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At least 433 records · Page 24Linked to original sources
PubMed1998

Poor diagnostic value of colonic CD44v6 expression and serum concentrations of its soluble form in the differentiation of ulcerative colitis from Crohn's disease.

BACKGROUND: Increased expression of CD44v6 on colonic crypt epithelial cells in ulcerative colitis has been suggested as a diagnostic tool to distinguish ulcerative colitis from colonic Crohn's disease. AIMS: To investigate colonic CD44v6 expression and serum concentrations of soluble CD44v6 (sCD44v6) in patients with ulcerative colitis and Crohn's disease. METHODS: Colonic biopsy samples were obtained from 16 patients with ulcerative colitis, 13 with ileocolonic Crohn's disease, and 10 undergoing polypectomy. Serum samples were obtained from 15 patients with active ulcerative colitis, 20 with active Crohn's disease, and 20 healthy donors. Colonic CD44v6 expression was evaluated immunohistochemically by monoclonal antibody 2F10 and the higher affinity monoclonal antibody VFF18. Serum sCD44v6 concentrations were measured by ELISA. RESULTS: 2F10 stained colonic epithelium of inflamed ulcerative colitis and Crohn's disease samples in 80% and 40% of cases, respectively, and VFF18 in 95% and 87%, respectively. Both monoclonal antibodies displayed a sensitivity and specificity of 60% and 87% to differentiate ulcerative colitis from colonic Crohn's disease. Serum concentrations of sCD44v6 were lower in patients with ulcerative colitis (median 153 ng/ml; interquartile range (IQR) 122-211) compared with Crohn's disease (219; IQR 180-243) and healthy donors (221; IQR 197-241 (p = 0.002)). Its sensitivity and specificity to discriminate ulcerative colitis from Crohn's disease was 75% and 71%, respectively. CONCLUSION: Colonic CD44v6 and serum sCD44v6 concentrations do not facilitate reliable differential diagnosis between ulcerative colitis and Crohn's disease.

Acute Disease↗
PubMed2001

Expression of nitric oxide synthases and effects of L-arginine and L-NMMA on nitric oxide production and fluid transport in collagenous colitis.

BACKGROUND AND AIMS: Luminal nitric oxide (NO) is greatly increased in the colon of patients with collagenous and ulcerative colitis. To define the source and consequence of enhanced NO production we have studied expression of NO synthase (NOS) isoforms and nitrotyrosine in mucosal biopsies from these patients. In addition, effects on colonic fluid transfer caused by manipulating the substrate of NOS were studied in patients with collagenous colitis. PATIENTS: Eight patients with collagenous colitis, nine with active ulcerative colitis, and 10 with uninflamed bowel were included. METHODS: Expression of NOS isoforms was quantified by western blotting. Inducible NOS (iNOS) and nitrotyrosine were localised by immunohistochemistry. Modulation of NOS activity by topical N(G)-monomethyl-L-arginine (L-NMMA) or L-arginine was assessed during perfusion of whole colon. Plasma and perfusate nitrite/nitrate (NOx) was measured by Griess' reaction. RESULTS: Both in collagenous and ulcerative colitis, expression of iNOS was 10(2)-10(3) higher (p<0.001) than in uninflamed bowel and localised primarily to the epithelium. Endothelial NOS was evenly expressed in all groups while neuronal NOS was undetectable. Nitrotyrosine was markedly expressed in active ulcerative colitis but rarely detected in collagenous colitis and never in uninflamed bowel. In collagenous colitis, the output of NOx was markedly increased compared with uninflamed bowel (283 (58) v <37 nmol/min; p<0.01) and fluid was net secreted. L-NMMA reduced the output of NOx by 13-66% (95% confidence intervals) and secretion of fluid by 25-109% whereas L-arginine increased the output of NOx by 3-39% and secretion of fluid by 15-93%. CONCLUSIONS: In collagenous colitis, as opposed to ulcerative colitis, upregulation of iNOS occurs in the absence of nitrotyrosine formation and mucosal damage. Excess generation of NO may be the primary cause of diarrhoea in this condition.

Adult↗
PubMed2006

CT imaging of colitis.

Computed tomography (CT) is widely used to assess patients with nonspecific abdominal pain or who are suspected of having colitis. The authors recommend multidetector CT with oral, rectal, and intravenous contrast material and thin sections, which can accurately demonstrate inflammatory changes in the colonic wall and help assess the extent of disease. In most cases, the final diagnosis of the type of colitis is based on clinical and laboratory data and colonoscopic and biopsy findings, but specific CT features help narrow the differential diagnosis. Ulcerative colitis is distinguished from granulomatous colitis (Crohn disease) in terms of location of involvement, extent and appearance of colonic wall thickening, and type of complications. Ulcerative colitis and Crohn disease (granulomatous colitis) are rarely associated with ascites, which is often seen in infectious, ischemic, and pseudomembranous colitis. Pseudomembranous colitis also demonstrates marked wall thickening and, occasionally, skip areas but is associated with broad-spectrum antibiotic treatment or chemotherapy. Neutropenic colitis is characterized by right-sided colonic and ileal involvement, whereas ischemic colitis is characterized by vascular distribution pattern and history. Diverticulitis is a focal asymmetric process with fascial thickening and inflamed diverticula. Dilatation of a thick-walled appendix with increased enhancement and adjacent stranding suggests appendicitis, but inflammatory changes may extend to the cecum and terminal ileum. Epiploic appendagitis is a focal rim-enhancing area next to the colon, usually without any substantial colonic wall thickening.

Colitis↗
PubMed2003

Bacterial load in animal models of acute and chronic 'reactivated' colitis.

BACKGROUND: The involvement of enteropathogenic microorganisms in the pathogenesis of inflammatory bowel disease (IBD) and their importance in the different phases of inflammation are still unknown. AIM: To quantify the aerobic bacterial load in models of acute and chronic 'reactivated' colitis, and correlate this with damage. METHODS: Acute colitis was induced in rats by administration of trinitrobenzene sulfonic acid (TNBS) or dextran sulfate sodium (DSS). Colitis was 'reactivated' 6 weeks later by intravenous administration of TNBS. The distal colon was removed and scored macroscopically before inoculating samples. RESULTS: Bacterial load in rats with acute colitis (72 h) and chronic 'reactivated' colitis or their controls was significantly higher than untreated (p < 0.05); however, there were significantly more bacteria in acute colitis than in chronic 'reactivated' or their controls (p < 0.05). Both acute and chronic 'reactivated' colitis had significantly higher damage scores than untreated animals (p < 0.05). Bacterial load and damage score were significantly correlated only with acute colitis. CONCLUSIONS: The role of enteric microflora in the pathogenesis of IBD is greater during the acute phase of colitis. The correlation between bacterial load and tissue damage suggests that damage contributes to bacterial multiplication and exacerbation of colitis. Normal colonic flora may contribute to the relapse of the disease.

Acute Disease↗
PubMed2004

Colonic ulceration and increase of neutrophil elastase activity in the acetic acid-induced colitis model in Syrian hamsters.

A novel colitis model using Syrian hamsters was developed. Colitis was induced by intracolonic administration of 1% acetic acid, and the ulcer area, tissue myeloperoxidase (MPO) activity, and luminal neutrophil elastase (NE) activity of the colon were determined at 1, 3, 8, 24 and 48 hr after colitis induction. The histopathological changes of the colon were also examined in this model. An increase of tissue MPO activity and NE activity was evident at 3 hr after induction of colitis, peaked at 24 hr, and decreased subsequently. The increase of luminal NE activity was well correlated with the colonic ulcer area. In histopathological examination, ulceration, erosion, crypt abscesses, neutrophil infiltration, hemorrhage, and edema were seen. The effects of prednisolone were examined to evaluate the adequacy of our colitis model. Syrian hamsters were treated orally with prednisolone at 18 and 1 hr before and at 6 hr after induction of colitis, and the ulcer area, tissue MPO activity, and luminal NE activity were evaluated at 24 hr after colitis induction. Prednisolone therapy had little effect on the tissue MPO activity. However, the NE activity of the prednisolone-treated group was significantly decreased. In addition, although prednisolone did not significantly decrease the ulcer area, a tendency toward decrease was noted. We conclude that this new model of experimental colitis in Syrian hamsters is useful for investigating the pathophysiology of colitis, especially useful for studying the relationship between colitis and NE activity.

Acetic Acid↗
PubMed2003

[Trends in the occurrence (1980-1999) and clinical features of Crohn's disease and ulcerative colitis in a university hospital in southeastern Brazil].

BACKGROUND: Crohn's disease and ulcerative colitis are regarded as uncommon in developing countries, but studies on their occurrence in Brazil are scarce. Aims - To determine the occurrence of Crohn's disease and ulcerative colitis in a Brazilian university hospital throughout a 20-year period, and analyze the demographical, clinical and evolutive features of these cases. METHODS: The frequencies of new cases of Crohn's disease and ulcerative colitis admitted from January 1980 up to December 1999 were calculated and a descriptive analysis of the features of all cases seen from January 1990 up to December 1999 was performed. RESULTS: A total of 257 new cases (126 with Crohn's disease and 131 with ulcerative colitis) was recorded. The frequencies of admissions for both Crohn's disease and ulcerative colitis have increased progressively from 40 up to 61 cases/10.000 new admissions and Crohn's disease gradually became more common than ulcerative colitis. For both diseases, there was predominance of women, age at admission in the range of 30-40 years, Caucasian origin, married state and non-smokers. Digestive symptoms presented were similar to those already described for both diseases and there were no differences between Crohn's disease and ulcerative colitis regarding the frequencies of general complaints and extra-intestinal manifestations (29.5% vs 23.3%), including thromboembolism (5.9% vs 5.4%). Obstruction and/or perforation were seen in up to 59.2% of Crohn's disease cases, whereas 53.7% of all ulcerative colitis cases presented as severe forms. In Crohn's disease cases with obstruction, smoking was significantly more common than in non-complicated cases. In ulcerative colitis cases of increased severity, general complaints, extra-intestinal manifestations and pancolitis were significantly more frequent than in less severe forms. CONCLUSIONS: For the last 20 years, there have been an increased frequency of admission of inflammatory bowel diseases, and Crohn's disease have become more prevalent than ulcerative colitis. Demographical, clinical and evolutive features of these diseases seems to be similar to those already described, but there seems to be a predominance of more severe forms of both diseases.

Adolescent↗
PubMed2003

Methimazole-induced hypothyroidism in rats ameliorates oxidative injury in experimental colitis.

Depression of metabolism by hypothyroidism decreases oxidant production and thus protects tIssues against oxidant damage. Moreover, it is well-known that abnormal gut motility is a common manifestation in hypo/hyperthyroidism. In this study, we aimed to investigate the putative beneficial effects of methimazole on oxidative injury and dysmotility in a rat colitis model. Methimazole (0.04%) was administered in drinking water starting 15 days prior to induction of colitis. Colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (30 mg/ml; 0.8 ml) in ethanol. Six days after the induction of colitis, the fecal output was measured and used as an index for colonic motility. All rats were decapitated on the seventh day. The distal colon was weighed and the mucosal lesions were scored. Colonic lipid peroxidation (LP) and glutathione (GSH) measurements were performed. The macroscopic score, the colonic wet weight and LP values of the euthyroid colitis group were found to be higher than those of the control group (P<0.05-0.001). All these parameters were reduced in the methimazole-treated colitis group (P<0.01-0.001). The decrease in colonic GSH levels in the colitis group was completely abolished in the methimazole-treated colitis rats (P<0.01). Induction of colitis increased the average fecal output compared with the control group (P<0.05) and methimazole in the colitis group exaggerated the fecal output (P<0.001). In conclusion, methimazole reduces colonic oxidative injury probably due to hypometabolism, which is associated with a decrease in the production of reactive oxygen intermediates and an increase in the response of antioxidant systems.

Analysis of Variance↗
PubMed2001

Ursodiol use is associated with lower prevalence of colonic neoplasia in patients with ulcerative colitis and primary sclerosing cholangitis.

BACKGROUND: Patients with ulcerative colitis and primary sclerosing cholangitis are at high risk for colonic dysplasia and cancer. This risk approaches 50% after 25 years of colitis. Ursodiol has been shown to protect against development of colorectal neoplasia in animal models. OBJECTIVE: To assess the relationship between ursodiol use and colonic dysplasia, the precursor to colon cancer, in patients with ulcerative colitis and primary sclerosing cholangitis. DESIGN: Cross-sectional study. SETTING: University medical center. PATIENTS: 59 patients with ulcerative colitis and primary sclerosing cholangitis who were undergoing colonoscopic surveillance for colonic dysplasia. MEASUREMENTS: Use of ursodiol was assessed in all patients. The presence or absence of colonic dysplasia was evaluated by colonoscopic surveillance. Other variables assessed were age at onset and duration of ulcerative colitis; duration of primary sclerosing cholangitis; Child-Pugh classification; and use of sulfasalazine, other 5-aminosalicylic acid preparations, prednisone, cyclosporine, azathioprine, and methotrexate. RESULTS: Ursodiol use was strongly associated with decreased prevalence of colonic dysplasia (odds ratio, 0.18 [95% CI, 0.05 to 0.61]; P = 0.005). The association between dysplasia and ursodiol use remained after adjustment for sex, age at onset of colitis, duration of colitis, duration of sclerosing cholangitis, severity of liver disease, and sulfasalazine use (adjusted odds ratio, 0.14 [CI, 0.03 to 0.64]; P = 0.01). Younger age at onset of colitis was associated with an increased risk for dysplasia. CONCLUSIONS: Ursodiol use appears to be associated with a lower frequency of colonic dysplasia in patients with ulcerative colitis and primary sclerosing cholangitis. A randomized trial investigating the chemoprotective effect of ursodiol in patients with ulcerative colitis may be warranted.

Adult↗
PubMed2005

Pathophysiological studies of trinitrobenzene sulfonic acid-induced colitis in Syrian hamsters (Mesocricetus auratus).

We developed a colitis model in Syrian hamsters (Mesocricetus auratus) to investigate the relationship between colitis and neutrophil elastase (NE). Colitis was induced by a single intracolonic dose of trinitrobenzene sulfonic acid (TNBS; 90 mg/ml) dissolved in 15% (vol/vol) ethanol. The ulcer area, tissue myeloperoxidase (MPO) activity, and luminal NE activity all were increased on Days 1 and 5, corresponding with the acute inflammatory histopathological changes. These acute inflammatory parameters subsequently decreased by Day 14, and chronic inflammatory histopathological changes became evident. Recurrence of inflammation was not observed during the period up to Day 28. To evaluate our colitis model, the effects of prednisolone were examined. Prednisolone was administered orally once on the day before induction of colitis, and animals were treated twice daily thereafter. Although prednisolone had little effect on the tissue MPO activity, prednisolone inhibited the ulcer area and NE activity. In addition, the effects of an NE-specific inhibitor (ONO-6818) on our TNBS-induced colitis model were examined. In the subcutaneous treatment study, ONO-6818 was administered once before the induction of colitis. Although ONO-6818 had little effect on the tissue MPO activity, the ulcer area and NE activity were decreased in the ONO-6818-treated group. The inhibitory effects on the ulcer area and NE activity were confirmed after oral treatment with ONO-6818 after induction of colitis. We conclude that our colitis model is useful for investigating the relationship between colitis and NE, and inhibition of NE activity can prevent the progression of ulceration.

Animals↗
PubMed2006

Autoantibody profiles in microscopic colitis.

OBJECTIVE: The etiology of microscopic colitis is unclear; an autoimmune response and pharmacological induction have been proposed as possible mechanisms. We conducted a multicentre cross-sectional study to compare the antibody profiles of patients with collagenous and lymphocytic colitis with those of a control group. METHODS: The medical histories and antibody profiles of 26 patients with collagenous and 16 patients with lymphocytic colitis were compared with the corresponding data of 43 controls without gastroenterological disease. Antibodies to the following structures were determined: intestinal goblet cells, antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies, anti-Saccharomyces cerevisiae antibody (ASCA), tissue transglutaminase, gliadin, pancreatic acini, glutamate decarboxylase, tyrosine phosphatase IA-2 and thyroid (microsomal anitbodies, MAB). RESULTS: Patients with collagenous and lymphocytic colitis had been treated significantly more often with H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs (P = 0.026 and 0.014, respectively). Additional diseases of presumed autoimmune etiology were present in 43% (18/42) of patients. Comparison with the controls showed significantly more positive findings for ANA immunoglobulin G (IgG), gliadin immunoglobulin A (IgA) and ASCA (IgA and IgG) in patients with collagenous colitis but not in those with lymphocytic colitis. Collagenous colitis was associated with positive ASCA in 15% of patients and lymphocytic colitis in 13%. CONCLUSIONS: The autoantibodies investigated are of no diagnostic relevance to microscopic colitis. Positive ANA and strong associations with other autoimmune diseases point to an autoimmune etiology. H(2)-receptor antagonists and non-steroidal anti-inflammatory drugs might also be of pathogenetic significance.

Adult↗
PubMed2006

Klebsiella oxytoca as a causative organism of antibiotic-associated hemorrhagic colitis.

BACKGROUND: Antibiotic-associated hemorrhagic colitis is a distinct form of antibiotic-associated colitis in which Clostridium difficile is absent. Although the cause is not known, previous reports have suggested a role of Klebsiella oxytoca. METHODS: We studied 22 consecutive patients who had suspected antibiotic-associated colitis and who were negative for C. difficile. Patients underwent diagnostic colonoscopy, and among those who received a diagnosis of antibiotic-associated hemorrhagic colitis, stool samples were cultured for K. oxytoca. We isolated K. oxytoca strains and tested them for cytotoxin production using a tissue-culture assay. In addition, we also cultured stool samples obtained from 385 healthy subjects for K. oxytoca. An in vivo animal model for antibiotic-associated hemorrhagic colitis was established with the use of Sprague-Dawley rats. RESULTS: Of the 22 patients, 6 had findings on colonoscopy that were consistent with the diagnosis of antibiotic-associated hemorrhagic colitis, and 5 of these 6 patients had positive cultures for K. oxytoca. No other common enteric pathogens were found in the five patients. Before the onset of colitis, all five were receiving penicillins, and two were also taking nonsteroidal antiinflammatory drugs (NSAIDs). All isolated K. oxytoca strains produced cytotoxin. K. oxytoca was found in 1.6% of the healthy subjects. In the animal model, K. oxytoca was found only in the colon of rats that received amoxicillin-clavulanate in addition to being inoculated with K. oxytoca. In these rats, infection with K. oxytoca induced a right-sided hemorrhagic colitis that was not observed in uninfected animals that received amoxicillin-clavulanate, indomethacin (an NSAID), or both. CONCLUSIONS: Our fulfillment of Koch's postulates for cytotoxin-producing K. oxytoca suggests that it is the causative organism in at least some cases of antibiotic-associated hemorrhagic colitis. Infection with K. oxytoca should be considered in patients with antibiotic-associated colitis who are negative for C. difficile.

Adult↗
PubMed1997

Non-infective colitis in infancy: evidence in favour of minor immunodeficiency in its pathogenesis.

Forty two infants below the age of 2 years presenting with chronic non-infective diarrhoea and shown to have histologically proved colitis were investigated over a five year period. Allergic colitis was the most common cause of colitis, accounting for 62% of the cases. Other colitides diagnosed included: non-specific colitis, autoimmune enterocolitis, and ulcerative colitis accounting for 10% each; severe combined immunodeficiency 7%, and Crohn's disease 3%. A positive family history and a personal history of atopy were obtained in 48% and 29% of the cases respectively. Serum immunoglobulin A, IgG2, and IgG4 were very low in over 50% of the entire cohort of infants with colitis; 66% of those with severe combined immunodeficiency, autoimmune enterocolitis, and ulcerative colitis (n = 11) had low CD3 and CD4 T lymphocytes with an accompanying increase in CD8 in two thirds of those with severe combined immunodeficiency. T lymphocytes were normal in those with allergic colitis. Thus infants with proved non-infective colitis as a group show a high prevalence of IgA, IgG2, and IgG4 deficiency. It is likely that this minor deficiency of mucosa associated immunoglobulin production has a role in the pathogenesis of the colitic process.

Autoimmune Diseases↗
PubMed1995

Histological discrimination of idiopathic inflammatory bowel disease from other types of colitis.

AIMS: To assess the value of histology in diagnosing inflammatory bowel disease (IBD) in colorectal biopsy specimens. METHODS: Retrospective, double blind evaluation of colorectal biopsy specimens from 41 patients with colitis (28 with ischaemic colitis and 13 with acute self-limited colitis) and 84 patients with IBD (42 with Crohn's disease and 42 with ulcerative colitis). RESULTS: The features distinguishing IBD from other forms of colitis included distorted architecture, lymphocyte and plasma cell infiltrate, excess of polymorphonuclear leucocytes, polymorphonuclear cryptitis, crypt abscesses, and basal lymphoid aggregates. The features discriminating between Crohn's disease and ulcerative colitis included an irregular or villous surface, distorted architecture, decrease in mucus content, and polymorphonuclear cryptitis. Using multivariate analysis, 90% of patients with Crohn's disease and 71% of those with ulcerative colitis were correctly classified, the former being strongly defined by epithelioid granulomas, microgranulomas and isolated giant cells, and the latter best defined by an irregular or villous surface, decrease in mucus content and crypt atrophy. CONCLUSIONS: Examination of colorectal biopsy specimens is a reliable method for diagnosing IBD. In the absence of epithelioid granulomas, microgranulomas and isolated giant cells a diagnosis of Crohn's disease is based on the absence of histological criteria favouring ulcerative colitis. The histological spectrum of indeterminate colitis remains to be clarified.

Adolescent↗
PubMed1999

[Differential diagnosis of colitis].

The aims of the bioptical diagnosis of colitis are delineated in introductory remarks. Subsequently, the range of normality is described for mucosal structures, and the term "nonspecific chronic colitis" is critically discussed. Furthermore, some characteristic (diagnostic) forms of colitis are presented together with their differential diagnoses. Also the "less" diagnostic features of infectious colitis and chronic inflammatory bowel disease are described. An algorithmus of the differential diagnosis of colitis is proposed. Excluding 83 cases of normal findings, the practical impact of such an algorithm was critically analysed in 381 consecutive biopsies of histologically proven colitis.--Several "characteristical" types of colitis could be distinguished in about 95% of the biopsies; in a small percentage of cases only a differential diagnosis could be offered, partly because of inconclusive morphological findings, partly because clinical data were completely lacking and partly because there were no separate rectal biopsies in these cases. We wish to stress, however, that the anamnestical data relating to the length of complaints and the therapeutic interventions are very relevant to the interpretation of the morphological differential diagnosis of chronic colitis, especially in chronic colitis with low activity or inactive disease.

Algorithms↗
PubMed1992

Microscopic colitis: can it be qualitatively and quantitatively characterized?

This study reports the histological features helpful in diagnosing microscopic colitis. Rectal biopsy specimens from 14 patients with microscopic colitis, 14 with active ulcerative colitis and 14 without colonic inflammation were pooled and then assessed by three observers according to a predetermined protocol. Inter-observer agreement was good except for Paneth cell metaplasia and endocrine cell metaplasia. Compared with healthy tissue, microscopic colitis showed a significant (p less than 0.05) increase in chronic inflammatory cells and a depletion of goblet cells but these changes were less pronounced than those seen in ulcerative colitis (p less than 0.05). In contrast to ulcerative colitis, microscopic colitis was associated with a more marked infiltration with eosinophils and an increase in intra-epithelial lymphocytes. These results show that microscopic colitis can be distinguished both from normal colonic tissue and from ulcerative colitis.

Adolescent↗
PubMed2004

Interventions for treating collagenous colitis.

BACKGROUND: Collagenous colitis is a disorder that is recognized as a cause of chronic diarrhea. Treatment has been based mainly on anecdotal evidence. This review was performed to identify therapies for collagenous colitis that have been proven in randomized trials. OBJECTIVES: To determine effective treatments for patients with clinically active collagenous colitis. SEARCH STRATEGY: Relevant papers published between 1970 and August 2003 were identified via the MEDLINE and PUBMED databases. Manual searches from the references of identified papers, as well as review papers on collagenous or microscopic colitis were performed to identify additional studies. Abstracts from major gastroenterological meetings were searched to identify research submitted in abstract form only. Finally, the Cochrane Controlled Trials Register and the Cochrane Inflammatory Bowel Disease Group Specialized Trials Register were searched for other studies. SELECTION CRITERIA: Five randomized trials were identified. One trial studied bismuth subsalicylate (published in abstract form only), one trial studied prednisolone, and 3 trials studied budesonide in the therapy of collagenous colitis. DATA COLLECTION AND ANALYSIS: Data were extracted independently by each author onto 2x2 tables (treatment versus placebo and response versus no response). For therapies assessed in one trial only, p-values were derived using the chi-square test. For therapies assessed in more than one trial, summary test statistics were derived using the Peto odds ratio and 95% confidence intervals. Data were combined for analysis only if the outcomes were sufficiently similar in definition. MAIN RESULTS: There were 9 patients with collagenous colitis in the trial studying bismuth subsalicylate (nine 262 mg tablets daily for 8 weeks). Those randomized to active drug were more likely to have clinical (p=0.003) and histological (p=0.003) improvement than those assigned to placebo. Eleven patients were enrolled in the trial studying prednisolone (50 mg daily for 2 weeks). There was a trend towards clinical response in patients on active medication compared to placebo (p=0.064). The effect of prednisolone on histologic improvement was not studied. A total of 94 patients were enrolled in 3 trials studying budesonide (9 mg daily or in a tapering schedule for 6 to 8 weeks). The pooled odds ratio for clinical response to treatment with budesonide was 12.32 (95% CI 5.53-27.46), with a number needed to treat of 2 patients. There was significant histological improvement with treatment in all 3 trials studying budesonide therapy. REVIEWER'S CONCLUSIONS: Budesonide is effective for the treatment of collagenous colitis. The evidence for benefit with bismuth subsalicylate is weaker. Prednisolone may be effective for treatment of collagenous colitis, but only a single very small study has been reported. The effectiveness of these and other therapies for induction or maintenance of remission (as opposed to producing clinical or histological improvement) of collagenous colitis is unknown.

Anti-Inflammatory Agents↗
PubMed1993

Effect of putative phospholipase A2 inhibitors on acetic acid-induced acute colitis in the rat.

Phospholipase activation may play an important role in ulcerative colitis. This hypothesis was tested by evaluating the effect of two non-selective phospholipase (PL) A2 inhibitors, quinacrine and p-bromophenacyl-bromide (pBPB), on acetic acid-induced colitis in the rat. The calcium antagonist verapamil, which may also act as a PLA2 inhibitor, was also tested. Acute colitis was induced in an isolated colonic segment by instillation of 4 per cent acetic acid for 15 s; this induces a uniform colitis after 4 days. The severity of colitis was evaluated histologically, by measuring myeloperoxidase (MPO) activity and by determining plasma exudation into the lumen of the colon (permeability) with 125I-labelled albumin given intravenously. All three putative PLA2 inhibitors tested were found to prevent the development of colitis. Intravenous administration of quinacrine 10 mg kg-1 at 30 min before instillation of acetic acid resulted in a normal mucosal appearance, normal MPO activity and a significantly reduced increase in plasma exudation into the colon. A similar effect was achieved using verapamil. Intracolonic administration of either quinacrine or pBPB also prevented acetic acid-induced colitis. However, three doses, starting immediately after acetic acid administration and repeated on the first and second days, were needed to achieve this, whereas one dose produced only a partial effect. PLA2 may play an important role in acetic acid-induced colitis and inhibition of its activity may offer an alternative mode of treatment in ulcerative colitis.

Acetates↗
PubMed2007

Comparative analysis of colonic gene expression of three experimental colitis models mimicking inflammatory bowel disease.

BACKGROUND: Mouse models of inflammatory bowel diseases (IBD) are used to unravel the pathophysiology of IBD and to study new treatment modalities, but their relationship to Crohn's disease (CD) or ulcerative colitis (UC) is speculative. METHODS: Using Agilent mouse TOX oligonucleotide microarrays, we analyzed colonic gene expression profiles in three widely used models of experimental colitis. In 2 of the models (TNBS and DSS-induced colitis), exogenous agents induce the colitis. In the third model the colitis is induced after transfer of a T-cell population (CD4(+)CD45RB(high) T cells) that lacks regulatory cells into an immunodeficient host. RESULTS: Compared with control mice, in DSS, TNBS, and the CD45RB transfer colitis mice, 387, 21, and 582 genes were more than 2-fold upregulated in the intestinal mucosa. Analyses of exclusively shared gene expression profiles between the different models revealed that DSS/transfer colitis share 69 concordantly upregulated genes, DSS/TNBS 6, and TNBS/transfer colitis 1. Seven genes were upregulated in all three models. The CD45RB transfer model expression profile included the most genes that are known to be upregulated in IBD. Of 32 genes that are known to change transcriptional activity in IBD (TNF, IFN-gamma, Ltbeta, IL-6, IL-16, IL-18R1, IL-22, CCR2, 7, CCL2, 3, 4, 5, 7, 11, 17, 20, CXCR3, CXCL1, 5, 10, Mmp3, 7,9, 14, Timp1, Reg3gamma, and Pap, S-100a8, S-100a9, Abcb1, and Ptgs2), 2/32 are upregulated in TNBS, 15/32 are upregulated or downregulated in DSS and 30/32 are upregulated or downregulated in the CD45RB transfer colitis. CONCLUSION: The pattern of gene expression in the CD45RB transfer model most closely reflects altered gene expression in IBD.

Animals↗