Correlation between oesophageal acid exposure and dyspeptic symptoms in patients with nonerosive reflux disease.

Oesophageal acidification induces dyspeptic symptoms in healthy individuals. This study aimed to evaluate the correlation between oesophageal acid exposure and dyspeptic symptoms in patients with nonerosive reflux disease. METHODS: A total of 68 patients with dominant symptoms of heartburn, negative upper gastrointestinal endoscopy and concomitant dyspeptic symptoms participated in the study. The severity of dyspepsia and reflux-related symptoms was evaluated, and 24-h gastro-oesophageal pH-monitoring study was performed in all patients at baseline and after 4 weeks of therapy with esomeprazole 40 mg. RESULTS: Oesophageal basal acid exposure was pathological in 43 patients and normal in 25 patients, with a similar prevalence and severity of individual dyspeptic symptoms in the two groups. A significant correlation between reflux and dyspepsia scores was observed in the subgroup of patients with normal, but not in those with abnormal pHmetry (r=0.4, P=0.04 and r=0.2 P=0.07, respectively). After esomeprazole, a reduction in severity of dyspepsia (>or=50% with respect to baseline) was observed, independent of improvement of reflux-associated symptoms. Improvement in dyspepsia was, however, similar in patients with normal and abnormal basal acid exposure (14/25 vs. 33/43, respectively, P=NS). CONCLUSION: Dyspeptic symptoms coexist in a subset of nonerosive reflux disease patients, but prevalence and severity of the symptoms seems to be independent of oesophageal acid exposure

Chronic constipation diagnosis and treatment evaluation: The "CHRO.CO.DI.T.E." study

Background: According to Rome criteria, chronic constipation (CC) includes functional constipation (FC) and irritable bowel syndrome with constipation (IBS-C). Some patients do not meet these criteria (No Rome Constipation, NRC). The aim of the study was is to evaluate the various clinical presentation and management of FC, IBS-C and NRC in Italy. Methods: During a 2-month period, 52 Italian gastroenterologists recorded clinical data of FC, IBS-C and NRC patients, using Bristol scale, PAC-SYM and PAC-QoL questionnaires. In addition, gastroenterologists were also asked to record whether the patients were clinically assessed for CC for the first time or were in follow up. Diagnostic tests and prescribed therapies were also recorded. Results: Eight hundred seventy-eight consecutive CC patients (706 F) were enrolled (FC 62.5%, IBS-C 31.3%, NRC 6.2%). PAC-SYM and PAC-QoL scores were higher in IBS-C than in FC and NRC. 49.5% were at their first gastroenterological evaluation for CC. In 48.5% CC duration was longer than 10 years. A specialist consultation was requested in 31.6%, more frequently in IBS-C than in NRC. Digital rectal examination was performed in only 56.4%. Diagnostic tests were prescribed to 80.0%. Faecal calprotectin, thyroid tests, celiac serology, breath tests were more frequently suggested in IBS-C and anorectal manometry in FC. More than 90% had at least one treatment suggested on chronic constipation, most frequently dietary changes, macrogol and fibers. Antispasmodics and psychotherapy were more frequently prescribed in IBS-C, prucalopride and pelvic floor rehabilitation in FC. Conclusions: Patients with IBS-C reported more severe symptoms and worse quality of life than FC and NRC. Digital rectal examination was often not performed but at least one diagnostic test was prescribed to most patients. Colonoscopy and blood tests were the "first line" diagnostic tools. Macrogol was the most prescribed laxative, and prucalopride and pelvic floor rehabilitation represented a "second line" approach. Diagnostic tests and prescribed therapies increased by increasing CC severity

Almost all irritable bowel syndromes are post-infectious and respond to probiotics: consensus issues.

Several reports have described post-infectious irritable bowel syndrome (Pi-IBS), while many animal and human studies have shown the presence of increased infiltration of inflammatory cells and hyperplasia of enterochromaffin cells in the intestinal mucosa after acute gastroenteritis. The potential value of probiotic bacteria in restoring normal gut function has been demonstrated by animal models of Pi-IBS. In humans, Pi-IBS can be prevented utilizing probiotics to reduce the duration of acute gastroenteritis, despite the variable efficacy shown in randomized control trials evaluating unspecified IBS. Here, advances in the pathophysiology supporting the post-infectious hypothesis are considered. In addition, the current role of probiotics in the management of Pi-IBS is discussed. 2007 S. Karger AG, Ba

Medical treatment of gastro-oesophageal reflux disease.

The introduction, in the last two decades, of strongly effective acid suppressant drugs, such as proton pump inhibitors has radically modified the way of treating gastro-oesophageal reflux disease. In clinical trials, these agents have constantly been demonostrated to be more effective than other acid-suppressant agents such as H2-receptor antagonists in relief of symptoms and healing of oesophagitis, the two main goals of gastro-oesophageal reflux disease treatment. They provide a prompt clinical benefit to most patients and can be safely used in long-term gastro-oesophageal reflux disease management for maintenance of clinical and endoscopic remission, because of their negligible adverse-events profile. Therapeutic protocols vary depending on the severity of symptoms and the degree of oesophageal injury. In patients with mild symptoms and with minimal lesions at endoscopy, a "step-down" therapy, in the short-term, is considered the best medical strategy, while in the long-term the therapy "on-demand" appears to be a reasonable approach. Patients with non-erosive disease seem to have a lower response rate to proton pump inhibitor treatment. More severe grades of oesophagitis must be treated with full-dose proton pump inhibitors without withdrawal. Data on the treatment of extra-oesophageal manifestations of gastro-oesophageal reflux disease are few and controversial. Overall, it appears that patients with extra-oesophageal symptoms of gastro-oesophageal reflux disease must be treated with higher doses of pharmacological treatment, principally with proton pump inhibitors, and with longer periods of treatment to achieve complete relief of symptoms, as compared with patients with typical symptoms of gastro-oesophageal reflux disease and erosive oesophagitis

La dispepsia post-infettiva: evoluzione sintomatologica- funzionale, predisposizione genetica, ruolo dell'Ossido Nitrico Sintetasi inducibile e coinvolgimento della glia entererica.

Functional gastrointestinal disorders are highly prevalent conditions affecting at least 30-40% of the western population. These disorders are characterized by occurrence of digestive symptoms in the absence of any identifiable organic cause. Mostly, functional abnormalities involve gastrointestinal motility and/or sensitivity, with a broad spectrum of symptoms severity. Several factors should be then considered to address the impact of the different gastrointestinal disorders: chronic idiopathic intestinal pseudo-obstruction for the severe prognosis, esophageal achalasia for the marked impact of patients'quality life, functional dyspepsia and irritable bowel syndrome for the high prevalence and the involvement of economic resources. Functional and/or structural damage of the enteric nervous system with its glial component seems likely to be a common trademark in each of these syndromes. Although the pathophysiological mechanisms underlying the damage of the enteric neuronal network are still not well defined, it has been recently proposed that functional gastrointestinal disorders may be secondary to transient infection of the digestive system. In keeping with this, different infectious agents may either directly, or through the activation of the immune system, alter the enteric nervous system and or gastrointestinal muscle with impaired motility, sensitivity or secretion and symptoms onset. Moreover, it should be noted that host response to infection is genetically determined, and thus it is possible that individual genetic determinants can be also involved. The general aim of the present research proposal is to study the pathophysiological mechanisms, the biomolecular aspects and the genetic determinants underlying post-infectious functional gastrointestinal disorders. Specifically, individual research units will collaborate in order to address: A) in an animal model of Herpes Simplex 1 virus (HSV-1) infection of the enteric neurons: i) the effect of neurotoxic agents, stress or high dose steroids on HSV-1 reactivation; ii) the correlation between HSV-1 reactivation in the enteric nervous system and the impairment of gastrointestinal motility; B) in an in vitro model of primary culture of human smooth muscle cells: i) the effect of bacterial products on cells contractility; ii) the mechanisms involved in bacterial products cells recognition's trough the analysis of Toll-Like Receptors (TLRs); iii) the intracellular effect of TLRs activation and its correlation with cell contractility; C) in patients with esophageal achalasia: i) the characterization of lymphocytes infiltrating the lower esophageal sphincter; ii) the specific viral epitopes involved in lymphocytes activation; D) in patients with post-infectious dyspepsia: i) mucosal inducible Nitric Oxide Synthase (iNOS) expression, the relative nitric oxide (NO) production and its association with impaired gastric sensitivity and motility and dyspeptic symptoms; ii) the role of enteric glia in NO production; E) the impact of HSV-1 infection and other neurotropic viruses in the enteric nervous system of patients with severe dysmotility related to an underlying neuropathy, such as intestinal pseudoobstruction; F) the role of intestinal inflammation in the pathophysiology of visceral hypersensitivity in patients with post-infectious irritable bowel syndrome; G) the association between the iNOS gene promoter polymorphisms and esophageal achalasia and post-infectious dyspepsia