Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009324 (ulcerative colitis)
17,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rectal folds are seen best in the lateral view. Normal values for the thickness of the folds have been established by measuring these in patients with a diagnosis of irritable bowel syndrome who had no evidence of rectal disease. In severe ulcerative colitis the valves disappear, but they are present earlier in the disease. The first barium enema examination in patients with ulcerative colitis was assessed. When the valve thickness could be measured in these patients it showed values significantly greater than normal. It is uncommon for this finding to be the sole indicator of disease. Patients with Crohn's disease of the rectum showed no increase in the fold thickness. This observation may be helpful in distinguishing between these two forms of colitis.
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PMID:Rectal fold thickness as an indicator of disease. 687 49

A quantitative morphometric study of the immunoglobulin-containing plasma cells in rectal biopsies from nine patients with ulcerative colitis and three patients with the irritable colon syndrome is presented. The results show that fixation of the biopsy specimens with formol-sublimate, a mercuric fixative, resulted in better staining with the immunoperoxidase method and that, by comparison with formol saline, higher cell counts were always obtained.
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PMID:A quantitative study of the influence of fixation on immunoperoxidase staining of rectal mucosal plasma cells. 699 88

In a 4-year period 45 patients were admitted to our gastroenterological u nit with acute infective colitis. The endemic pathogens responsible for the colitis were Yersinia enterocolitica (46%), Campylobacter fetus jejuni (20%), common Salmonellae (13%), less virulent strains of Shigella (9%), Entamoeba hystolytica (7%) and Cytomegalovirus (4%). These microorganisms caused very severe disease in 18% of the patients, who were mostly predisposed. While Salmonella- and amoebic colitis always mimicked ulcerative colitis by the presence of diffuse lesions, the other pathogens caused focal colitis, thus necessitating differential diagnosis vis a vis Crohn's colitis. Two patients (4%) died of complications, while 93% of the patients were cured by proper antimicrobial therapy. In the same period 12 patients were admitted with an acute attack of inflammatory bowel disease due to an intercurrent infection with the same pathogens. In most of these patients clinical remission of IBD was achieved by treating the intercurrent infection. These data indicate that in the presence of an acute attack of colitis an infective etiologic agent must always be sought, and that an attack of chronic idiopathic inflammatory bowel disease may be caused by an intercurrent infection.
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PMID:Acute infective colitis caused by endemic pathogens in western Europe: endoscopic features. 714 Jun 55

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

We studied 27 patients with severe chronic diarrhea for which extensive investigations carried out at other institutions had failed to reveal a diagnosis. They were studied by standard diagnostic methods as well as by careful fecal analysis and intestinal perfusion. If they were incontinent of feces, anal sphincter function tests were performed. Although many were suspected of having pancreatic cholera syndrome, this diagnosis could not be established in a single patient. The most common diagnosis that could be established was surreptitious ingestion of drugs (laxatives in 7 patients and diuretics in 2). Other specific diagnoses included ulcerative colitis in 2 patients, allergy to beef in 1, and bacterial overgrowth of the small intestine in 1. Thus, we were able to establish a specific diagnosis in 13 patients. Of the remaining 14 patients, 8 had findings suggestive of irritable bowel syndrome, and 2 others had anal sphincter dysfunction as the major cause of their disability. The other 4 undiagnosed patients had severe secretory (3 patients) or osmotic (1 patient) diarrhea. Follow-up interviews at 6 mo-6 yr failed to reveal evidence of a cause for diarrhea that had been overlooked during our studies. The diagnostic approach to patients with unexplained diarrhea is discussed. The importance of a search for surreptitious drug ingestion and accurate measurement of bowel movement frequency and stool weight is emphasized.
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PMID:Chronic diarrhea of unknown origin. 735 49

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

The activity of monoamine oxidase (MAO) was studied during functional, inflammatory and tumoral diseases of the large intestine. In the patients with the irritable colon syndrome, the enzymatic activity was decreased by 34% at the acute stage of the disease and in those with nonspecific ulcerative colitis it was increased by 44%. Follow-ups of MAO activity may serve as an indicator of the adequacy and efficiency of the treatment performed.
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PMID:[The role of monoamine oxidase in large intestine pathology]. 761 5

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


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