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.

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.

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.

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.

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.

Short bowel syndrome (SBS) is the main cause of intestinal failure especially in children. The colon is a crucial partner for small intestine adaptation and function in patients who have undergone extensive small bowel resection. However, SBS predisposes the patient to small intestine bacterial overgrowth (SIBO), explaining its high prevalence in patients with this disorder. SIBO may significantly compromise digestive and absorptive functions and may delay or prevent weaning from total parenteral nutrition (TPN). Moreover, SIBO may be one of the causes of intestinal failure-associated liver disease, requiring liver transplantation in some cases. Traditional tests for assessing SIBO may be unreliable in SBS patients. Management of SIBO with antibiotic therapy as a first-line approach remains a matter of debate, while other approaches, including probiotics, offer potential based on experimental evidence, though only few data from human studies are available.

Le syndrome du grêle court (SGC) est la principale cause d’insuffisance intestinale, particulièrement chez l’enfant. Le côlon joue un rôle crucial pour l’adaptation et le fonctionnement de l’intestin grêle chez les patients qui ont eu une résection étendue de l’intestin grêle. Cependant, le SGC prédispose à une pullulation bactérienne dans l’intestin grêle (PBIG), expliquant son importante prévalence chez ces patients. La PBIG peut altérer sigm’ficativement les fonctions de digestion et d’absorption intestinales peut retarder ou empêcher l’arrêt de la nutrition parentérale totale. de plus, la PBIG peut être l’une des causes de complications hépatiques associées à l’insuffisance intestinale, pouvant nécessiter le recours à une transplantation hépatique dans certains cas. Les tests cliniques habituellement utilisés pour évaluer la PBIG sont généralement peu fiables chez les patients avec SGC. Le traitement de la PBIG par une antibiothérapie de première intention reste très débattue, alors que d’autres approches, incluant les probiotiques, apparaissent potentiellement intéressantes sur la base de données expérimentales mais reposent encore sur peu de données validées par des études chez l’Homme.