vasoactive-intestinal-peptide and Malabsorption-Syndromes

Small intestinal dysfunction has been described in patients with ulcerative colitis and in experimental animal models of colitis. This is demonstrated by a decrease in fluid, electrolyte, amino acid, fat and carbohydrate absorption as well as by deranged intestinal motility. Histopathological changes in the small intestines in colitis have not been consistently demonstrated, but there is evidence of structural and biochemical alterations as shown by increased intestinal permeability and a decrease in the expression of multiple brush border membrane enzymes such as disaccharidases and aminopetidases, in both humans and experimental animals. The pathophysiology of this dysfunction has not been elucidated, but it is thought to include alterations in neural circuitry such as increased neuronal excitability, neuronal damage and changes of neuropeptidergic innervation and receptors as well as an increase in local production of pro-inflammatory cytokines and alterations in the production of some neurohumoral mediators. In the following, we provide an update on the advancement of clinical and scientific contributions to elucidate the underlying mechanisms of the alteration of the functions of apparently intact small intestinal segments, induced by ulcerative colitis.

Topics: Animals; Colitis, Ulcerative; Cytokines; Enteric Nervous System; Gastrointestinal Motility; Humans; Intestine, Small; Malabsorption Syndromes; Nitric Oxide; Permeability; Serotonin; Vasoactive Intestinal Peptide

Topics: alpha 1-Antitrypsin; Bacterial Toxins; Cholestyramine Resin; Colonic Diseases; Deoxycholic Acid; Diarrhea; Humans; Immunoglobulin G; Iodine Radioisotopes; Malabsorption Syndromes; Prostaglandins; Protein-Losing Enteropathies; Serum Albumin; Vasoactive Intestinal Peptide; Water-Electrolyte Imbalance

Short bowel syndrome is a complex disease that is almost always seen with diarrhea. VIP is known to act powerfully on gut motility, and elevated VIP plasma levels have been reported in several diarrheal conditions. In this study VIP plasma levels were measured by radioimmunoassay in 8 patients with short bowel syndrome versus 30 healthy control subjects under basal conditions. VIP plasma levels were significantly higher in the short bowel syndrome group (p less than 0.05). The explanations that could account for these elevated levels are (1) an increased gastric acid load in the residual bowel, (2) a compensatory increase in blood supply to the gut, (3) removal of an inhibitory factor arising from the small intestine, or (4) mucosal stress due to unadsorbed food. An etiologic role of VIP in the occurrence of diarrhea in patients with short bowel syndrome seems to be an unproved hypothesis.

Topics: Female; Gastrointestinal Hormones; Humans; Malabsorption Syndromes; Male; Middle Aged; Short Bowel Syndrome; Vasoactive Intestinal Peptide