Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010346 (Crohn's disease)
 21,615 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is hypothesized that chronic gastritis and ulcerative colitis both are induced by viral infection, and that such chronic infection of the mucosa may lead to ulceration and occasionally cancer. Duodenal ulcer disease and Crohn's disease may on the other hand, be due to activation of latent viral infection of the corresponding neural ganglions, with subsequent migration of virus along the nerves to the gut wall. The gastric acid hypersecretion often occurring in patients with duodenal ulcer disease might be a consequence of viral interference with the efferent nerve function of vagal ganglions. Correspondingly, non-ulcer dyspepsia as well as irritable colon may reflect viral infection of afferent nerve function leading to pain and discomfort.
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PMID:Gastritis, peptic ulcer disease, inflammatory bowel disease, and stomach and colon cancers- are they all caused by viral infections? 732 19

Ulcerative colitis and Crohn's disease are significant childhood illnesses. With their many extraintestinal manifestations, they may masquerade as fever of unknown etiology, arthritis, anorexia nervosa, growth hormone deficiency, collagen-vascular disease, idiopathic growth retardation and even irritable bowel syndrome of childhood. In any child who presents with growth failure and/or chronic abdominal pain with fever or weight loss, the diagnosis of inflammatory bowel disease must be considered. As in any other chronic disease of childhood, long-term management will often challenge the physician emotionally and intellectually. As the etiology is yet unknown and a definitive cure is lacking, proper treatment depends on optimal medical and surgical management and supportive care.
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PMID:Inflammatory bowel disease in children and adolescents. 737 73

Fecal alpha-1-antitrypsin is recommended as a marker of enteric protein loss and in patients with Crohn's disease as an index of intestinal inflammatory activity. We describe our experience in 88 patients with chronic diarrhea or suspicion of protein-losing enteropathy. We measured alpha-1-antitrypsin concentration in random stool samples (n = 7), quantitative alpha-1-antitrypsin excretion in a 24 h feces collection (n = 59) and fecal alpha-1-antitrypsin clearance (n = 22). 13 of 88 patients with the following diagnoses had increased values: Crohn's disease (3/9), other inflammatory diseases of the small intestine (3/3, Whipple's disease, eosinophilic gastroenteritis, celiac disease), hypertrophic gastropathy (1/4), infectious diarrhea (2/6), irritable bowel syndrome (2/29), chronic pancreatitis (2/32) and diarrhea of other reasons (0/5). In patients with Crohn's disease, alpha-1-antitrypsin excretion correlated with the clinical disease activity. All 3 patients with other inflammatory diseases of the small intestine showed increased fecal alpha-1-antitrypsin. All but 2 of the 32 patients with diarrhea due to chronic pancreatitis had normal values. Of 29 patients with idiopathic diarrhea, only 2 showed slightly increased fecal alpha-1-antitrypsin. 10 of the 11 patients with increased alpha-1-antitrypsin excretion in 24 h stool collection had normal alpha-1-antitrypsin concentration in random stool samples. Of the 5 patients with increased alpha-1-antitrypsin clearance, 4 also had increased alpha-1-antitrypsin in 24 h stool collection, but only one had increased alpha-1-antitrypsin concentration in random stool sample. Fecal alpha-1-antitrypsin measurement proved helpful in differing between inflammatory and non-inflammatory diarrhea.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Initial personal experiences with alpha-1-antitrypsin determination in feces]. 748 35

Approximately 60% of sera from ulcerative colitis (UC) patients contains Igs reactive with neutrophil components, raising the question of the origin of these anti-neutrophil cytoplasmic Abs (ANCA). Our assertion that ANCA is a marker for a mucosal disease-related immune response predicts the existence of ANCA producing B cell clones in the lamina propria lymphocyte (LPL) fraction of UC patients. This hypothesis was tested by examining 12-day culture supernatants of LPL ANCA expression. LPL were isolated from surgically removed mucosa from patients with UC, Crohn's disease (CD), and diverticulitis. Normal mucosa was obtained from accident victims or normal margins of colon cancer resections. Supernatants were assayed by a fixed neutrophil ELISA. The ANCA staining pattern of supernatants expressing ANCA, as determined by ELISA, was assessed by indirect immunofluorescent staining of alcohol-fixed neutrophils. ANCA was found in 70% of culture supernatants from UC LPL fractions. In contrast, only approximately 11% of supernatants from CD and diverticulitis/normal (noninflammatory bowel disease (IBD)) LPL displayed ANCA binding. A perinuclear (pANCA) staining pattern was obtained with 70% of ANCA-expressing UC LPL supernatants, whereas ANCA-expressing CD and non-IBD LPL supernatants displayed a cytoplasmic reaction. PBL and mesenteric lymph node lymphocytes lacked spontaneous pANCA production, and pANCA production from PBL was not inducible. These findings indicate the existence of pANCA-producing B cell clones in mucosal lesions of UC patients and support our hypothesis that pANCA production is a consequence of a mucosal immune response specific to UC.
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PMID:Perinuclear anti-neutrophil cytoplasmic antibodies are spontaneously produced by mucosal B cells of ulcerative colitis patients. 767 39

IBD is characterized by increased serum concentrations of different cytokines. IL-10 inhibits the production of proinflammatory cytokines such as IL-1, tumour necrosis factor-alpha (TNF-a), interferon-gamma (IFN-gamma) and IL-6 through inhibitory action on Th1 cells and macrophages, and it is thought to be a suppressor type cytokine. In the present study we determined serum concentrations of IL-10 in patients with ulcerative colitis (UC) and Crohn's disease (CD). We measured human IL-10 by our own newly established ELISA system using PharMingen antibodies. Serum antibodies were assessed in 44 patients with UC, 40 patients with CD, and in 30 healthy controls. Human IL-10 serum levels were significantly increased in patients with active UC (144 +/- 34 pg/ml (mean +/- s.e.m.), P < 0.001) and in active CD (132 +/- 32 pg/ml, P < 0.001) compared with healthy controls (44 +/- 9.5 pg/ml). Only patients with active CD and active UC presented with significantly increased IL-10 serum levels, while patients with inactive disease did not show any significant increase. There was no statistically significant difference between IL-10 serum levels in patients with CD or UC. Compared with clinical disease activity indices there was a significant correlation between IL-10 serum concentration and CDAI in patients with CD (r = 0.45, P < 0.01) and CAI in UC patients (r = 0.39, P < 0.05). Comparing IL-10 serum levels with serum concentrations of other proinflammatory cytokines there was a significant correlation to serum levels of sIL-2R (r = 0.417, P < 0.05) and IL-6 (r = 0.387, P < 0.05) in patients with CD. Serum cytokine levels in patients with UC did not show any significant correlation to IL-10 serum concentration. IL-10 is elevated in serum of patients with active CD and UC, suggesting that IL-10 acts as a naturally occurring damper in the acute inflammatory process of IBD.
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PMID:Circulating antiinflammatory cytokine IL-10 in patients with inflammatory bowel disease (IBD). 777 55

Morphological and functional changes were examined in the upper jejunum and terminal ileum of 18 patients suffering from Crohn's disease. Intestinal permeability, biochemical determination of enzymatic activities, and morphologic evaluation of the severity of the lesions were evaluated. Ulcerative colitis and irritable bowel syndrome patients served as controls. We found abnormal lactulose-mannitol tests in all patients with active Crohn's disease. Permeability changes correlated with increased crypt cell proliferation, as indicated by thymidine kinase activity. A significant reduction in brush border enzyme activities was seen in the terminal ileum, but no significant change was observed in the unaffected upper jejunum. The number of mast cells was increased in the diseased ileum. We conclude that the site of inflammation and the healing capacity of the epithelium are important in determining functional and biochemical abnormalities in active Crohn's disease. Changes may be dependent on the type and number of immune cells involved in the inflammatory process.
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PMID:Functional and morphological changes in small bowel of Crohn's disease patients. Influence of site of disease. 778 65

Researchers have recently challenged long-held concepts of psychological origins to inflammatory bowel disease, in particular with ulcerative colitis. The purpose of this paper is to review published studies on psychiatric factors in Crohn's disease to determine whether available evidence points to the absence or presence of a significant relationship between Crohn's disease and stressful life events or psychiatric symptoms or disorders. Twelve articles with > or = 10 subjects on which statistical data were reported from standardized instruments of measure were found. Most reported a significant association between Crohn's disease and psychiatric factors. Many of the investigative groups reporting such an association in Crohn's disease had also studied ulcerative colitis and failed to find a similar association in that disease. Published data indicate that Crohn's disease, unlike ulcerative colitis, may be statistically associated with lifetime psychiatric disorders. This association appears to be more modest than in irritable bowel syndrome, in which far higher rates of psychiatric disorders are reported than in Crohn's disease.
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PMID:A review of studies of psychiatric factors in Crohn's disease: etiologic implications. 780 87

The intestinal population of gamma delta T cell receptor (TCR)-bearing cells was characterized with regard to V delta and V gamma subtype expression. For this purpose, we utilized V gene-specific PCR of mRNA prepared from intestinal biopsies. Predominant expression of the V delta 1 subtype was demonstrated in the small intestine of patients with coeliac disease and in the inflamed colon of patients with inflammatory bowel diseases (IBD: ulcerative colitis and Crohn's disease) as well as in colon biopsies taken from macroscopically normal areas of colon. Although intestinal gamma delta T cells preferentially expressed V delta 1, other V delta transcripts could be detected, of which V delta 2 and V delta 5 were commonly expressed. Analysis of biopsies from mesenteric lymph nodes demonstrated a V delta repertoire similar to the mucosa. In peripheral blood on the other hand, high expression of both V delta 2 and V delta 1 was found. The predominant expression of V delta 1 transcripts in the intestinal mucosa of IBD patients correlated well with protein cell surface expression as analysed by flow cytometry using V delta 1- and V delta 2-specific antibodies. Selective expansion of gamma delta T cells could not be demonstrated within the inflamed mucosa as shown by mRNA analysis and flow cytometry. Instead, IBD patients demonstrated a decreased proportion of TCR gamma delta-carrying T cells in the inflamed mucosa compared with macroscopically normal area of colon. On the other hand, a significantly increased percentage of T cells bearing the gamma delta TCR was found in peripheral blood of patients with Crohn's disease compared with healthy individuals, indicating that local mucosal inflammation may influence the circulating gamma delta T cell population.
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PMID:Analysis of gamma delta V region usage in normal and diseased human intestinal biopsies and peripheral blood by polymerase chain reaction (PCR) and flow cytometry. 781 10

Atypical forms of IBD include the microscopic colitides, collagenous and lymphocytic colitis, and two macroscopic colitides, SRUS and diversion colitis. Clinical presentations include chronic, watery diarrhea and intermittant rectal bleeding. Constitutional symptoms are typically absent; laboratory data are often nonspecific. Colonoscopic evaluation and mucosal biopsy are essential in establishing these diagnoses and excluding more classic forms of IBD (i.e., Crohn's disease or idiopathic ulcerative colitis). Prognosis and response to treatment are variable; potential therapeutic options include dietary manipulations, topical or systemic anti-inflammatory agents, and, in refractory cases, surgical intervention.
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PMID:Atypical forms of inflammatory bowel disease. 796 8

Management strategies in Crohn's disease and ulcerative colitis should be based on up-to-date information on disease distribution, extent, activity and complications. A system of structured analysis is suggested, with separate consideration of destructive ulceration, inflammatory activity and other factors. Direct investigation of gut immunity by using whole gut lavage fluid (WGLF) is a valuable new technique of clinical investigation in IBD and related disorders. Recent studies have shown that the concentrations of plasma-derived proteins in WGLF provide objective measures of disease activity; and that this activity is a separate phenomenon from destructive ulceration and fibrosis. Neutrophils in the lumen can be in- investigated by cytology, or by assay of neutrophil elastase in WGLF. Cytokines and other immuno-regulatory mediators can also be detected. These new techniques can provide a description of intestinal immunity and inflammation, based on a non-invasive test of 2-4 h duration. Work in progress shows that patients who respond clinically to elemental diet treatment have unusually high concentrations of soluble IL2 receptor in WGLF; cytokine profiles may facilitate the selection of patients suitable for other new treatment modalities.
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PMID:Analysis of disease distribution, activity and complications in the patient with inflammatory bowel disease. 797 42


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