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PubMed1998

The immunohistological diagnosis of E. coli O157:H7 colitis: possible association with colonic ischemia.

OBJECTIVE: E. coli O157:H7 may cause hemorrhagic colitis resembling ischemic colitis. Diagnosis is usually made by finding sorbitol-negative colonies on MacConkey agar that react with O157 and H7 antisera. Most ischemic colitis is idiopathic, but some may be caused by E. coli O157:H7, inasmuch as this organism can produce fibrin thrombi in colon vasculature. The objectives of this study were to determine whether E. coli O157:H7 infection can be diagnosed retrospectively from paraffin blocks of colon sections and whether an association exists between E. coli O157:H7 infection and colonic ischemia. METHODS: Paraffin-embedded sections of normal colon (n = 2) and various colitides [ischemic (n = 11), E. coli O157:H7 (n = 2), IBD (n = 8) and pseudomembranous (n = 3)] were used. Sections were deparaffinized, rehydrated, incubated with 3% peroxide in methanol, rinsed, and incubated with peroxidase-labeled antibody isolated from goats immunized with whole E. coli O157:H7. Sections were stained with peroxidase chromagen reagent and counterstained with hematoxylin. Coarse, granular, orange-brown staining was considered positive. To determine the localization of the chromagen deposits, three cases that stained positive, including one of the culture-proved E. coli O157:H7 colitis and two of colonic ischemia, were processed for electron microscopy. RESULTS: Both cases (100%) of E. coli O157:H7 colitis and three of 11 (27.3%) cases of ischemic colitis stained positive by light microscopy. In one culture-proved case, electron microscopy demonstrated staining of bacillary structures; in two cases of colonic ischemia, extensive deposits of chromagen material were present that were associated neither with inflammatory cells nor with bacterial forms. CONCLUSIONS: Immunoperoxidase staining of archival sections may be used to diagnose E. coli O157:H7 infection. An etiological role for this organism is possible in some cases of colonic ischemia.

Aged↗

PubMed1979

Chronic immune colitis in rabbits.

A chronic colitis has been induced in rabbits having many of the histological features of human ulcerative colitis. Animals were first immunised with the common enterobacterial antigen of Kunin and haemagglutinating antibodies demonstrated in high titre. An immune complex colitis was then established by the injection of soluble immune complexes following mild irritation of the rectum with dilute formalin as previously described. The rabbits developed an acute colitis within the first week but, in contrast with unsensitised rabbits, the inflammation persisted and was still present at six months as assessed by proctoscopy and rectal biopsy. Kunin-sensitised rabbits receiving intravenous saline, antigen, or antibody alone did not develop a chronic colitis. It is suggested that hypersensitivity to colonic bacterial antigens may be one mechanism whereby an acute colitis becomes chronic.

Animals↗

PubMed2001

IL-4 exacerbates disease in a Th1 cell transfer model of colitis.

IL-4 is associated with Th2-type immune responses and can either inhibit or, in some cases, promote Th1-type responses. We tested the effect of IL-4 treatment on the development of inflammation in the CD4(+)CD45RB(high) T cell transfer model of colitis, which has been characterized as a Th1-dependent disease. IL-4 treatment significantly accelerated the development of colitis in immunodeficient recipients (recombinase-activating gene-2 (Rag2)(-/-)) of CD4(+)CD45RB(high) T cells. Quantitative analysis of mRNA expression in the colons of IL-4-treated mice showed an up-regulation of both Th1- and Th2-associated molecules, including IFN-gamma, IP-10, MIG, CXCR3, chemokine receptor-8, and IL-4. However, cotreatment with either IL-10 or anti-IL-12 mAb effectively blocked the development of colitis in the presence of exogenous IL-4. These data indicate that IL-4 treatment exacerbates a Th1-mediated disease rather than induces Th2-mediated inflammation. As other cell types besides T cells express the receptor for IL-4, the proinflammatory effects of IL-4 on host cells in Rag2(-/-) recipients were assessed. IL-4 treatment was able to moderately exacerbate colitis in Rag2(-/-) mice that were reconstituted with IL-4Ralpha-deficient (IL-4Ralpha(-/-)) CD4(+)CD45RB(high) T cells, suggesting that the IL-4 has proinflammatory effects on both non-T and T cells in this model. IL-4 did not cause colitis in Rag2(-/-) mice in the absence of T cells, but did induce an increase in MHC class II expression in the lamina propria of the colon, which was blocked by cotreatment with IL-10. Together these results indicate that IL-4 can indirectly promote Th1-type inflammation in the CD4(+)CD45RB(high) T cell transfer model of colitis.

Adjuvants, Immunologic↗

PubMed1999

[Differential diagnosis of ulcerative colitis].

Important points during differential diagnosis of ulcerative colitis from other inflammatory disorders are endoscopic examination and microbial studies of stools. In acute phase of enterocolitis in which waterly diarrhea with bloody stool and abdominal pain appeared, infectious enterocolitis by Shigella, Salmonella, Campylobacter and Yersinia, which sometimes causes mucosal edema, hyperemia, erosions and ulceration should be distinguished carefully. Microbial studies of stool would bring helpful information in such situation. In chronic phase of inflammatory diseases of bowel, they often showed chronic diarrhea associated with mucobloody stools and abdominal pain. They often revealed mucosal inflammation mimicking ulcerative colitis during endoscopic evaluation. Among them, most important diseases are amebic colitis, ischemic colitis, radiation colitis and antibiotics associated hemorrhagic colitis.

Bacterial Infections↗

PubMed1981

Colitis in the elderly. A reappraisal.

The records of 81 patients with colitis whose symptoms began after the age of 50 years were analyzed to determine the importance of ischemia as a cause of colitis in this age group and to evaluate the accuracy of previous diagnoses. Patients were classified by clinical, roentgenological and pathologic criteria. A retrospective diagnosis of ischemic colitis was made in three-fourths of the patients, one-half of whom had original discharge diagnoses of ulcerative, Crohn's or nonspecific colitis. This study supports our belief that ischemia is the most common cause of colitis beginning in patients older than 50 years of age. Moreover, the incorrect diagnosis of idiopathic inflammatory bowel disease in a large proportion of these patients may explain why colitis has been reported to behave differently in the elderly than in the young.

Aged↗

PubMed1981

[Ischaemic colitis (author's transl)].

Attention must be drawn to the fact that especially in elderly patients with acute onset of abdominal pain concomitant with haemorrhagic, mucous diarrhoea, ischaemic colitis must be considered in the differential diagnosis. Ischaemic colitis arises as a consequence of insufficient blood flow through the peripheral branches of the middle colic artery and inferior mesenteric artery and mostly strikes the left colonic flexure, the colon descendens or sigmoid. Because of the segmental involvement and the macroscopic appearance on X-ray and endoscopy the disease is sometimes indistinguishable from Crohn's disease or ulcerative colitis. In every day clinical life ischaemic colitis is a relatively rare phenomenon, in spite of the high incidence of arterial occlusive disease in the patients treated at this unit. The increasing frequency of ulcerative colitis in elderly patients, as reported in the literature, may be partly associated with unidentified cases of ischaemic colitis and this possibility is discussed.

Aged↗

PubMed1998

Primary sclerosing cholangitis and colorectal carcinoma in patients with chronic ulcerative colitis: a case-control study.

BACKGROUND: Controversy persists regarding primary sclerosing cholangitis (PSC) as a risk factor for colorectal carcinoma in patients with chronic ulcerative colitis. Small sample size and differing endpoints have contributed to variation among reported studies. This large case-control study was conducted to examine the possible association between PSC and colon carcinoma in patients with ulcerative colitis. METHODS: From Mayo Clinic records spanning 1976-1994, 171 cases with both ulcerative colitis and colorectal carcinoma and 171 contemporaneous controls with ulcerative colitis but no colorectal neoplasia matched with regard to age, gender, extent, and duration of colitis were identified. The diagnosis of PSC required cholangiographic confirmation. Analysis employed a multivariate logistic regression model. RESULTS: The prevalence of PSC was similar in cases (18%) and controls (15%) (P = 0.54). The adjusted odds ratio for colorectal carcinoma with PSC was 1.23 (95% confidence interval, 0.62-2.42). CONCLUSIONS: Based on this large case-control study, there was no association between PSC and colorectal carcinoma in patients with ulcerative colitis.

Adolescent↗

PubMed2007

CD4(+) T lymphocytes mediate colitis in HLA-B27 transgenic rats monoassociated with nonpathogenic Bacteroides vulgatus.

BACKGROUND: HLA-B27/beta2 microglobulin transgenic (TG) rats develop spontaneous colitis when raised under specific pathogen-free (SPF) conditions or after mono-association with Bacteroides vulgatus (B. vulgatus), whereas germ-free TG rats fail to develop intestinal inflammation. SPF HLA-B27 TG rnu/rnu rats, which are congenitally athymic, remain disease free. These results indicate that commensal intestinal bacteria and T cells are both pivotal for the development of colitis in TG rats. However, it is not known if T cells are also required in the induction of colitis by a single bacterial strain. The aim of this study was therefore to investigate the role of T cells in the development of colitis in B. vulgatus-monoassociated HLA-B27 TG rats. METHODS: HLA-B27 TG rnu/rnu and rnu/+ rats were monoassociated with B. vulgatus for 8-12 weeks. CD4(+) T cells from mesenteric lymph nodes (MLNs) of B. vulgatus-monoassociated rnu/+ TG donor rats were transferred into B. vulgatus-monoassociated rnu/rnu TG recipients. RESULTS: B. vulgatus-monoassociated rnu/+ rats showed higher histologic inflammatory scores and elevated colonic interferon-gamma mRNA, cecal myeloperoxidase, and cecal IL-1beta levels compared to those in rnu/rnu TG rats that did not contain T cells. After transfer of CD4(+) cells from colitic B. vulgatus-monoassociated rnu/+ TG donor rats, B. vulgatus-monoassociated rnu/rnu TG recipients developed colitis that was accompanied by B. vulgatus-induced IFN-gamma production by MLN cells in vitro and inflammatory parameters similar to rnu/+ TG rats. CONCLUSIONS: These results implicate CD4(+) T cells in the development of colitis in HLA-B27 TG rats monoassociated with the nonpathogenic bacterial strain B. vulgatus.

Animals↗

PubMed2007

Fecal excretion of deoxyribonucleic acid in long-term follow-up of patients with inactive ulcerative colitis.

BACKGROUND: We have developed a technique for measuring fecal excretion of human DNA by assuming that luminal desquamation of epithelial and inflammatory cells increases in damaged colonic mucosa. However, the clinical usefulness of this technique in the follow-up of patients with ulcerative colitis has not been established. The aim of this study was to determine the stability of fecal DNA in inactive ulcerative colitis and its potential value as an indicator of relapse. METHODS: The 54 patients with clinically quiescent ulcerative colitis in this prospective study were followed for 12 months or until clinical relapse (clinical activity index > 7). Fecal calprotectin concentration was determined by ELISA, and fecal DNA concentration was determined by quantitative PCR. RESULTS: During the year of follow-up, 23 of the 54 patients relapsed, with a median increase in the colitis activity index from 1.0 to 8.0 (P < 0.01). Median fecal DNA remained unchanged in patients with stable, inactive colitis, ranging from 6.8 copies/microg at inclusion to 1.7 copies/microg at the end of follow-up. Fecal calprotectin level also was unchanged, ranging from 414.0 microg/g at inclusion to 128.9 microg/g at the end of follow-up. In contrast, fecal DNA concentration increased significantly in patients who relapsed (259.0 versus 3.9 copies/microg at entry; P < 0.01). Similar increases in relapsing patients were also observed with fecal calprotectin. ROC curve analysis to assess the accuracy of fecal DNA and calprotectin in detecting relapses during follow-up yielded similar results. CONCLUSIONS: Fecal DNA concentration remained stable in patients with inactive ulcerative colitis but increased significantly with relapses. Determining fecal DNA concentration may be a new objective instrument to use in the follow-up of patients.

Adult↗

PubMed2000

E-Selectin expression in a murine model of chronic colitis.

The objective of this study was to quantify E-selectin surface expression in the colon as well as other tissues in a CD4(+) T-cell model of chronic colitis in mice using the newly developed dual radiolabel monoclonal antibody technique. Male SCID mice were reconstituted with either 5 x 10(5) CD4(+) CD45RB(low) or CD45RB(high) T-cells isolated from normal CB-17 donor mouse spleens and subsequently monitored for clinical signs of colitis. We found that animals injected with CD45RB(high) but not CD45RB(low) T-cells nor PBS developed colitis at 6-8 weeks following reconstitution as assessed by loss of body weight, development of loose stools and/or diarrhea, and histopathology. Concurrent with the onset of distal bowel inflammation was enhanced expression of E-selectin compared to SCID mice injected with PBS or reconstituted with CD45RB(low) T-cells, both of which did not develop colitis. We also observed significant increases in E-selectin expression in cecum, small intestine, mesentery, and liver of colitic mice. Our data confirm that reconstitution of SCID mice with CD45RB(high) but not CD45RB(low) T-cells induces chronic colitis and demonstrate that this chronic colitis is associated with enhanced expression of an endothelial cell-specific adhesion molecule. Furthermore, our studies demonstrate that reconstitution of SCID mice with CD45RB(high) T-cells enhances E-selectin expression in a variety of tissues distant from the site of active inflammation.

Animals↗

PubMed1995

Development of ulcerative colitis-associated anti-idiotype antibody using a novel monoclonal antibody against a colonic autoantigen.

Earlier studies have established reactivity of ulcerative colitis colon-bound IgG antibody with an autoantigen recognized by a novel monoclonal antibody, 7E12H12 (IgM isotype). Purified 7E12H12-IgM was used to raise anti-idiotype antibody in the rabbit, and the presence of disease-specific idiotype(s) was evaluated in patients with ulcerative colitis. F(ab')2 fragments were prepared from serum-IgG of the rabbit immunized with 7E12H12-IgM and extensively absorbed against unrelated mouse IgM and purified serum IgG from 4 normal subjects. The reactivity of the absorbed F(ab')2 fragment was tested in an ELISA against the serum from 19 patients with ulcerative colitis, 15 patients with Crohn's disease, and 10 normal subjects. The OD values with ulcerative colitis sera were significantly (P < 0.0005) higher than those with Crohn's disease and normal sera. Blood serum from 84% of patients with ulcerative colitis contains antibodies that are reactive to the F(ab')2 fragments of the immune rabbit serum-IgG. Further studies of the anti-idiotype antibodies may elucidate autoimmune processes in ulcerative colitis and may have diagnostic and therapeutic values.

Animals↗

PubMed1999

Effect of dehydroleucodine in experimental colitis in rats and mice.

Dehydroleucodine (DhL), a sesquiterpene lactone (SQL) of the guaianolide type isolated from Artemisia douglasiana Besser, shows a pharmacological cytoprotective effect and significantly prevents the formation of gastric and duodenal lesions induced by various necrotising agents in rodents. The effects of DhL, on two models of experimental colitis were examined. Colitis was produced in male Wistar rats by rectal instillation of 5 and 10% acetic acid, following the methods of Eliakim et al. and Le Duc et al., respectively. In mice colitis was produced by rectal instillation of 0.1 ml of 2,4,6-trinitrobenzene sulphonic acid (5 mg in 50% ethanol) (TNB) as previously described by Chin et al. In this study, the administration of DhL 40 mg kg(-1)(1 h before the induction of colitis) significantly decreased mucosal damage. This effect was consistent in both models. The protection provided by DhL was accompanied by significant decreases in diarrhoea and colon weight; and histologically normal mucosa without ulceration and mucus production were observed. This study shows that both TNB and acetic acid colitis can be pharmacologically controlled by DhL. Our results suggest that the protective activity of DhL in experimental colitis is mediated, at least in part, through the increase of glycoprotein synthesis, anti-inflammatory effect and inhibition of COX-2 induction, and by inhibiting the degranulation of cells containing monoamines.

Acetic Acid↗

PubMed1994

Collagenous, microscopic and lymphocytic colitis. An evolving concept.

Collagenous colitis and lymphocytic colitis (previously described as microscopic colitis) are two newly recognised forms of colitis. Both have generated much controversy and continue to do so; their aetiology and pathogenesis are unresolved and their association with a variety of immune-related disorders is intriguing. Response to available therapeutic modalities is often disappointing. The possible relationship or overlap between these two conditions remains a controversial issue. The aim of this review is essentially to present an overview of collagenous colitis and lymphocytic colitis and to propose an unifying concept with an adapted terminology.

Child↗

PubMed1996

Non-steroidal anti-inflammatory drug-induced colitis.

Non-steroidal anti-inflammatory drugs (NSAIDs) may adversely affect the colon, either by causing a non-specific colitis or by exacerbating a preexisting colonic disease. Patients with NSAID-induced colitis present with bloody diarrhoea, weight loss, iron deficiency anaemia and sometimes abdominal pain. Colonoscopy may be normal or may show inflammation, ulceration or diaphragm-like stricture. Histology often concludes to non-specific colitis. NSAIDs may cause perforation or bleeding of colonic diverticula, may cause relapse to inflammatory bowel disease and may exacerbate bleeding of colonic angiodysplasia. Pathogenesis of NSAID-induced colitis is still controversial. Local and/or systemic effects of NSAIDs on mucosal cells might lead to an increased intestinal permeability, which is a prerequisite for colitis. Treatment of NSAID-induced colitis should be to discontinue the drug, or at least, to reduce the dose as much as possible. Sulphasalazine and Metronidazole have been successfully used in few studies. Surgery is often indicated in case of life threatening complications or untractable symptoms.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1975

Colonic epithelial cells and polymorphonuclear leukocytes in ulcerative colitis. An electron-microscopic study.

The following study cinfirms previously reported electron-microscopic findings in ulcerative colitis and agrees with the nonspecific nature of those findings. The study extends these observations in regard to relationship of PMN leukocytes, eosinophil leukocytes, and mast cells to colonic epithelial cells. Strong, though not conclusive, data that PMN and eosinophil leukocytes extensively invade epithelial cells in ulcerative colitis is presented. This finding also is not specific to ulcerative colitis and was found with much less frequency in Crohn's disease of the colon and in salmonella colitis. The presence of intravascular degranulation of PMN leukocytes in ulcerative colitis is confirmed. This study adds additional support to the concept that the major abnormality in ulcerative colitis resides within the colonic epithelial cell.

Animals↗

PubMed1997

Colonic cancer in a patient with primary sclerosing cholangitis and long-standing ulcerative colitis.

A 27-year-old woman with a 9-year history of ulcerative colitis involving the entire colon was admitted to our hospital in August 1992 because of bloody stools and left lower abdominal pain. She had been treated with sulfasalazine since 1983 and the colitis had been clinically quiescent or mild for 7 years. She had also been diagnosed as having primary sclerosing cholangitis (PSC) 4 years prior to this admission, based on the clinical, laboratory, and cholangiographic findings. A barium enema and colonoscopy showed an irregular mass obstructing the bowel lumen in the distal portion of the descending colon. Biopsy specimens taken from the mass revealed moderately differentiated adenocarcinoma, and a subtotal colectomy was performed. Histologic examination of the mass lesion showed moderately differentiated adenocarcinoma invading the pericolic adipose tissue. She is currently alive 3 years after surgery. PSC has recently been reported as a risk factor for colonic neoplasia in patients with long-standing ulcerative colitis. In Japan, however, colorectal cancer associated with PSC and ulcerative colitis has rarely been reported. The present case suggests that the risk of colonic cancer is higher in patients with ulcerative colitis and PSC than in patients with ulcerative colitis alone.

Adenocarcinoma↗

PubMed1983

Polymorphonuclear leukocyte function in ulcerative colitis and Crohn's disease.

The aim of this study was to determine whether polymorphonuclear leukocyte chemotaxis, adhesion, and electrophoretic mobility were altered in inflammatory bowel disease and whether such alterations could be related to prior ingestion of immune complexes. Polymorphonuclear leukocytes from patients with ulcerative colitis and Crohn's disease showed significantly impaired stimulated migration (P less than 0.05), increased adhesiveness (P less than 0.01 in ulcerative colitis, P less than 0.001 in Crohn's disease), and reduced electrophoretic mobility (P less than 0.02 in ulcerative colitis, P less than 0.001 in Crohn's disease) compared with healthy controls. The disease control of patients with rheumatoid arthritis demonstrated reduced stimulated migration (P less than 0.025) but normal adhesion. Preincubating normal cells in inflammatory bowel disease sera suggested that the altered migration and adhesion were due to circulating serum factors. Circulating immune complexes, detected by the C1q PEG binding assay, were present in 12.5% of patients with ulcerative colitis and 30% with Crohn's disease. Direct immunofluorescence of polymorphonuclear leukocytes suggested binding and/or ingestion of complexes in 57% of patients with ulcerative colitis, and 67% with Crohn's disease. There was a direct correlation between positive immunofluorescence and impaired cell migration in ulcerative colitis (P less than 0.05), but no such relationship was found in the other parameters of polymorph function.

Antigen-Antibody Complex↗

PubMed1993

Clinical patterns, natural history, and progression of ulcerative colitis. A long-term follow-up of 1116 patients.

We studied the natural history of ulcerative colitis (UC) by following 1116 patients in whom UC had been diagnosed or confirmed at The Cleveland Clinic Foundation between 1960 and 1983. Data before 1973 were obtained retrospectively. Criteria for inclusion in the study were: a diagnosis of UC confirmed by clinical, radiographic, endoscopic, and histologic examination; disease location that could be defined as one of three categories (proctosigmoiditis, pancolitis, or left-sided colitis); and a follow-up of at least five years (mean = 12.7 years). Mean age at diagnosis was 32 years. Of the 1116 patients, 46.2% (516) had proctosigmoiditis; 36.7% (410) had pancolitis (colitis of the entire large intestine); and 17.0% (190) had left-sided colitis (from the dentate line to the splenic flexure). Early complications (within two years of diagnosis) included colonic hemorrhage (16.7%) and toxic colitis (12.7%). Complications were highest among patients with pancolitis. Surgery was required for 37.6% of the patients. Primary indications for surgery included chronic or intractable disability (40.2%), fulminating medical failure (16.9%), and colonic dilatation (18.4%). At the most recent follow-up, the disease had extended (progressed to a more serious category) in 53.8% of the patients, although 67.2% were asymptomatic and only 37.0% were on medications. Both the final disease destination and the initial diagnosis impacted cumulative colectomy-ileostomy rates. Factors associated with extension were toxic colitis (P < 0.0001); extent of disease at diagnosis (P < 0.0001); joint symptoms (P = 0.0008); younger age at diagnosis (P = 0.06); and severe bleeding (P = 0.07).

Adolescent↗