Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0021390 (inflammatory bowel disease)
 23,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present review is concerned by the main features of zinc metabolism (requirements, intestinal absorption, tissue distribution, excretion). The relationships between zinc variations and gut pathology are discussed with respect to the following points: criteria for the diagnostic of zinc deficiency, pathophysiological mechanisms, clinical consequences, therapeutic implications. Evidence for zinc malabsorption is present in Acrodermatitis enteropathica and in chronic zinc deficiency observed in Middle-East. During last decade zinc deficiency has been frequently reported in total parenteral feeding. Alterations in plasma zinc concentrations have been described in coeliac disease and inflammatory bowel disease but a true deficiency remains to be established in this pathological states.
 ...
PMID:[Zinc in digestive diseases (author's transl)]. 10 78

We have developed an enzymatic technique for isolating human intestinal mucosal lymphoid cells. This method was found to be superior to mechanical methods in regard to cell yield and survival. It is based on treating mucosa with serum-free solutions containing collagenase and deoxyribonuclease, followed by isolating the lymphoid cells through centrifugation steps involving fetal calf serum and ficoll-hypaque. Exposure of peripheral blood lymphocytes to the components of the enzymatic solution did not appreciably alter their uptake of tritiated thymidine in the presence or absence of mitogens. Application of the method to derive lymphoid cells from Crohn's disease, ulcerative colitis, and normal intestinal mucosa has shown that gut mucosal lymphocytes from inflammatory bowel disease (1) exceed the number of those from normal mucosa by a factor of 3 to 5; (2) show different degrees of tritiated thymidine uptake, spontaneously and in response to mitogens, depending upon the time they are harvested during the dissociation process; (3) are better stimulators than responders in the allogeneic mixed lymphocyte reaction; (4) generate suppressor cell activity comparable to that of peripheral blood lymphocytes; (5) cannot, in contrast to peripheral blood lymphocytes, generate antibody-dependent cell mediated cytotoxicity; and (6) produce an average of 5 times more IgM than equal numbers of peripheral blood lymphocytes.
 ...
PMID:Gut mucosal lymphocytes in inflammatory bowel disease: isolation and preliminary functional characterization. 15 97

In order to investigate the prevalence of iodine depletion in chronic inflammatory bowel disease two separate studies have been performed. One was devoted to the 24-hour urinary iodine excretion and 50 patients with ulcerative colitis or Crohn's disease were examined and compared with 102 controls. In the other study the thyroid 131I uptake was compared in 38 patients and 36 controls. Ten of the 50 patients with chronic inflammatory bowel disease had a 24-hour urinary iodine excretion less than 40 mug, compared with 5 of the 102 controls (p greater than 0.01). Sixteen of the 38 patients had a 24-hour thyroid 131I uptake of 50% or more of the administered test does, compared with 4 of the 36 controls (p smaller than 0.01). These results are compatible with an increased occurrence of iodine deficiency in patients with chronic inflammatory bowel disease. Treatment with corticosteroids or Salazopyrin or a milk-free diet did not influence these findings. No evidence was found of an impaired absorption of inorganic iodide from the gut.?31
 ...
PMID:The thyroid in ulcerative colitis and Crohn's disease. I. Thyroid radioiodide uptake and urinary iodine excretion. 23 26

Lympho-plasmacytic infiltrates in cryostat sections (resected small intestine or colon specimens and rectal biopsies) from 29 patients with Crohn's disease (CD) were studied with the immunoperoxidase and immunofluorescence technique, by means of specific anti-human lymphocyte globulin (ALG) and specific anti-human T-lymphocyte globulin (ATG). Control specimens were obtained from 16 patients with ulcerative colitis (UC) and 12 subjects without inflammatory bowel disease. Characteristic transmural inflammatory infiltrates in CD consisted mainly of lymphocytes. A wide variation of the relative T-cell proportion was observed. However, in contrast with UC, abundant numbers of T-lymphocytes in CD were often detected, particularly in the deeper layers of the bowel wall. Furthermore, in serial sections immunoglobulin-containing plasma cells were counted, using specific anti-IgA, -IgM, and -IgG antisera. A significant reduction of the IgA/IgM plasma cell-ratio was found in CD in comparison with UC and controls. Our results indicate that in CD a chronic cellular immune reaction is going on within the diseases gut, involving increased numbers of lymphocytes and particularly T-cells. It remains to be established whether a deficient IgA barrier has to be considered of primary pathogenetic importance.
 ...
PMID:Analysis of the lympho-plasmacytic infiltrate in Crohn's disease with special reference to identification of lymphocyte-subpopulations. 79 55

Many patients with the inflammatory bowel diseases, Crohn's disease, or ulcerative colitis have significant protein-calorie malnutrition and micronutrient deficiencies. Factors that contribute to these nutritional deficits include inadequate nutrient intake, malabsorption, excessive nutrient secretion across the diseased gastrointestinal tract, drug-nutrient interactions, and increased nutrient requirements. In this review, the use of enteral and parenteral nutrition support as primary therapy for active Crohn's disease and ulcerative colitis is discussed. Other roles for nutrition support in patients with inflammatory bowel disease, including preoperative nutrition support, nutritional treatment of intestinal fistulas and growth retardation, and home parenteral nutrition for gut failure, are also reviewed.
 ...
PMID:Nutrition support in inflammatory bowel disease. 129 78

1. The expression of leucocyte antigens CD11/CD18 and complement receptor 1 was studied on the circulating leucocytes of 13 patients with inflammatory bowel disease and 13 age- and sex-matched healthy control subjects. 2. Monoclonal antibodies against CD11/CD18 and complement receptor 1 were added to leucocyte suspensions from patients and control subjects. Antibody binding was detected using a fluorescein-conjugated rabbit anti-mouse antibody and flow cytometry. The proportions of lymphocytes, monocytes and granulocytes expressing these molecules and the density of antigen expression, measured as mean fluorescence intensity, were determined. 3. There were no differences between patients and control subjects in the mean fluorescence intensity of antibody staining of surface molecules or in the proportion of cells expressing each molecule for any cell type. Analysis of subgroups of patients according to disease type, severity or treatment also showed no difference compared with control subjects. 4. We conclude that failure to identify a population of circulating leucocytes whose adhesion molecules or complement receptors are upregulated may arise because cells are only activated locally within the gut vasculature. Alternatively, structural changes in these molecules, rather than an increase in their number or the expression of other surface glycoproteins, may be more important in mediating adhesive interactions in inflammatory bowel disease.
 ...
PMID:Expression of adhesion molecules on circulating leucocytes in patients with inflammatory bowel disease. 135 84

To detect and measure occult gastrointestinal bleeding, we have measured haemoglobin concentrations (by HemoQuant) in the clear fluid obtained after whole-gut lavage. In subjects with healthy gastrointestinal tracts, lavage-fluid haemoglobin concentrations were 0.5-5.1 mg/L, equivalent to daily blood loss of 0.1-1.1 mL. High concentrations were found for patients with colorectal cancer, severe diverticular disease, and rectal varices, in seven of sixteen patients with active inflammatory bowel disease, and in four patients with iron-deficiency anaemia thought to be due to gastrointestinal bleeding. In these four patients, estimated blood loss ranged from 2.6-24.5 mL per day. This method could have various research and clinical applications.
 ...
PMID:Haemoglobin in gut lavage fluid as a measure of gastrointestinal blood loss. 136 92

Neuropeptides form a part of the brain-gut axis which may regulate gastrointestinal functions, including immune regulation. Various changes in the neuropeptides--most important, vasoactive intestinal peptide and substances P (VIP and SP)--have been described in inflammatory bowel disease. We employed a sensitive immunoperoxidase (avidin-biotin-peroxidase complex) technique, using anti-VIP and anti-SP antibodies to localize and compare the distribution of VIP and SP in the colon. Colon specimens from 19 normal subjects, eight patients with ulcerative colitis (UC), and eight with Crohn's disease (CD) were used. In the normal colon, VIP and SP immunoreactivity (IR) were localized in the muscularis mucosa, circular muscles, walls of blood vessels, nerve fibers, and some distinct cells, probably enterochromaffin cells. SP-IR was also present in the epithelial cells, mainly along the basolateral domain. VIP-IR was considerably diminished at all locations in patients with UC and CD. However, the SP-IR was increased in UC in the colonic epithelial cells along the basolateral areas. The SP-IR was intense in patients with CD, in the epithelium, the granulomas, cells lining the mucosal fissure, and in the muscle layers. In contrast to normals, SP-IR in patients with CD was observed both in the longitudinal and circular muscles. We conclude that VIP-IR and SP-IR are distributed widely in the mucosa, submucosa, and in the circular muscle in normal colon. VIP-IR is decreased in UC and CD, whereas SP-IR is increased in both, but more so in CD.
 ...
PMID:Immunocytochemical localization of vasoactive intestinal peptide and substance P in the colon from normal subjects and patients with inflammatory bowel disease. 137 Aug 72

Heat-shock proteins (HSPs) are highly conserved immunogenic intracellular molecules that are induced by inflammatory mediators and may induce autoimmune phenomena in vivo. We have recently demonstrated the increased expression of HSP-60 in the colonocytes of patients with ulcerative colitis. To study further the role of HSP-60 in inflammatory bowel disease, we have now measured antibodies to recombinant mycobacterial HSP-65 (a member of the HSP-60 family) in patients with Crohn's disease, ulcerative colitis, healthy volunteers and, as disease controls, patients with confirmed bacterial diarrhoea. In comparison with healthy controls (n = 20; median level of 89 ELISA units; range 24-292), serum IgA HSP-60 antibodies were elevated in Crohn's disease (n = 21; 157; 57-364; P < 0.05) and active ulcerative colitis (n = 16; 188; 58-373; P < 0.01) but not bacterial diarrhoea (n = 10; 106; 51-285). Increased IgA HSP-60 antibody levels in patients with inflammatory bowel disease may occur as the result of HSP release from injured gut epithelium; alternatively, increased intestinal permeability could facilitate mucosal access of luminal antigens and the generation of cross-reactive anti-bacterial HSP antibodies.
 ...
PMID:Circulating antibodies to heat-shock protein 60 in Crohn's disease and ulcerative colitis. 142 86

There are many avenues where molecular biology is important in studying the gut, and here we explore methods for defining expression of a new gene family in the gut. We have defined the pattern of trefoil peptide gene expression in the ulceration-associated cell lineage (UACL) and in the nearby mucosa in Crohn's disease. In the UACL, human spasmolytic polypeptide mRNA and peptide are expressed in the acinar and proximal duct cells, whereas pS2 mRNA and peptide are found in the distal duct cells and in the surface cells. In adjacent mucosa, pS2 mRNA and protein are expressed ectopically by goblet cells. Ultrastructural immunolocalisation showed the pS2 to be co-packaged in the mucous cell granules. pS2 peptide was demonstrated in local neuroendocrine cells and was also co-packaged with the neuroendocrine granules. The crypts associated with the UACL also showed marked neuroendocrine cell hyperplasia. We have also cloned the newest trefoil peptide intestinal trefoil factor from human and rat intestinal mucosa and shown its co-expression with mucus by normal intestinal goblet cells. The co-packaging of the same secretory protein in both mucous and neuroendocrine granules, which have different functions, is unusual and indicates an important role for pS2 in the secretory process itself or as a ligand delivered to its receptor via multiple routes. We conclude that the trefoil peptides are widely distributed in the intestine in inflammatory bowel disease and are of considerable potential functional importance.
 ...
PMID:Trefoil peptide expression in intestinal adaptation and renewal. 143 65


1 2 3 4 5 6 7 8 9 10 Next >>