Gastroenterologie Clinique Et Biologique最新文献

Aim

The purpose of this study was to measure the bone mineral density (BMD) of children with Crohn's disease (CD) and to prospectively assess its evolution.

Patients and methods

A total of 27 children (20 boys, seven girls), aged 12.1 ± 2.5 years, were recruited at the time of CD diagnosis. Dual-energy X-ray absorptiometry (DEXA) was used to measure BMD, expressed as Z scores for chronological age (BMD/CA) and bone age (BMD/BA). One year later, BMD was measured again to identify any correlations with disease activity [group A (active disease) vs group R (remission)].

Results

BMD/CA and BMD/BA were negatively correlated with delay in diagnosis (P < 0.0001 and P < 0.05, respectively). BMD/CA was less than −2 standard deviation (SD) in nine patients and BMD/BA was less −2 SD in four patients. At the follow-up, the increase in BMD was smaller in group A (n = 14), whether expressed as absolute values (−0.002 vs 0.040 g/cm² per year; P < 0.024) or as percentages (−0.2 vs 6.6%; P < 0.041); changes in BMD/CA (−0.5 vs −0.1 SD/year) and BMD/BA (−0.3 vs 0 SD/year) did not differ.

Conclusion

Diagnostic delay greatly affects BMD in children with CD even prior to corticosteroid therapy. The risk of low BMD increases with persistent CD activity, although the risk is reduced in association with bone maturation delay.

Epithelial-mesenchymal transition (EMT) is a physiological process occuring in the embryo. In adult organism, EMT could be involved in disease development. In the liver, the possibility that EMT of liver epithelial cells participate to liver fibrosis is increasingly discussed. Furthermore, the involvement of hepatocyte EMT to liver cancer biology has also been documented over the past few years. In this review, we will first describe how EMT participates to embryological development. We will then discuss the involvement of hepatocytes and biliary epithelial cells in liver fibrosis. Finally, we will describe how EMT may impact the metastatic process and resistance to therapy in hepatocellular carcinoma.

Background/aim

Sociodemographic factors associated with colorectal cancer screening participation have been extensively analysed although few, if any, studies have focused on regional/geographical factors as determinants of non-participation rates. The purpose of this study was to investigate the effects of individual and geographical determinants on the variable participation rates seen for colorectal cancer screening.

Methods

The study population comprised 183,978 individuals in the first round of screening and 175,596 in the second round, all of whom were residents of the city of Marseille in France. The influence of age, gender and regional/geographical characteristics, such as proportion of migrants and property prices per square meter, on participation rates was assessed by multilevel analysis.

Results

The participation rate was lower for men (0.85; 95% CI: 0.83–0.86), and higher for those aged 65–69 years. Univariate analysis showed that participation rates were significantly different across the 16 municipal districts of Marseille (range: 22.8–36.7%; OR: 1.97; 95% CI: 1.86–2.08). On multivariate analysis, having a higher proportion of migrants in the district population was still associated with lower participation (OR: 0.96; 95% CI: 0.95–0.97).

Conclusion

In addition to individual factors, regional/geographical factors appear to be relevant determinants of participation rates in urban colorectal cancer screening programs.

The frequency of obesity has been increasing worldwide for 20 years. Many epidemiological studies support a correlation between obesity and increased risk of cancer, particularly digestive cancers in both genders, and gynaecological cancer in women. Currently, about 5% of cancers could be directly related to overweight. Carcinogenesis mechanisms induced by obesity involve insulin resistance, adipokine and angiogenic factor secretions, and inflammation. Experimental and clinical evidence suggest that insulin resistance plays a major role in carcinogenesis. Insulin and non-protein banded IGF-1, whose levels are increased in type 2 diabetes, stimulate cellular growth and inhibit apoptosis. Abnormalities in adipokine secretion by the central adipose tissue play a role at different stages of obesity-induced carcinogenesis. Excess of leptin and PAI-1, associated with a decrease in adiponectin secretion in obese people, contributes to carcinogenesis through cellular growth and angiogenesis stimulation. Remodelling of the extracellular matrix due to metalloproteinase stimulation by PAI-1 is also able to promote cell migration. Obesity not only increases cancer frequency, but is also liable to modify the prognosis and the response to antiangiogenic therapy of digestive cancers. This data suggests the need for clinicians to take into account overweight in cancer risk evaluation and to consider obesity and metabolic disorders as confounding factors in designing therapeutic studies.

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.

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.

Les analogues nucléosidiques ou nucléotidiques de 2^e génération permettent une viro-suppression optimale après 48 à 96 semaines de traitement, chez la plupart des patients quel que soit le type de virus (sauvage ou mutant pré-C), d’hépatopathie sous-jacente (cirrhose ou non) ou de statut immunitaire (mono- ou co-infection VIH/ VHB). Cette efficacité antivirale peut s’accompagner d’une séroconversion HBe voire d’une séroconversion HBs ; elle a un impact clinique majeur puisque l’inactivation de l’activité nécrotico-inflammatoire permet, en l’absence de co-morbidités hépatiques, une stabilisation puis une régression de la fibrose voire de la cirrhose, et de la survenue de ses complications carcinomateuses ou non carcinomateuses. Le problème à l’avenir sera donc celui d’une part de l’observance du traitement pour permettre une efficacité durable et d’autre part de la tolérance du fait de la nécessité d’un traitement antiviral au long cours. Les échecs thérapeutiques sont habituellement dus à une mauvaise observance plus qu’à un problème de résistance. À l’avenir, l’observance des patients doit être optimisée par des consultations d’éducation thérapeutique et l’éducation des médecins. La tolérance à long terme doit être systématiquement évaluée : plus que les risques neuro-musculaires voire d’acidose lactique, seront surveillés, prévenus et traités par le respect des bonnes pratiques cliniques les risques rénaux et osseux.

Second generation nucleos (t) idic analogues result in a complete viral suppression after 48 to 96 weeks of therapy in most patients, regardless of the virus (HBV genotype, wild type or pre-C mutant), the underlying liver disease (cirrhosis or not) or the immune status (mono- or HIV/HBV co-infection). This antiviral efficacy may result in HBe or HBs seroconversion. Its clinical impact is important since inactivation of necroinflammation allows, in the absence of liver comorbidities, a stabilisation then a reversal of fibrosis and cirrhosis, and consequently a decrease in the occurrence of carcinomatous or non-carcinomatous complications. The future issues for long-term anti-HBV therapy will be adherence on the one hand and safety on the other hand. Therapeutic failures are mainly related to poor adherence more than to viral resistance. Adherence of patients has to be optimized by therapeutic education and education of physicians. Long-term safety has to be systematically evaluated. More than the neuromuscular or metabolic side effects (lactic acidosis), the renal and bone-related adverse events have to be monitored, followed-up and anticipated by good clinical practices.

Enteral nutrition is a nutritional therapy that is used in up to 10% of hospitalized patients. It involves 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 level of between-subject variability, this dysbiosis is characterized by a decrease in the dominant flora, an increase in potentially pathogenic 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. Saccharomyces boulardii 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 harvesting and changes in the nutritional status. Manipulations of the microbiota may therefore be a novel way to increase feeding efficiency in tube-fed patients.

La nutrition entérale est une thérapeutique nutritionnelle utilisée chez les patients hospitalisés, jusque chez 10% d’entre eux. Elle représente un changement considérable dans l’apport des nutriments à l’intestin, ce qui, de concours avec le stress métabolique et les médicaments utilisés, est responsable d’une dysbiose marquée. Même s’il existe une 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 chez ces patients. Saccharomyces boulardii est capable de prévenir la diarrhée associée à la nutrition entérale, probablement via une augmentation de la production des acides gras à chaîne courte. En parallèle à son rôle sur l’apparition et la prévention de la diarrhée, le microbiote peut être impliqué dans l’homéostasie (stockage) énergétique et les modifications du statut nutritionnel; les manipulations du microbiote intestinal peuvent donc représenter une nouvelle voie pour augmenter l’efficacité de l’apport nutritionnel chez les patients sous alimentation artificielle.