of cases. Viral suppression is associated with normal ALT values and progressive histological improvement of not only necroinflammatory lesions but also fibrosis. Regression of cirrhosis can be observed in severe cases. With the use of second-generation nucleoside or nucleotide analogues, the risk of mutation resistance is rare or inexistent. Finally, negativation and seroconversion of the HBs antigen can be observed in the medium-term. This seroconversion is usually associated with a decreased risk of complications and morbidity-mortality improvement.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S109-S111"},"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)70029-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29484209","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":"Liver transplantation for multiple angiomyolipomas complicating tuberous sclerosis complex","authors":"J. Dumortier ,&nbsp;O. Guillaud ,&nbsp;T. Walter ,&nbsp;C.E. Ber ,&nbsp;C. Partensky ,&nbsp;O. Boillot ,&nbsp;J.-Y. Scoazec","doi":"10.1016/j.gcb.2010.06.005","DOIUrl":"10.1016/j.gcb.2010.06.005","url":null,"abstract":"<div><p>Tuberous sclerosis complex is a genetic multisystem disorder characterised by widespread hamartomas in several organs, including the brain, heart, skin, eyes, kidney, lung, and liver. Hepatic multiple, bilateral angiomyolipomas are a rare and usually asymptomatic complication in patients with tuberous sclerosis. We report here the case of a patient who needed liver transplantation because of debilitating manifestations and mechanical complications of massive liver involvement by multiple angiomyolipomas (severe malnutrition, anorexia and abdominal pain). Seventeen tumors, from 2 to 16<!--> <!-->cm in diameter, were identified at examination of the liver explant. No feature suggestive of malignant behaviour was identified at histological examination. In conclusion, this unusual indication of liver transplantation underlines the interest of this therapeutic approach for benign tumors for which the multiplicity of the lesions and their huge volume prevent any attempt at surgical resection.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 494-498"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.06.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29161403","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":"Role and limitations of 18F-FDG positron emission tomography (PET) in the management of patients with pancreatic lesions","authors":"C. Pery ,&nbsp;G. Meurette ,&nbsp;C. Ansquer ,&nbsp;E. Frampas ,&nbsp;N. Regenet","doi":"10.1016/j.gcb.2009.04.014","DOIUrl":"10.1016/j.gcb.2009.04.014","url":null,"abstract":"<div><p>The 18-fluorine-18-fluoro-2-deoxyglucose Positron Emission Tomography coupled with computed tomography is a non invasive exploration. Several studies have shown that PET-CT has superior efficacy over conventional imaging techniques in distinguishing a benign pancreatic tumor from a malignant one. It contributes to the diagnosis of cancer in patients with a doubtful mass, much more in case of chronic pancreatitis. PET-CT is also an important help for the diagnosis of cystic tumors of the pancreas; the results can affect the management strategy. It is interesting for the endocrine tumors, particularly since the emergence of new markers. The aim of this paper is to summarize the role and limitations of 18-F-FDG PET-CT in the management of patients with pancreatic lesions (adenocarcinoma, cystic tumors, endocrine tumors, etc…) concerning the malignancy diagnosis, the detection of metastases, the monitoring after non surgical treatments and to evaluate interpretation difficulties, particularly in case of diabetes or chronic pancreatitis.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 465-474"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2009.04.014","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29171035","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":"Fermentative metabolism by the human gut microbiota","authors":"A. Bernalier-Donadille","doi":"10.1016/S0399-8320(10)70016-6","DOIUrl":"10.1016/S0399-8320(10)70016-6","url":null,"abstract":"<div><p>The human large intestine is colonized by a complex community of microorganisms, largely composed of strictly anaerobic bacteria with numerous physiological functions which impact on the host nutrition and health. Among these functions, the fermentation of substrates is of major importance for host health through the production of a wide variety of metabolites. The metabolic functions of the human gut microbiota are correlated with the nature of the substrates available for fermentation in the colon. These substrates are from exogenous (dietary fibers that are mainly plant polysaccharides) and endogenous (produced by the host and represent important source of nitrogen) sources. The metabolites produced from the microbial fermentation process in the gut are mainly absorbed and used by the host. Most of them have health benefits, but some may also have deleterious effects. The gut microbiota should thus be considered in relation to its environment, including dietary food and host factors. The interactions between food, intestinal microbiota and the host are fundamental to the maintenance of homeostasis in the ecosystem. Any disruption of this equilibrium could modify the functionality of the gut microbiota and lead to a pathological state.</p></div><div><p>Le côlon humain héberge une communauté microbienne extrêmement dense, composée essentiellement d’espèces anaérobies strictes. Ce microbiote intestinal exerce de nombreuses fonctions physiologiques ayant des répercussions importantes sur la nutrition et la santé de l’hôte. Parmi ces fonctions, la fermentation des substrats joue un rôle majeur par la diversité des métabolites produits. Ces processus fermentaires sont fortement corrélés à la nature des substrats disponibles. Ceux-ci sont de deux origines: exogène (alimentaire/polyosides d’origine végétale) et endogène (produit par l’hôte, source importante d’azote). La plupart des métabolites fermentaires synthétisés par le microbiote intestinal sont absorbés puis utilisés par l’hôte. La majorité de ces métabolites sont potentiellement bénéfiques pour l’hôte, toutefois certains peuvent avoir des effets délétères pour la santé. Les interactions entre l’aliment, le microbiote intestinal et l’hôte ont donc un rôle essentiel dans le maintien de l’homéostasie de l’écosystème. Toute rupture de l’équilibre entre ces éléments est susceptible de modifier le fonctionnement de l’écosystème et de conduire à un état pathologique, en particulier au niveau digestif.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S16-S22"},"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)70016-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29326522","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":"Bithérapie par analogues dans le traitement de l’hépatite chronique B : de novo ou en cas d’échec","authors":"A. Kahloun ,&nbsp;M. Bourlière ,&nbsp;F. Zoulim","doi":"10.1016/S0399-8320(10)70032-4","DOIUrl":"10.1016/S0399-8320(10)70032-4","url":null,"abstract":"<div><p>Hepatitis B virus (HBV) genomic variability is responsible for the complexity of the viral quasi-species and its evolution during the course of infection. The persistence of infected cells promotes the selection of drug-resistant strains. The development of nucleoside analogs without cross-resistance has provided a rationale for combination therapy. <em>De novo</em> combination, with low genetic barrier drugs, prevents the emergence of resistance in the short-term for drugs with a low genetic barrier and improves the control of infection. Lont-term studies are needed to determine whether <em>de novo</em> combination is beneficial for analogs with a high genetic barrier as well. The add-on strategy is a standard in case of emergence of resistant mutants. This strategy needs to be implemented as early as possible before the virological breakthrough, especially if the viral suppression is sub-optimal. Clinical trials are mandatory in order to assess whether a) <em>de novo</em> combination is better than an early add-on strategy; and b) whether in case of sub-optimal viral suppression, an early add-on strategy is better in the long-term than a switch to a more potent drug with a high genetic barrier.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 ","pages":"Pages S126-S135"},"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)70032-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29484212","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":"Nutrition entérale et microbiote","authors":"S.-M. Schneider","doi":"10.1016/S0399-8320(10)70009-9","DOIUrl":"10.1016/S0399-8320(10)70009-9","url":null,"abstract":"<div><p>La nutrition entérale est une thérapeutique nutritionnelle utilisée chez les patients hospitalisés, jusque chez 10% d’entre eux. Elle représente dans l’apport des nutriments à l’intestin une modification brutale qui, jointe au stress métabolique et à l’impact des médicaments, est responsable d’une dysbiose marquée. Même s’il existe une très large variabilité entre sujets, la dysbiose est caractérisée par une diminution de la flore intestinale dominante, une augmentation des micro-organismes potentiellement pathogènes et une réduction du nombre de souches bactériennes individuelles. La caractéristique principale de ces modifications du microbiote est une diarrhée, avec ses multiples conséquences pour les patients. <em>Saccharomyces boulardii</em> est capable de prévenir la diarrhée associée à la nutrition entérale, probablement <em>via</em> une augmentation de la production des acides gras à chaîne courte. Outre son rôle dans l’apparition ou la prévention de la diarrhée, le microbiote peut être impliqué dans l’apport énergétique et les modifications du statut nutritionnel ; les manipulations du microbiote intestinal peuvent ainsi représenter une voie nouvelle pour augmenter l’efficacité de l’apport nutritionnel chez les patients alimentés par sonde.</p></div><div><p>Enteral nutrition is a nutritional therapy that is used in up to 10% of hospitalized patients. It represents a dramatic change in the provision of nutrients to the intestine and this, along with metabolic stress and drugs used, is responsible for a marked dysbiosis. Even though there is a huge between-subject variability, this dysbiosis is characterized by a decrease in the dominant flora, an increase in potentially pathogen microorganisms and a reduction in the number of individual strains. The main characteristic of these changes in the microbiota is diarrhea, which has many consequences in these patients. <em>Saccharomyces boulardii</em> is able to prevent enteral nutrition-associated diarrhea, probably through an increase in short-chain fatty acid production. Alongside its role in the onset and prevention of diarrhea, the microbiota may be involved in energy harvest and changes in the nutritional status. Manipulations of the microbiota may therefore be a novel way to increase feeding efficiency in tube-fed patients.</p></div>","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 4","pages":"Pages 61-66"},"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)70009-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115080459","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":"IgA anti-actin antibodies in celiac disease","authors":"A. Achour ,&nbsp;Y. Thabet ,&nbsp;W. Sakly ,&nbsp;A. Mankai ,&nbsp;N. Sakly ,&nbsp;A. Ayadi ,&nbsp;M.T. Sfar ,&nbsp;F. Amri ,&nbsp;A. Harbi ,&nbsp;A.S. Essoussi ,&nbsp;A. Krifa ,&nbsp;S. Ajmi ,&nbsp;I. Ghedira","doi":"10.1016/j.gcb.2010.01.023","DOIUrl":"10.1016/j.gcb.2010.01.023","url":null,"abstract":"<div><h3>Aims</h3><p>The purpose of this study was to determine the sensitivity and specificity of IgA anti-actin antibodies (IgA-AAA) for celiac disease (CD), to investigate their usefulness as a marker of compliance in CD patients to the gluten-free diet (GFD), and to assess the relationship between their presence in the sera of CD patients and severity of intestinal mucosal damage.</p></div><div><h3>Patients and methods</h3><p>A total of 182 patients with CD were studied: 63 patients were untreated; 50 patients were following a strict GFD; and 69 patients were non-compliant with a GFD. IgA-AAA was detected using a homemade enzyme-linked immunosorbent assay (ELISA).</p></div><div><h3>Results</h3><p>IgA-AAA showed a sensitivity of 41.3% and a specificity of 71.4% for a diagnosis of CD. In children, the frequency of IgA-AAA detection was lower in those following a strict GFD (23.1%) compared with untreated patients (39.4%) and those not complying with a GFD (32.5%). In patients following a strict GFD, IgA-AAA detection was significantly less frequent in children than in adults (23.1% vs. 58.3%, respectively; <em>P</em> <!-->&lt;<!--> <!-->0.001). IgA-AAA was found in 17 out of 52 CD patients with total villous atrophy (32.7%), and in one out of 11 patients with subtotal villous atrophy (9%).</p></div><div><h3>Conclusion</h3><p>IgA-AAA cannot replace anti-endomysium and anti-tissue transglutaminase antibodies in the diagnosis algorithm of CD, but it can serve as a reliable marker of severe intestinal mucosal damage in CD patients.</p></div><div><h3>Objectif</h3><p>Déterminer la sensibilité et la spécificité des anticorps anti-actine d’isotype IgA (AAA-IgA) au cours de la maladie cœliaque (MC), évaluer la relation entre leur présence dans le sérum de patients cœliaques et la gravité des dommages au niveau de la muqueuse intestinale, et déterminer leur utilité dans le contrôle de la compliance au régime sans gluten (RSG).</p></div><div><h3>Patients et méthodes</h3><p>L’étude a porté sur 182 sérums prélevés chez des patients cœliaques. Soixante-trois patients sont non-traités, 50 sont sous RSG strict et 69 sont sous RSG mal suivi. Les AAA-IgA sont recherchés par une technique Elisa maison.</p></div><div><h3>Résultats</h3><p>La sensibilité des AAA-IgA est de 41,3 % et sa spécificité est de 71,4 %. Chez les enfants, mais pas chez les adultes, les AAA-IgA sont moins fréquents chez les patients sous RSG strict (23,1 %) que chez les patients non traités (39,4 %) et ceux qui ne suivent pas leur régime (32,5 %). Chez les patients sous RSG strict, les AAA-IgA sont significativement moins fréquents chez les enfants que chez les adultes (23,1 % versus 58,3 %, p &lt;0,001). Les AAA-IgA sont détectés dans 17 cas parmi les 52 patients cœliaques présentant une atrophie villositaire totale (32,7 %) et dans un cas sur 11 chez les patients présentant une atrophie villositaire subtotale (9 %).</p></div><div><h3>Conclusion</h3><p>Les AAA-IgA ne peuvent pas remplacer le","PeriodicalId":12508,"journal":{"name":"Gastroenterologie Clinique Et Biologique","volume":"34 8","pages":"Pages 483-487"},"PeriodicalIF":0.0,"publicationDate":"2010-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.gcb.2010.01.023","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"29141641","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}