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At least 199 records · Page 11Linked to original sources
PubMed1990

Anxiety and the gastrointestinal system.

There is a growing recognition that a link exists between anxiety and the gastrointestinal tract. This is evident in studies examining the effects of stress on gastrointestinal function and also in studies assessing psychopathology in patients with functional gastrointestinal disorders which demonstrate a high prevalence of anxiety disorders and depression in these individuals. The recent conceptualization of anxiety as resulting from dysfunction in separable subsystems of the brain as well as experimental evidence linking the brain with the GI tract may allow for testing hypotheses that the high prevalence of anxiety in patients with functional GI disorders may be due to common or interacting pathophysiology. The similarity between the ENS and the CNS may also be a plausible explanation for this association. The high prevalence of anxiety disorders in functional GI patients suggests that medications useful in the treatment of anxiety disorders (anxiolytics and antidepressants) may be useful in the treatment of functional GI disorders especially refractory cases, but further treatment studies are needed.

Anxiety Disorders↗
PubMed1985

[Potential adaptation of the gastrointestinal system. Existence of an enteropancreatic trophic axis, the role of hormones and polyamines].

The evidence for an enteropancreatic trophic axis is reviewed. Luminal nutrition is essential for the maintenance of normal intestinal mucosal, as well as exocrine pancreatic structure and function. Exclusion of luminal nutrition leads to mucosal hypoplasia and hypofunction with similar changes in the pancreas. The trophic effect of luminal nutrition may be mediated through the release of regulatory peptides with endocrine or paracrine effects. Enteroglucagon is the strongest candidate for the role of "enterotrophin" while cholecystokinin (CCK) markedly influences pancreatic growth. Thus, CCK not only stimulates exocrine pancreatic secretion but makes acinar cells divide and the pancreas grow. The cellular mechanisms whereby trophic peptides influence normal and adaptive growth are also discussed with emphasis on polyamines (putrescine, spermidine and spermine) and the key enzymes controlling their synthesis (ornithine decarboxylase [ODC]) and degradation (diamine oxidase [DAO]). When polyamine synthesis is blocked with the ODC inhibitor difluoromethyl ornithine (DFMO), the adaptive intestinal hyperplasia of pancreaticobiliary diversion is either inhibited or completely prevented. A proposed sequence of events might be: luminal nutrients, particularly long chain fat, reach the ileum and colon and stimulate increased enteroglucagon release. Enteroglucagon binds to cell receptors and triggers an intracellular cascade involving ODC and the polyamines which, in turn, stimulate RNA polymerase, DNA, RNA and protein synthesis, cell division and adaptive tissue growth.

Adaptation, Physiological↗
PubMed1993

Effects of sandostatin on neuroendocrine tumours of the gastrointestinal system.

Sandostatin is a drug of immense importance in the management of NETs of the gastrointestinal tract. Its effect in some syndromes is life-saving, in particular in VIPoma. Dramatic effects have also been reported in the glucagonoma syndrome. The quality of life is considerably improved in the carcinoid syndrome and it is potentially life-saving in carcinoid crises. The drug is effective in gastrinomas, but other therapy is more effective. Its value is controversial in insulinoma although some patients are clearly improved. Not all patients respond and this may be related to the abundance of Sandostatin receptors on the tumour or simply to tumour bulk. There is no clear-cut evidence that Sandostatin has an anti-tumour effect in these patients.

Carcinoid Tumor↗
PubMed2005

Moderate alcohol consumption and diseases of the gastrointestinal system: a review of pathophysiological processes.

BACKGROUND/AIMS: Alcohol drinking is responsible for a number of gastrointestinal diseases and cancers. Although heavy drinking episodes and chronic drinking are well linked to mechanisms of disease, moderate alcohol consumption and its effects are less well known. This review attempts to fill a gap in the literature surrounding moderate alcohol consumption. METHODS: A systematic review of the English literature using PubMed was used. RESULTS: A dose-response risk relationship exists between alcohol consumption and digestive disease risk. Acetaldehyde is the main factor in alcohol-related damage in moderate alcohol consumption and acts through numerous methods to exert damaging effects. CONCLUSION: Zero alcohol intake is recommended for lowest risk of alcohol-related digestive tract diseases and conditions. However, given the lowest overall mortality is associated with moderate drinking, moderate drinking with no bingeing episodes is recommended.

Adult↗
PubMed1984

[Usefulness of metoclopramidum-Polfa in the roentgenological diagnosis of defects of the gastrointestinal system in children].

The purpose of this report is estimation of influence of Metoclopramidum on gastrointestinal tract in children and advantages of its administration in gastrointestinal examination. Between October 1980 and August 1981 70 children had contrast gastrointestinal studies with administrations Metoclopramidum. In the cases of suspicion pylorostenosis administration Metoclopramidum make possible correct diagnosis with minimal irradiation of child. After administration Metoclopramidum the roentgenological sing of hiatus hernia and reflux gastro-oesophageal are better visible.

Adolescent↗
PubMed1998

Developmental expression of mucin genes in the human gastrointestinal system.

BACKGROUND AND AIMS: Mucin glycoproteins play a key role in the normal function of the epithelium lining the gastrointestinal tract. The expression of mucin genes, MUC 3, 4, 5AC, 5B, 6, 7, and 8 in human fetal tissues was examined to establish the localisation and age of onset of expression of each mucin gene during human development. METHODS: Mucin gene expression was assayed by mRNA in situ hybridisation. RESULTS: Expression of MUC3 was detected in the small intestine and colon from 13 weeks gestation onwards and at low levels in the main pancreatic duct at 13 weeks only. MUC4 expression was seen at a low level in the colonic epithelium from 13 weeks of gestation but not elsewhere in the gastrointestinal tract. MUC5AC mRNA was detected in the colon at 17 weeks and at high levels in the stomach at 23 weeks. MUC6 transcripts were evident in the pancreatic ducts from 13 weeks of gestation and at high levels in the stomach at 23 weeks. MUC5B, MUC7, and MUC8 transcripts were not detected. CONCLUSIONS: Mucin genes are expressed from the early mid-trimester of gestation in the developing human fetal gastrointestinal tract.

Colon↗