Pathophysiological role of fundic tension receptors in functional dyspepsia

This work has tried to provide better insight in some pathophysiological factors involved in functional dyspepsia. We have identified several experimental evidences supporting the hypothesis that activation of transducers of wall tension at the level the proximal stomach might be the key to the genesis of at least some of the symptoms. One of the mechanisms by which this activation may be enhanced in patients is the presence of defective accommodation of the proximal stomach in response to a meal. This abnormality was present in a large subgroup of patients and was associated to the presence of early satiety. Pharmacological modulation of the gastric wall tension resulted in concomitant changes in symptom severity, both in health and in functional dyspepsia patients. Special attention has been given to provide the clinician with better tools to investigate his patient, in the perspective of the prescription of a treatment aimed at restoring a defective mechanismCe travail a tenté d'améliorer la compréhension de certains mécanismes physiopathologiques de la dyspepsie fonctionnelle. Nous avons identifié plusieurs arguments expérimentaux soutenant l'hypothèse disant que c'est l'activation de mécanorécepteurs sensibles à la tension pariétale qui est reponsable d'au moins un des symptômes de l'affection. Un des mécanismes par lesquels cette activation peut accrue chez les patients est la présence d'un défaut de l'accommodation gastrique post-prandiale. Cette anomalie a été retrouvée dans une large proportion des patients et est associée à la présence de satiété précoce. Les modifications du tonus gastrique ont résulté dans de modifications concomitantes des symptômes aussi bien chez les volontaires que chez les patients atteints de dyspepsie fonctionnelle.Une attention particulière a été portée sur le développement de nouveaux outils permettant de caractériser les patients dans la perspective de la prescription d'un traitement visant à corriger un mécanisme défectueux.(MED 3) -- UCL, 200

A Hard Nut to Crack: Bouveret's Syndrome.

An 81-year-old man presented with a brutal upper abdominal pain, malaise, sweating and vomiting. Computed tomography revealed an important distension of both the stomach and the first portion of the duodenum consistent with intestinal obstruction as well as a 3cm biliary stone in the second portion of the duodenum.[...

Personalized medicine in metastatic colorectal cancer treated with anti-epidermal growth factor receptor agents: A future opportunity?

Treatment options for colorectal cancer have increased substantially in the past decade, with the introduction of novel biological therapies targeting cancer-specific molecules leading to significantly improved outcomes. Despite access to these treatments, we are not yet in an era where we can fully personalize treatment choices for patients with colorectal cancer. A number of prognostic and predictive markers have been identified that appear to be directly related to sensitivity to targeted therapies, such as those against epidermal growth factor receptor. However, the sensitivities of individual tumors toward different biological agents appear to be more complex. It seems that a more complete molecular signature of the tumor must be taken into account when making individual treatment choices. In the absence of having fully elucidated the influence of these prognostic or predictive markers, other surrogate markers of early treatment success may be useful in determining whether to continue treatment with a particular agent. In this review, we discuss the role of molecular markers in choosing appropriate treatment for the individual patient, along with the use of measuring the depth of response to a particular agent to assist decisions on whether to continue therapy in colorectal cancer. © 2014 Wiley Publishing Asia Pty Ltd

Irritable bowel syndrome: the role of the intestinal microbiota, pathogenesis and therapeutic targets

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder that predominantly affects women and accounts for up to 40% of the gastroenterology unit outpatient visits. The pathophysiology is complex and multifactorial. In the present review we will focus on the role of intestinal dysbiosis in its pathogenesis and treatment. Post-infectious IBS (PI-IBS) can put light on the mechanisms underlying IBS. Modified commensal gut flora may lead to mucosal inflammation. Several changes such as an increase in mucosal cellularity (enterochromaffin cells, lamina propria T lymphocytes and mast cells), modified pro-inflammatory/anti-inflammatory cytokine balance and disordered neurotransmission have been observed. The normal microbiota is an essential factor in health. A modification of the flora, such as small intestinal bacterial overgrowth (SIBO) is thought to play a pathogenic role in IBS. Changes in the composition of the luminal and mucosal colonic flora have been linked to IBS. It is not clear however, whether these changes are a cause or a consequence of the syndrome. The comprehension of the interaction between the dysbiotic microbiota and the host will probably lead to the development of focused therapies. Based on these assumptions, treatments modulating the microbiota have been investigated. On the one hand several probiotics have shown a reduction in IBS symptoms by an immunomodulatory and analgesic effects. On the other hand antibiotic treatment has proven efficacy in treating IBS with or without associated SIBO. Due to its complex pathophysiology, treating IBS nowadays implies multiple approaches, one of which may be modulation of the intestinal flora

LA NÉPHROTOXICITÉ DESIPP : PLUS FRÉQUENTE QU’ON NELE PENSAIT ?

no abstract availabl