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PubMed2003

IgA and IgG tissue transglutaminase antibody prevalence and clinical significance in connective tissue diseases, inflammatory bowel disease, and primary biliary cirrhosis.

An association between celiac disease (CD) and other autoimmune diseases such as connective tissue diseases (CTD), inflammatory bowel diseases (IBD), and primary biliary cirrhosis (PBC) has been reported in several studies. However, a high rate of false positives in autoantibody testing was noted, especially when tissue transglutaminase (tTG) from guinea pig liver was used. Thus, the real prevalence of CD in CTD, IBD, and PBC is unclear. In a case-control study, 400 patients with CTD, 170 with IBD, 48 with PBC, and 120 healthy subjects were investigated for CD by the analysis of IgA and IgG tTG antibodies using the more specific human recombinant tTG immunoenzymatic assay. Patients and controls with positive findings were further tested for antiendomysial antibodies by indirect immunofluorescence and HLA typing, and those found positive by either of these tests underwent duodenal biopsy to confirm a possible diagnosis of CD. Twelve patients were positive for IgA or IgG tTG antibodies, showing an overall prevalence of 1.9%. Only 1 healthy subject (0.8%) had a low level positive reaction for IgA anti-tTG. Among the 12 patients and the healthy subject, only 2 (1 SLE and 1 ulcerative colitis patient) were subsequently confirmed to be affected with CD by positive EMA, HLA, and small bowel biopsy findings. The highest rate of false positives was found in PBC patients (10.4%). For these reasons, serological screening testing for CD is not recommended in CTD patients or in subjects affected with IBD or PBC, unless there is a relevant clinical suspicion of CD.

Adult↗

PubMedDate not supplied

Salivary SIgA and SIgA 1 in coeliac disease, inflammatory bowel disease and controls.

Levels of secretory IgA1 (SIgA1) in the saliva have not been measured previously in either coeliac disease (CD) or inflammatory bowel disease (IBD). Saliva was collected from coeliacs, IBD patients and controls. The concentration of total SIgA in saliva was measured by enzyme linked immunosorbent assay (ELISA) with an anti-human SIgA antibody as the bound phase and human SIgA isolated from colostrum as the standard. The concentration of SIgA1 was determined using an ELISA with a lectin with a high affinity for human SIgA1. The IBD patients have a significantly higher concentration of SIgA1 than the controls. The rate of secretion of saliva and %SIgA1 was significantly lower in coeliacs than in the control and IBD groups. The rate of secretion of SIgA1 was significantly higher in the IBD than in the coeliacs. We describe hitherto unreported levels of SIgA1 in CD and IBD.

Adult↗

PubMed2004

Johne's disease, inflammatory bowel disease, and Mycobacterium paratuberculosis.

Johne's disease is a chronic diarrhea affecting all ruminants. Mycobacterium avium subsp. paratuberculosis (MAP), a slowly growing mycobacteria, is the etiologic agent. There is also a concern that MAP might be a causative agent of some cases of inflammatory bowel disease in humans, especially Crohn's disease. Food products including pasteurized bovine milk have been suggested as potential sources of human infection. This review addresses microbial factors that may contribute to its pathogenicity. In addition, the experimental evidence defining MAP as the cause of Johne's disease and the issues and controversies surrounding its potential pathogenic role in humans are discussed.

Animals↗

PubMed2002

Hepatic manifestations of gastrointestinal diseases. Inflammatory bowel disease, celiac disease, and Whipple's disease.

The gastrointestinal tract and the liver are closely related anatomically, physiologically, and pathologically. Some disease associations are well documented, such as PSC in association with IBD, whereas others are less well defined. A heightened clinical suspicion is required in these patients who do not present with the classical disease associations. The underlying causes of their diseases are the subject of much debate and research, and their diagnosis and management remain challenging.

Animals↗

PubMed1981

Gastritis, peptic ulcer disease, inflammatory bowel disease, and stomach and colon cancers- are they all caused by viral infections?

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.

Chronic Disease↗

PubMed1978

Ankylosing spondylitis and inflammatory bowel disease. I. Prevalence of inflammatory bowel disease in patients suffering from ankylosing spondylitis.

To establish the prevalence of inflammatory bowel disease in ankylosing spondylitis (AS), 79 AS patients underwent detailed medical screening, including sigmoidoscopic and roentgenological examination, 48 had gastrointestinal symptoms and the others did not. In 3 patients a diagnosis of Crohn's disease was made which was previously established. In all other patients inflammatory bowel disease could be excluded. The prevalence of inflammatory bowel disease in this series of patients with AS therefore was 3.8%.

Enteritis↗

PubMed1990

Histamine release from gut mast cells from patients with inflammatory bowel diseases.

Inflammatory mediators from intestinal mast cells may serve as initiators of acute and delayed inflammation. Mast cell histamine release was measured in 19 patients with inflammatory bowel diseases using gut mast cells from enzymatically dispersed endoscopic forceps biopsy specimens of macroscopically inflamed and normal tissue. Mast cells and corresponding basophils were challenged with anti-IgE, anti-IgG, subclass anti-IgG4, and formyl-methionyl-leucyl-phenylalanine (FMLP) and results were compared with those from nine patient control subjects. The mast cell count in patients with ulcerative colitis was increased compared with that in control subjects and patients with Crohn's disease, and the mast cell count obtained from inflamed tissue was greater than that of normal tissue. The study also shows the heterogeneity of the responsiveness of the histamine releasing cells to various secretagogues. Thus, mast cells released 0.4 (0.0-2.0) (median (range)) ng histamine per sample at anti-IgE challenge, and basophils were also anti-IgE responsive. In contrast, mast cells did not respond to FMLP but the corresponding basophils did. Gut mast cells released 0.3 (0.0-1.0) (median (range)) ng histamine per sample at anti-IgG4 challenge; however, the corresponding basophils did not respond to anti-IgG4. In addition, the anti-IgG4 mediated histamine release was primarily confined to patients with inflammatory bowel disease. This study substantiates previous histopathological findings that mast cells may play a functional role in the inflammatory process of inflammatory bowel diseases and provides evidence for a possible role of subclass IgG4 as a reaginic antibody.

Adolescent↗

PubMed2001

Inflammatory bowel disease: clinics and pathology. Do inflammatory bowel disease and periodontal disease have similar immunopathogeneses?

Inflammatory bowel disease (IBD) comprises two chronic, tissue-destructive, clinical entities Crohn disease (CD) and ulcerative colitis (UC) both apparently caused by immunological overreaction (hypersensitivity) to commensal gut bacteria. Under normal conditions the intestinal immune system shows a down-regulating tone ('oral tolerance') against dietary antigens and the indigenous microbiota. This local homeostasis is disturbed in IBD, leading to hyperactivation of T helper 1 (Th1) cells with abundant secretion of interferon-gamma and tumor necrosis factor (TNF) and production of IgG antibodies against commensal bacteria. In addition, UC includes genetically determined autoimmunity, particularly IgG1-mediated cytotoxic epithelial attack. Breaching of the epithelium is the best-defined event underlying abrogation of oral tolerance, but immune deviation caused by cytokines fiom irritated epithelial cells or subepithelial elements (for example, mast cells, natural killer cells, macrophages) may also be involved. Endogenous infection with local hypersensitivity likewise causes periodontal disease, reflecting 'frustrated' immune elimination mechanisms entertained by antigens from dental plaque. Altogether, perturbation of a tightly controlled cytokine network, with abnormal crosstalk between several cell types, apparently explains the progressive immunopathology of chronic inflammatory mucosal diseases in general. This adverse development will be influenced by numerous immunity genes, the dosage and potential pathogeniciy of commensal bacteria, general health, nutritional status, and psychological factors. Several targets for new therapy have tentatively been identified to block immunopathological mechanisms in IBD, and inhibition of TNF has a striking beneficial effect in CD, supporting a central role of this cytokine.

Animals↗

PubMed2000

Risk of lymphoma in inflammatory bowel disease.

OBJECTIVE: Inflammatory bowel disease with a subsequent diagnosis of non-Hodgkin's lymphoma has been reported. There is concern that the risk of developing lymphoma will rise with increasing use of immune modifier therapy. We determined the risk of non-Hodgkin's lymphoma in an U.S. population-based inception cohort, and evaluated the association between inflammatory bowel disease and lymphoma in our referral practice. METHODS: The records of all incidence cases of inflammatory bowel disease in Olmsted County, Minnesota, between 1950 and 1993 were reviewed for the diagnosis of lymphoma. Standardized incidence ratios (observed/expected) were used to estimate relative risk. In addition, the clinical features and outcomes of all patients with inflammatory bowel disease and lymphoma seen at Mayo Clinic between 1976 and 1997 were reviewed. RESULTS: Among 454 county residents diagnosed with inflammatory bowel disease, a single non-Hodgkin's lymphoma occurred in a patient with Crohn's disease. No cases were seen with ulcerative colitis. The estimated relative risk of lymphoma was 2.4 in Crohn's disease (95% confidence interval, 0.1-13), 0 in ulcerative colitis (0-6), and 1.0 in inflammatory bowel disease overall (0.03-6). Between 1976 and June 1997, 61 patients with inflammatory bowel disease and lymphoma (approximately 0.41%) were seen in the referral practice. In four patients with Crohn's disease (13%), potential neoplastic risk factors were identified-therapeutic radiation in 1, and use of purine analogs in 3 (median length of use, 11 months). CONCLUSIONS: Our population-based cohort study demonstrated that the absolute risk of non-Hodgkin's lymphoma remains quite small (0.01% per person-year). This risk may not exceed that in the general population. In our referral practice, immune modifier therapy could be potentially implicated in only 5% of cases of lymphoma occurring in the setting of inflammatory bowel disease.

Cohort Studies↗

PubMed1992

Technetium-99m hexamethyl propylene amine oxine leucocytes in the assessment of disease activity in inflammatory bowel disease.

The inflammatory activity in 108 bowel segments of 40 patients with suspected or known inflammatory bowel disease was assessed macroscopically by endoscopy, histology and technetium-99m hexamethyl propylene amine oxine (99mTc-HMPAO) leucocytes using a numerical grading system (scores 0-3). A 4-h series of scintigrams showed a significant correlation with both histological and macroscopical assessment of disease activity (rho = 0.850, P less than 0.001 and rho = 0.773, P less than 0.001, respectively). Sensitivity, specificity and accuracy of scintigraphy in detecting active inflammatory segments were 85%, 92% and 89%, respectively. A normal scintigram did not completely exclude mild inflammatory activity, especially in the rectosigmoid area. 99mTc-HMPAO leucocytes offer an accurate and non-invasive alternative for the assessment of disease activity in ulcerative colitis and Crohn's disease.

Adult↗

PubMed1993

[Articular and extraarticular involvement in inflammatory bowel diseases].

Idiopathic inflammatory bowel disease include basically two disorders: ulcerative colitis and Crohn's disease. Both diseases are chronic and of unknown etiology and extraintestinal manifestations are seen in a high number of these patients. We studied 18 patients (7 female, 11 male) with previous diagnosis of inflammatory bowel disease (14 ulcerative colitis, 2 Crohn's disease, 1 pancolitis, 1 ulcerative proctitis) in order to search for extraintestinal manifestations with emphasis on osteoarticular and ocular involvement. The mean age at the time of diagnosis of the inflammatory bowel disease was 44 years (range 20 to 71 years). Mean time duration of the inflammatory bowel disease was 7 years (range 1 to 24 years) and of the articular manifestations 3.2 years (range 1 to 8 years). The osteoarticular manifestations developed after the diagnosis of the bowel disease in all but one patient (simultaneously) 17/18 patients had artralgias, 7/18 lumbalgia, 3/18 talalgia, 1/18 knee arthritis. (table I) Only six of the 17 patients with orteoarticular involvement has simultaneous activity of the underlying bowel disease. All the 18 patients were taking 2 g/day of sulfasalazine. Radiographic screening in all patients revealed sacroiliitis in 10. (table II) Of the 10 radiographic sacroiliitis 4 were grade I (confirmed by technetium phosphate scans, 2 were grade II and 4 grade III-IV. Three of the ten patients with radiographic sacroiliitis were asymptomatic (table II). Axial computed tomography was performed done in two patients: a) in one case to exclude osteitis condensens ilii, and b) in the other case to exclude septic arthritis. The severity of the sacroiliac damage was related with a longer duration of the inflammatory bowel disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2002

Immunomodulation by the autonomic nervous system: therapeutic approach for cancer, collagen diseases, and inflammatory bowel diseases.

The distribution of leukocytes is regulated by the autonomic nervous system in humans and animals. The number and function of granulocytes are stimulated by sympathetic nerves whereas those of lymphocytes are stimulated by parasympathetic nerves. This is because granulocytes bear adrenergic receptors, but lymphocytes bear cholinergic receptors on the surface. These regulations may be beneficial to protect the body of living beings. However, when the autonomic nervous system deviates too much to one direction, we fall victim to certain diseases. For example, severe physical or mental stress --> sympathetic nerve activation --> granulocytosis --> tissue damage, including collagen diseases, inflammatory bowel diseases, and cancer. If we introduce the concept of immunomodulation by the autonomic nervous system, a new approach for collagen diseases, inflammatory bowel diseases, and even cancer is raised. With this approach, we believe that these diseases are no longer incurable.

Animals↗

PubMed2004

Expression of endothelial protein C receptor and thrombomodulin in the intestinal tissue of patients with inflammatory bowel disease.

OBJECTIVE: Inflammatory bowel diseases are characterized by disorders of immunity, thrombosis of large vessels, and microthrombosis of mucosal vessels. The expression of endothelial protein C receptor (EPCR) and thrombomodulin-two receptors of the protein C pathway involved in thrombin scavenging and inflammation-was studied in intestinal resection specimens or mucosal biopsies from patients with inflammatory bowel disease and from controls. The soluble forms of the receptors in plasma were measured. DATA SOURCE: This study involved patients from two large university hospitals. After surgery or biopsy, tissue samples were either frozen or fixed in formalin and embedded in paraffin. Sections for immunohistochemistry examination were cut and tested with the specific antibodies to EPCR and thrombomodulin. RNA was extracted from frozen tissue for amplification via reverse-transcriptase polymerase chain reaction. Normal intestinal and diverticulitis tissue was used as a control. Resection samples from 36 patients with ulcerative colitis, 38 with Crohn's disease, 38 with colonic cancer, and 32 with diverticulitis were studied by immunohistochemistry, and frozen sections from the same patients were studied by immunofluorescence. Twelve biopsy specimens of adjacent intestinal areas from six patients with inflammatory bowel disease were included in the study for reverse-transcriptase polymerase chain reaction. Soluble receptors were measured in the plasma of 52 inflammatory bowel disease patients and 52 controls. DATA SUMMARY: EPCR and thrombomodulin were expressed on the mucosal endothelium of controls, and the intensity of the signal decreased in inflammatory bowel disease patients. EPCR was expressed by dendritic-like cells in controls, which also stained positive for CD21. The EPCR/CD21 dendritic-like cells were not as commonly observed in sections from ulcerative colitis patients as they were in sections from control patients (12.0 +/- 3.6 cells per high-power field vs. 23.8 +/- 10.4 cells per high-power field, p =.03), and this decrease was less evident in sections from Crohn's disease patients. Levels of messenger RNA for EPCR paralleled protein expression. Soluble thrombomodulin and EPCR levels were both higher in patients than in controls: 41.5 vs. 26.0 ng/mL (p <.0001) and 141 vs. 130 ng/mL (p <.05), respectively. CONCLUSIONS: EPCR expression on dendritic-like cells that bear the key complement receptor CD21 suggests a role for EPCR in innate immunity. The reduced expression of thrombomodulin and EPCR in the mucosal vessels in inflammatory bowel disease impairs protein C activation, favoring microthrombosis.

Adult↗

PubMedDate not supplied

Scavenging effect of 5-aminosalicylic acid on neutrophil-derived oxidants. Possible contribution to the mechanism of action in inflammatory bowel disease.

Inflammatory phagocytic leukocytes produce superoxide and hydrogen peroxide and secrete myeloperoxidase (MPO) into the extracellular medium. MPO catalyzes the oxidation of Cl- by H2O2 to yield chlorinated oxidants (e.g. HOCl and NH2Cl), which have been shown to induce pathologic changes in mucosal function. We examined the ability of 5-aminosalicylic acid (5-ASA), a drug used to treat inflammatory bowel disease (IBD), to inhibit oxidation of L-cysteine by NH2Cl, HOCl and H2O2. NH2Cl and HOCl were especially strong oxidants against L-cysteine. 5-ASA prevented L-cysteine oxidation by NH2Cl and HOCl; an interaction associated with the formation of characteristic absorption spectra due to the oxidation of 5-ASA was observed. NH2Cl and HOCl evoked characteristic increases in short-circuit current (Isc), indicative of net electrolyte transport, when added to the serosal side of stripped rat colon mounted in Ussing chambers. Premixing of NH2Cl with 5-ASA 10 min before addition to the tissue markedly reduced the secretory response to NH2Cl. In contrast, 5-ASA immediately reduced the response to HOCl. The reduction in the functional response to NH2Cl and HOCl by 5-ASA may contribute to its mechanism of action in the treatment of the symptoms of IBD.

Aminosalicylic Acids↗

PubMed1991

Inflammatory bowel disease: primary health care management of ulcerative colitis and Crohn's disease.

Inflammatory bowel disease encompasses both ulcerative colitis and Crohn's disease, two conditions so alike clinically that they are frequently indistinguishable from one another. Inflammatory bowel disease occurs at a rate of approximately five per 100,000 people. It tends to cluster in families and is seen four to five times more often in Jewish Caucasians than in other Caucasians. The etiology is unknown. Increasing attention is being paid to autoimmune factors, genetic factors and food allergies, and the notion that inflammatory bowel disease has its roots in a psychological disorder continues to pale for want of empirically sound evidence. Disease pattern is one of remission and exacerbation. The aim of therapy is to maintain an optimal lifestyle in remission through an individually tailored protocol of medications. Sulfasalazine remains the medication of choice; corticosteroids have short-term utility in exacerbation; and immunosuppressants, though controversial, are thought to have some steroid-sparing benefits during acute flare-ups. Indications for surgery vary, depending on whether or not a clear differential diagnosis has been made between ulcerative colitis and Crohn's disease. There is no cure for inflammatory bowel disease except for total colectomy in clearly diagnosed ulcerative colitis. Current research endeavors seek a cause or causes for inflammatory bowel disease, but the literature does not solidly support any one possibility above other rival etiologies.

Colitis, Ulcerative↗

PubMed2006

Novel susceptibility genes in inflammatory bowel disease.

The inflammatory bowel disease, Crohn's disease and ulcerative colitis, are polygenic disorders with important environmental interactions. To date, the most widely adopted approach to identifying susceptibility genes in complex diseases has involved genome wide linkage studies followed by studies of positional candidate genes in loci of interest. This review encompasses data from studies into novel candidate genes implicated in the pathogenesis of inflammatory bowel disease. Novel techniques to identify candidate genes-genome wide association studies, yeast-two hybrid screening, microarray gene expression studies and proteomic profiling, are also reviewed and their potential role in unravelling the pathogenesis of inflammatory bowel disease are discussed.

Adaptor Proteins, Signal Transducing↗

PubMed2004

Association between enhanced soluble CD40 ligand and prothrombotic state in inflammatory bowel disease.

BACKGROUND: Inflammatory bowel disease is associated with an increased incidence of thromboembolic complications. The aim of this study was to investigate the role of the soluble CD40 ligand (sCD40L), which displays prothrombotic properties, in patients with ulcerative colitis (UC) and Crohn's disease (CD) in comparison with inflammatory and healthy controls. METHODS: Plasma levels of sCD40L, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin (TAT) complex and soluble P-selectin were measured in 104 inflammatory bowel disease patients (54 ulcerative colitis and 50 Crohn's disease), in 18 cases with other causes of intestinal inflammation and in 80 healthy controls using commercially available enzyme-linked immunosorbent assays. Plasma levels of sCD40L were correlated with disease activity, type, localization and treatment as well as with the measured thrombophilic parameters. RESULTS: CD patients had significantly higher sCD40L levels than both groups of controls (CD vs HC P < 0.001; CD vs non-IBD P < 0.05). UC patients had higher but not significantly different sCD40L levels compared with the controls. Both UC and CD patients with active disease had significantly higher sCD40L levels in comparison with patients with inactive disease. Plasma levels of sCD40L were correlated with platelet count (r = 0.27, P = 0.001). They also showed a correlation with prothrombin F1+2 (r = 0.16, r = 0.03) and TAT (r = 0.15, r = 0.04) as well as with P-selectin (r = 0.19, P = 0.01). CONCLUSIONS: The increased sCD40L plasma levels may represent, at least in some degree, a molecular link between inflammatory bowel disease and the procoagualant state.

Adult↗

PubMedDate not supplied

Information for patients about inflammatory bowel disease.

In inflammatory bowel disease it is important that patients understand their condition since this helps to improve long-term management of the disease. The aim of this study was to assess the information given to patients with inflammatory bowel disease about their condition, its treatment and the National Association for Colitis and Crohn's disease. Two surveys were performed, using anonymous questionnaires. One was of all association members in north-east England, the other was a sample of patients attending medical outpatients. The surveys showed that more patients heard of the National Association for Colitis and Crohn's disease from the media than from medical sources. Of patients seen in medical clinics, 75% would welcome more information about their disease. In four of the six participating centres less than half the patients had been told about the existence of a patients' association. There was considerable variation in the instructions on what action to take in the event of a relapse. These findings suggest that the opportunity offered by out-patient clinics to educate and inform patients is often wasted. Clinicians often neglect to mention the National Association for Colitis and Crohn's disease, especially to patients with long-standing disease. A higher priority should be given to providing patients with appropriate information on inflammatory bowel disease. Three simple audit standards for the organisation of outpatient clinic information are proposed.

Adult↗