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)

To assess the importance of disease-induced increases in plasma concentrations of alpha1 acid glycoprotein (an acute-phase plasma protein that binds cationic drugs), we determined binding of propranolol in plasma from 53 patients and 25 healthy volunteers. Binding was increased in 10 patients with Crohn's disease (P less than 0.002), nine with inflammatory arthritis (P less than 0.002) and eight with chronic renal failure with superimposed inflammatory disease (P less than 0.01) as compared with healthy controls. The plasma binding of control subjects did not differ from that of 12 patients with chronic hepatic disease (P greater than 0.45) or 14 with uncomplicated renal failure (P greater than 0.80). Chlorpromazine binding, determined in 60 subjects, yielded similar results. Percentage of free drug and alpha1 acid glycoprotein concentration were inversely correlated (r = -0.77 with propranolol, P less than 0.001, and r = -0.69 with chlorpromazine, P less than 0.001). Increases in plasma protein binding in patients with inflammatory disease appear mediated by increases in alpha1 acid glycoprotein concentration, which may influence drug kinetics.
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PMID:Increased plasma protein binding of propranolol and chlorpromazine mediated by disease-induced elevations of plasma alpha1 acid glycoprotein. 8 6

Increased serum concentrations of acute-phase proteins can be found in active inflammatory bowel disease. Because interleukin 6 (IL-6) is one of the main mediators of acute-phase protein synthesis by the liver, the serum concentrations of IL-6 and the acute-phase proteins C-reactive protein, alpha 1-antitrypsin, and alpha 1-acid glycoprotein were determined in 70 patients with Crohn's disease (CD) and 23 patients with ulcerative colitis (UC). Disease activities were determined by established clinical activity indices. Serum IL-6 concentrations were significantly (P less than 0.005) increased in patients with CD (mean +/- SEM, 6.8 +/- 0.9 U/mL) compared with patients with UC (mean, less than 4 U/mL) and healthy controls (mean, less than 4 U/mL). Of patients with CD, 68.5% had serum IL-6 concentrations of greater than or equal to 4 U/mL, compared with 21.7% of patients with UC and 0% of healthy controls. There was a tendency toward higher serum IL-6 concentrations in patients with active CD than in patients with inactive disease. However, these differences were not statistically significant. There was no correlation between IL-6 serum concentrations and clinical activity indices, possibly because of the short circulatory lifetime and rapid hepatic clearance of IL-6 from the portal venous blood. In contrast to serum IL-6, acute-phase proteins, which have a longer circulatory lifetime, were significantly correlated with clinical activity indices. Only the follow-up of individual patients with initially highly active disease showed a further increase in IL-6 levels during acute exacerbations of the inflammatory process. The results show that most patients with even moderately active CD have significantly increased serum concentrations of IL-6, most probably reflecting a continuous stimulation of IL-6-producing cells.
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PMID:Evidence for continuous stimulation of interleukin-6 production in Crohn's disease. 149 21

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

We studied the activity assessment of ulcerative colitis and Crohn's disease by 5 acute phase reactants: C-reactive protein (CRP), alpha 1-acid glycoprotein, alpha 1 antitrypsin, haptoglobin and fibrinogen. From a large register of patients with inflammatory bowel disease (IBD) we chose randomly 91 patients: 61 with ulcerative colitis and 30 with Crohn's disease. As a reference point in the disease activity assessment we used standard clinical indices. Statistical analysis was performed by non-parametric methods: the Kruskal-Wallis and Fisher's exact test. The disease activity assessment in patients with ulcerative colitis by the index according to Powell-Tuck indicated that the patients with active disease (N = 19) had significantly higher levels of all acute phase proteins mentioned above except fibrinogen (alpha less than 0.05 to 0.001) than patients in remission (N = 42). Analysis of the same data by Fisher's exact test indicated that there had been a probability for all the proteins measured to be higher than the normal values, particullary CRP (p less than 10(-8) and the other somewhat less. In patients with Crohn's disease, the disease activity assessment was performed by 2 indices. According to "The Crohn's Disease Activity Index" (CDAI), only alpha-1 acid glycoprotein and haptoglobin (alpha less than 0.05) were higher in patients with active disease (N = 4) than in patients with remission (N = 26).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serum acute phase proteins for determining disease activity of ulcerative colitis and Crohn disease]. 172 73

A panel of 12 monoclonal antibodies were produced by immunization of Balb/c mice with small bowel epithelial cells obtained from a patient with active well-documented Crohn's disease. The clones were derived by screening with immunofluorescence microscopy; those with staining patterns suggestive of mucin directed epitopes were chosen for study. Several distinct patterns of staining reactivity were noted, including reagents with homogeneous, luminal, heterogeneous and peripheral goblet cell activity. In addition, SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting analysis revealed reactivity to high molecular weight mucin. The reactive antigen was resistant to proteinase digestion. No endoneuraminidase activity was detected; however, one neuraminidase sensitive sialic acid epitope was demonstrated. Confirmation of glycoprotein epitopes was accomplished by testing purified mucins from several areas of the gastrointestinal tract by ELISA. Finally, individual small bowel goblet cell heterogeneity was demonstrated by immunofluorescence, Western blotting, and antibody affinity chromatography. These data demonstrate both by morphology and specific binding of antibody affinity chromatography a significant degree of small bowel goblet cell mucin heterogeneity.
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PMID:Characterization and heterogeneity of monoclonal antibodies directed to intestinal mucin derived from Crohn's disease small bowel. 187 17

Previous reports of a selective mucin subclass defect in ulcerative colitis have been reassessed using high performance chromatography (Superose 6 and Mono Q) for mucin purification and fractionation coupled with analysis of the fractions obtained using a combination of enzyme linked lectin and mucin antibody assays. Mucin samples purified from snap frozen rectal biopsy specimens obtained from patients with ulcerative colitis (n = 12), Crohn's disease (n = 5), and non-inflammatory bowel disease control subjects (n = 9) were subject to ion exchange chromatography using a continuous 0-0.35 mol/l NaCl salt gradient with a final 2.5 mol/l NaCl step. In all samples the major proportion (mean (SD) 86.7 (8.9)%) of the mucin detectable by wheat germ agglutinin binding eluted between 0.15 and 0.35 mol/l NaCl with no significant difference in elution profile between ulcerative colitis and control subjects. Significant elution of glycoprotein at less than 0.15 mol/l NaCl did occur, however, when a lower molecular weight mucin containing fraction which contained concanavalin A positive (glucose or mannose containing) material was analysed similarly. Similar ion exchange profiles were obtained when (3H)N-acetylglucosamine labelled mucins were studied after tissue culture of rectal biopsy specimens. No significant alteration in the ion exchange profile of purified mucins in ulcerative colitis has been shown in these studies. It is possible that the previously reported relative depletion of mucin subclass IV (eluting with 0.20 mol/l NaCl) may simply have reflected mucin depletion.
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PMID:Ion exchange chromatography of purified colonic mucus glycoproteins in inflammatory bowel disease: absence of a selective subclass defect. 195 68

Colonic glycoprotein composition was evaluated in monozygotic twins with inflammatory bowel disease using ion-exchange chromatography. Fifty-three individuals, 12 pairs and 1 single twin with ulcerative colitis and 14 pairs with Crohn's disease, were evaluated. Seven twin pairs were concordant for the presence of ulcerative colitis or Crohn's disease, whereas twin siblings of 10 ulcerative colitis probands and 9 Crohn's disease probands were not known to have inflammatory bowel disease. Content of one chromatographically defined component of colonic mucin, designated HCM species IV, was reduced in both patients with ulcerative colitis (1040 +/- 300 cpm/10,000 cpm total HCM) and their apparently healthy twins (1340 +/- 540 cpm/10,000 cpm total HCM) compared with control subjects (4030 +/- 1,000 cpm/10,000 cpm total HCM). Composition of mucin in Crohn's disease patients and their nonaffected twins was not significantly different than in controls. These observations suggest that altered profiles of mucin glycoprotein may be present before the onset of ulcerative colitis and may be genetically defined. Conversely, it appears that alterations in glycoproteins only are not sufficient to initiate mucosal inflammation.
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PMID:Colonic glycoproteins in monozygotic twins with inflammatory bowel disease. 198 38

Alpha-1-antitrypsin is a glycoprotein which is excreted in feces under three different forms of molecular weight 38, 45 and 51 kDa. The 45 and 38 kDa forms are the result of a partial or total removal of the carbohydrate moiety, respectively. We determined the molecular forms of fecal alpha-1-antitrypsin in 10 controls, 13 patients with protein-losing enteropathy other than inflammatory bowel disease, 70 patients with active (n = 55) (CDAI greater than 150) and inactive (n = 15) (CDAI less than 150) Crohn's disease, 14 patients with active (n = 12) and inactive (n = 2) ulcerative colitis, and 17 patients with ileostomy. Fecal 38 kDa alpha-1-antitrypsin was found in all controls, all patients with protein-losing enteropathy, in 82 percent of patients with inactive inflammatory bowel disease, and in 20 percent of patients with active inflammatory bowel disease. In contrast, the 51 kDa and 45 kDa forms were present in feces of 80 percent of patients with active inflammatory bowel disease, and in only 17 percent of patients with inactive inflammatory bowel disease. Patients with Crohn's disease and the 51 kDa form (n = 39) had significantly higher values of activity index (CDAI) and orosomucoid than patients with Crohn's disease and the 38 kDa form (n = 26) (P less than 0.01). Deglycosylated 38 kDa alpha-1-antitrypsin was never recovered in ileostomy samples. This suggests that deglycosylation of alpha-1-antitrypsin occurred in the colon and is impaired in patients with active inflammatory bowel disease.
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PMID:[Qualitative study of fecal alpha-1-antitrypsin in patients with inflammatory digestive disease and patients with ileostomy]. 206 Jul 40

Supernatants of faecal suspensions from patients with Crohn's disease (CD) showed much lower viscosity than those from healthy subjects. Material responsible for the viscosity could be precipitated with ethanol. Gel filtration indicated that the viscosity was not due to the glycoprotein fraction but to a fraction with higher molecular weight and relatively high contents of muramic acid suggesting a bacterial origin. The concentration and viscosity of this fraction are less in faeces from patients with CD than in that of healthy subjects.
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PMID:Effect of a soluble bacterial carbohydrate fraction on the viscosity of intestinal contents in healthy subjects and patients with Crohn's disease. 249 63

The expression of the 220,000 MW (p220) glycoprotein component of the leucocyte common antigen (LCA) family by intestinal mucosal lymphocytes was studied using the CD45R monoclonal antibody WR16. In normal intestine, a proportion of CD3+ mucosal T cells were WR16+ and this population resided predominantly in the mid-villus and crypt region of lamina propria. In the inflammatory infiltrates of both coeliac disease and Crohn's disease the CD3+, WR16+ population was markedly reduced. The monoclonal antibody UCHL1 identifies the 180,000 MW member of the LCA family and is expressed on T cells and in macrophages. CD3+ lymphocytes expressing this marker were widespread in normal lamina propria and epithelium. In contrast with WR16, UCHL1+ cells remained at a high level in coeliac disease and Crohn's disease. Our results support the view that loss of the p220 molecule occurs upon T-cell activation in inflammation.
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PMID:Leucocyte common antigen expression on T cells in normal and inflamed human gut. 253 Jan 54


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