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At least 1,261 records · Page 70Linked to original sources
PubMed2007

Results at up to 20 years after ileal pouch-anal anastomosis for chronic ulcerative colitis.

BACKGROUND: Ileal pouch-anal anastomosis (IPAA) is performed routinely for chronic ulcerative colitis. METHODS: Using data from a prospective database and annual standardized questionnaires, functional outcome, complications and quality of life (QoL) after IPAA were assessed. RESULTS: Some 1885 IPAA operations were performed for chronic ulcerative colitis over a 20-year period (mean follow-up 11 years). The mean age at the time of IPAA was 34.1 years, increasing from 31.2 years (1981-1985) to 36.3 years (1996-2000). The overall rate of pouch success at 5, 10, 15 and 20 years was 96.3, 93.3, 92.4 and 92.1 per cent respectively. Mean daytime stool frequency increased from 5.7 at 1 year to 6.4 at 20 years (P < 0.001), and also increased at night (from 1.5 to 2.0; P < 0.001). The incidence of frequent daytime faecal incontinence increased from 5 to 11 per cent during the day (P < 0.001) and from 12 to 21 per cent at night (P < 0.001). QoL remained unchanged and 92 per cent remained in the same employment. Seventy-six patients were eventually diagnosed with indeterminate colitis and 47 with Crohn's disease. CONCLUSION: IPAA is a reliable surgical procedure for patients requiring proctocolectomy for chronic ulcerative colitis and indeterminate colitis. The clinical and functional outcomes are excellent and stable for 20 years after operation.

Adolescent↗
PubMedDate not supplied

Serum paraoxonase 1 activity and malondialdehyde levels in patients with ulcerative colitis.

This study was designed to evaluate the oxidative and antioxidative status in patients with ulcerative colitis by detecting antioxidant enzyme paraoxonase 1 activity together with the level of a well-known marker of oxidative stress, malondialdehyde. Serum paraoxonase 1 activity and malondialdehyde levels were analysed in 30 patients with ulcerative colitis and 30 controls using a spectrophotometric method; correlation analysis was made between these variables. Serum malondialdehyde levels were higher in the ulcerative colitis group (median: 2.5, range: 0.5-9.4 nmol ml(-1)) than among the controls (median:1.1, range: 0.5-2.3 nmol ml(-1); p < 0.001) whereas paraoxonase 1 activities were lower in the ulcerative colitis group (median: 158.4, range: 61.6-264.1 U l(-1)) than in the control group (median: 233.3, range: 114.4-431.0 U l(-1); p < 0.001). There was no correlation between serum malondialdehyde level, paraoxonase 1 activity and disease activity. (1) Increased reactive oxygen metabolites levels in ulcerative colitis may result in a pro-oxidation environment, which in turn could result in decreased antioxidant paraoxonase 1 activity and increased malondialdehyde levels, (2) increased cytokines may be a possible cause of decreased paraoxonase 1 activity and (3) decreased serum paraoxonase 1 activity may be a part of an inflammatory response.

Adult↗
PubMed2005

Long-term treatment with anti-alpha 4 integrin antibodies aggravates colitis in G alpha i2-deficient mice.

Targeted deletion of the heterotrimeric G protein, Galphai2, in mice induces lethal colitis closely resembling ulcerative colitis. In chronic colitis, migration of circulating leukocytes into the intestinal mucosa is partially dependent on alpha4 integrins. In previous studies, short-term administration of anti-alpha4 integrin antibodies has been shown to attenuate intestinal inflammation, and here we elucidate the effect of long-term administration of anti-alpha4 integrin antibodies on colitis in Galphai2(-/- )mice. Long-term blockade of alpha4 integrin significantly increased the severity of colitis in Galphai2(-/-) mice. The inflammation was confined to the colon, associated with increased cancer in situ, destruction of crypt architecture, and increased production of IL-1beta, TNF-alpha and IFN-gamma. Blockade of alpha4 integrin reduced the recruitment of activated T cells to the small intestine. In strong contrast, there were significantly higher numbers of activated T cells in the colonic lamina propria and epithelium, most probably due to in situ proliferation. Furthermore, treatment with alpha4 integrin antibodies induced decreased levels of total IgA and IgG in sera, whereas total IgM levels were unchanged. These new findings may have implications in the understanding of the progression of chronic intestinal inflammation.

Animals↗
PubMed1989

Tumor-associated glycoprotein (TAG-72) expression in ulcerative colitis.

Monoclonal antibody (MAb) B72.3 reactive with the high-molecular-weight (Mr greater than 10(6) tumor-associated glycoprotein (TAG)-72 is being increasingly utilized in vivo and in vitro for a variety of purposes in colon cancer patients. Recent evidence has suggested that the TAG-72 antigen expression may be enhanced in inflammatory bowel disease, particularly ulcerative colitis (Thor et al., 1986a: Cancer Res., 46, 3118-3124). We have utilized 117 paraffin-embedded formalin-fixed colonic specimens from 56 ulcerative colitis patients which demonstrate a spectrum of epithelial abnormalities (reactive atypia, dysplasia, and carcinoma) as well as 11 inflammatory controls to evaluate TAG-72 expression. Our selected patient population all had pan-colitis and demonstrated a generally increasing incidence of dysplasia or carcinoma with duration of disease (20% at 0 to 10 years, 50% at 11 to 20 years, 59% at 21 to 30 years, and 100% at more than 31 years). TAG-72 expression was similar in the control and non-dysplastic colonic epithelia, and increased with low- or high-grade dysplasia as well as carcinomatous lesions (mean cellular reactivities 23.7%, 26.5%, 36.7%, 70% and 84.3%, respectively). Epithelium with low-grade dysplasia exhibited a focal perinuclear, superficial crypt staining (when present). High-grade dysplastic epithelium showed pancytoplasmic, pan-cryptic reactivity. Invasive disease showed cytoplasmic as well as extracellular mucin staining. Biopsies from patients with active disease showed significantly more immunoreactive cells for TAG-72 than patients with quiescent disease. For any given biopsy specimen the percentage of cells reactive did not always correlate with the degree of dysplasia. TAG-72 expression in quiescent disease generally increased with duration of disease, in contrast to active disease which showed no correlation between MAb B72.3 staining and duration of disease. The frequent expression of TAG-72 in actively inflamed colonic mucosa (ulcerative colitis and other colitides) may limit the clinical utility of this antigen for detecting colon cancer in ulcerative colitis patients by serological assay or in vivo radiolocalization techniques. The tendency for TAG-72 expression to correlate with disease duration in patients with quiescent disease and to increase with more severe degrees of dysplasia suggests that the expression of this gene product correlates with the dysplasia-to-carcinoma sequence.

Adolescent↗
PubMed1992

Ulcerative colitis and colon cancer: biology and surveillance.

The risk of colorectal carcinoma is increased among patients with longstanding ulcerative colitis and Crohn's disease. The development of cancer in inflammatory bowel disease is hypothesized to evolve by a multistep process involving genetic instability, clonal expansion and the development of a malignant phenotype. The contribution of nutritional factors such as folate deficiency is of great interest; molecular genetic mechanisms are under study. In contrast to sporadic colorectal carcinoma, carcinomas in ulcerative colitis are associated with a long prior history of chronic inflammation and the subsequent development of epithelial dysplasia. Dysplasia is defined as an unequivocal neoplastic alteration of the colonic mucosa. The object of surveillance is prevention of death from cancer by detection at a premalignant or early curable stage. Patients at greatest risk of cancer who customarily undergo endoscopic surveillance are those with extensive colitis of more than 8 years duration. Dysplastic epithelium may occur in flat mucosa, and may produce a plaque or a nodular/villiform appearance. Dysplasia is not present in all patients with cancer in colitis. It is important to develop more sensitive and specific markers for the presence of precancer or cancer in colitis. Under study are proliferation-associated markers detected by immunohistochemistry, lectin binding, flow cytometry and laser-induced fluorescence coupled with endoscopy.

Carcinoma↗
PubMedDate not supplied

Ultrasound findings in Crohn's disease and ulcerative colitis: a prospective study.

In a prospective study, 118 patients with Crohn's disease, 51 patients with ulcerative colitis, and 72 patients with no disease of the intestine proximal to the rectum were evaluated by ultrasound. In Crohn's disease, thickening of the bowel wall and inflammatory masses were detected in 72.0% of the patients. With a transducer having optimal imaging properties in the near range, these findings were detected in 87.2% of a group of 47 patients. In ulcerative colitis, bowel wall thickening was detected in 52.9% of all patients. Thickening of the bowel wall was more marked in Crohn's disease than in ulcerative colitis. Most pathologic findings in Crohn's disease were located in the right lower abdomen, whereas those in ulcerative colitis were in the left abdomen, in particular in the lower quadrant. The frequency of wall thickening was correlated to the activity of the disease in ulcerative colitis but not in Crohn's disease. Considerably increased wall thickness, when localized in the right lower quadrant and found in combination with inflammatory masses or an abscess, suggests Crohn's disease.

Adolescent↗
PubMed1992

Detection of herpesvirus DNA in the large intestine of patients with ulcerative colitis and Crohn's disease using the nested polymerase chain reaction.

The prevalence of herpesvirus DNA was examined in inflammatory bowel disease tissue. DNA was extracted from resection and biopsy specimens of the large intestine from patients with ulcerative colitis (n = 21), patients with Crohn's disease (n = 29), and patients with noninflammatory bowel disease (controls) (n = 21). The nested polymerase chain reaction was used to detect viral DNA using primer pairs specific for either cytomegalovirus (CMV), herpes simplex virus 1 (HSV1), human herpesvirus 6 (HHV6), varicella zoster virus (VZV), or Epstein Barr virus (EBV). HSV1 and VZV DNA were not detected in any of tissue samples. There was a high prevalence of CMV (81%), HHV6 (76%), and EBV (76%) DNA in ulcerative colitis tissue compared to Crohn's disease tissues (CMV 66%, HHV6 45%, EBV 55%). Control tissue had a relatively low frequency of CMV (29%) and EBV (19%) DNA but a prevalence of HHV6 DNA similar to that of ulcerative colitis (86%). However, the simultaneous presence of HHV6 and CMV and/or EBV DNA in ulcerative colitis tissue (76%) was much greater than in either Crohn's disease tissues (38%) or control tissue (29%) (P < 0.05). There was a low prevalence of CMV, HHV6, and EBV DNA in peripheral blood mononuclear cells from all patient groups. CMV and EBV are capable of reactivating HHV6: the high prevalence of coexistent HHV6 infection with either or both of these two viruses in ulcerative colitis tissue suggests that they may play a synergistic role in the pathogenesis of this disease.

Adolescent↗
PubMed1986

Variation in the argyrophil cell population of the rectum in ulcerative colitis and adenocarcinoma.

Longstanding ulcerative colitis predisposes to carcinoma of the colon. Argyrophil cell hyperplasia has been observed in association with dysplasia and neoplasia in ulcerative colitis. As the argyrophil cell population includes those cells producing enterglucagon, a hormone thought to stimulate mucosal proliferation, this study was designed to determine whether there was any consistent variation in the argyrophil cell population in longstanding ulcerative colitis. Argyrophil cells were demonstrated by the Grimelius method of silver impregnation in sections of non-tumour bearing mucosa from the rectosigmoid colon of normal bowel, ulcerative colitis with and without tumour, and mucosa adjacent to, and distant from, carcinoma arising in otherwise normal bowel. Cell numbers were expressed as ratios of argyrophil cells per crypt, per mm of epithelium, and per mm of underlying muscularis mucosae. There was marked individual variation within all groups in all parameters. Between groups, the only significant difference was an increase in argyrophil cells per crypt in ulcerative colitis. The significance of this finding is discussed.

Adenocarcinoma↗
PubMed1989

Studies on the mechanisms of mucous cell depletion in experimental colitis.

Mucous cell depletion is an important histological discriminator in favour of ulcerative colitis. The mechanism of this change was investigated in guinea pigs with experimental colitis induced by intrarectal instillation of acetic acid or dinitrochlorobenzene (DNCB) in sensitized animals. Both models showed mucous cell depletion. Increased numbers of mucous cells were flash-labelled with tritiated thymidine (3HTdR), indicating an increased pool of proliferating (oligo-) mucous cells; mucous cell production was in fact increased absolutely compared with control animals, and there was a marked increase in the rate of turnover of mucous cells. The results indicate that in colitis there is (i) increased mucous cell production and (ii) an increased rate of mucous cell turnover due to increased loss of older mucous cells. It is concluded that the disease process in experimental colitis leads to premature discharge of mucin, so that mucous cells are no longer recognizable by light microscopy. This explains the increase in mucin production in ulcerative colitis, which occurs even in the presence of significant mucous cell depletion.

Acetates↗
PubMed2000

Immunoglobulin leakiness in scid mice with CD4(+) T-cell-induced chronic colitis.

Inflammatory bowel disease in scid mice is initiated by transplantation of CD4(+) T-cells from immunocompetent syngenic donor mice. As the disease progresses, immunoglobulin (Ig)-containing cells appear in the gut lamina propria, suggesting that locally accumulating Ig may play a role in disease development. In the present work we have investigated the relationship between disease progression and patterns or levels of Ig isotypes in the feces of scid mice suffering from an ongoing colitis. The data clearly showed that the severity or progression of the disease did not influence the levels of IgA, IgG1, IgG2a, IgG2b, and IgG3, whereas the level of fecal IgM increased during the course of colitis. The presence of the serum protein alpha-1-antitrypsin in fecal extracts from diseased mice suggests that some of the fecal Ig has leaked through the inflamed epithelial membrane into the gut lumen. Finally, Ig-containing cells were observed in mesenteric lymph nodes and in the spleen, suggesting that the fecal Ig is produced both systemically and locally in the gut wall. In conclusion, the present results demonstrate that the level of IgM increases as colitis progresses. Also, the five remaining major Ig isotypes are increased in the gut lumen of scid mice with colitis, but the individual Ig types vary randomly during the course of the disease. Thus, it is unlikely that immunoglobulins are involved in the immunopathogenesis of this model of colitis.

Animals↗
PubMed2000

Analysis of cytokine production in the colon of nude mice with experimental colitis induced by adoptive transfer of immunocompetent cells from mice infected with a murine retrovirus.

LP-BM5 murine leukemia virus (MuLV) is known to induce murine AIDS (MAIDS). We have shown that Sjögren's syndrome (SjS)-like exocrinopathy can be induced in mice with MAIDS and that adoptive transfer of spleen cells from MAIDS mice can induce inflammatory bowel disease-like colitis as well as SjS-like exocrinopathy in nude mice. To assess the role of interferon (IFN)-gamma and interleukin (IL)-10 in the pathogenesis of our experimental model, we tried to identify the cells producing these cytokines and their localization in the colitis lesions in situ. Expression of mRNA for IFN-gamma and IL-10 was assessed by RT-PCR, and protein expression of these cytokines was also analyzed in frozen sections of colon by double-color-staining immunofluorescence (IF). An increase of IFN-gamma and IL-10 mRNA was detected in the colon of mice with colitis, but not in that of control mice. Double-color IF showed that Mac-1(+) cells were positive for IFN-gamma or IL-10 and that most CD4(+) T cells were positive for IL-10, although the population of IFN-gamma-positive CD4(+) T cells was low. In our experimental colitis model, Mac-1(+) macrophages that produce both IFN-gamma and IL-10 might play a crucial role in the pathogenesis of colitis in combination with CD4(+) T cells.

Adoptive Transfer↗
PubMed2002

Colitis-related public T cells are selected in the colonic lamina propria of IL-10-deficient mice.

IL-10 is an important regulatory cytokine in the mucosal immune system, as supported by the fact that mice deficient in IL-10 spontaneously develop Crohn's disease-like colitis. An aberrant, Th1-driven CD4(+) T-cell response to enteric bacteria seems to be important in the pathogenesis of this murine colitis. However, no specific bacteria or bacterial products have been identified, and whether the colitis is mediated by the activation of CD4(+) T cells that recognize specific peptide-MHC complexes is controversial. In this study, we analyzed the TCR beta chain complementarity determining region 3 length spectratype of colonic CD4(+) T cells isolated from diseased IL-10-deficient mice by using the Immunoscope technique. Screening of the diseased interleukin-10-deficient mice resulted in a restricted clonotype in TCR V beta 13 and 14 subfamilies of colonic CD4(+) T cells. In contrast, a Gaussian distribution of clonotype of individual TCR V beta subsets was observed in CD4(+) T cells from the peripheral lymphoid tissues. Although individual variability in the disease-related response was also noted in other IL-10-deficient mice maintained in La Jolla and Osaka, perhaps because of different stages of the disease, genetic background, or the housing environment, colitis-related public clones seemed to be shared in all the diseased mice tested. To address whether public clones were involved, we determined the DNA sequence of the clones. Public motifs were shared in colonic CD4(+) T cells from different background interleukin-10-deficient mice with colitis. The frequently found motifs were SXDWG and SATGNYAEQ. These motifs were not seen in the peripheral lymphoid tissues of diseased mice as well as the colon of non-diseased mice. Thus, the common motif may be related to a public gut-derived antigen, which could be important for the development of pathogenic CD4(+) T cells in this inflammatory bowel disease (IBD) model. The selection of V beta-J beta usage is perhaps stochastic in individual mice; however, the epigenetic generation of SXDWG motif by the recombination machinery and selection for this motif in the gut environment could be important for triggering IBD.

Aging↗
PubMed2002

Alteration in expression of beta 2 integrins on lamina propria lymphocytes in ulcerative colitis and Crohn's disease.

We have previously demonstrated by immunohistochemistry that mucosal expression of beta 2 integrins was enhanced in Crohn's disease and ulcerative colitis as compared to normal controls. We aimed, therefore, to determine whether there was a corresponding alteration in the expression of CD11a/CD18 (LFA-1), the primary lymphocyte beta 2 integrin, among the principal subsets of lamina propria lymphocytes (LPLs). Accordingly, LPLs were extracted from surgical resection specimens derived from patients with Crohn's colitis, ulcerative colitis, and from noninflamed controls. Following immunofluorescent staining, three-color flow-cytometry analysis identified LPLs on the basis of CD45 side scatter gating, which in turn, were further subdivided into CD4(+), CD8(+), and CD19(+) cells to account for the predominant T and B cells in the lamina propria. Expression patterns of CD11a, the alpha-subunit of LFA-1; CD18, the beta-subunit of LFA-1; and alpha d, a novel alpha-subunit of the beta 2 integrin family were assessed for each of these lymphocyte subsets. In Crohn's disease and ulcerative colitis there was an increased mean percentage expression of CD4(+) cells and CD11a(+) cells compared with noninflamed controls. CD11a was more likely to be expressed on CD4(+) cells in both Crohn's disease and ulcerative colitis and compared with controls and less expressed on CD19(+) cells. It is likely that an influx of CD4(+)11a(+) cells into the lamina propria accounted for these changes. These results suggest that although currently there is great interest in harnessing alpha 4 beta 7 in treatment of inflammatory bowel disease, further consideration should be given to the role of CD11a in these disease states.

Antigens, CD19↗
PubMed1996

The role of transient mucosal ischemia in acetic acid-induced colitis in the rat.

The importance of early microcirculatory changes in the rat colon after exposure to acetic acid was investigated. Administration of 4% acetic acid for 15 sec into an exteriorized colonic segment induced a marked, transient (starting 2 min after the challenge with acetic acid and persisting for 15 min) decrease in the colonic blood flow as estimated by a laser-Doppler flowmeter. Four days after acetic acid administration, a uniform colitis had developed in the exteriorized colonic segment with a total morphological score (TMS) of 15.1 +/- 0.8, myeloperoxidase activity (MPO) increased more than threefold, and plasma exudation into the colonic lumen increased sevenfold. Administration of hydrochloric acid (HCl) with the same pH as the acetic acid or sodium acetate (pH 7.0) did not affect colonic blood flow or produce colitis. Mechanical colonic ischemia, induced by a controlled increase in the intraluminal pressure, resulted in several pathological features of colitis with a TMS of 7.3 +/- 0.2, combined with a significant increase in MPO activity. The TMS and MPO were further increased when mechanical colonic ischemia was combined with HCl or sodium acetate. Pretreatment with SOD and catalase 5 or 15 min before acetic acid administration did not affect the transient ischemia immediately following acetic acid administration. However, it partially prevented the development of colitis. It is concluded that immediate transient ischemia accompanied by the generation of oxygen free radicals might be of importance in the pathogenesis of acetic acid-induced colitis in the rat.

Acetic Acid↗
PubMed2000

Effect of D-002 on acetic acid-induced colitis in rats at single and repeated doses.

D-002 is a natural mixture of higher aliphatic primary alcohols purified from beeswax, with mild anti-inflammatory and effective antiulcer effects experimentally proved. Furthermore, it reduces leukotriene (LTB(4)) in the exudate of carrageenan-induced pleurisy and has a protective effect on the pre-ulcerative phase of carrageenan-induced colonic ulceration in the guinea pig. This study was conducted to determine the effect of D-002 on acetic acid-induced colitis in rats at single and repeated doses. In a first series, D-002 was orally administered at 25 and 50 mg kg(-1), 24 h before the induction of colitis, meanwhile, in a second series, it was administered 24 h after the induction of colitis. Two other series (III and IV) examined the protective and therapeutic effect of D-002 administered for 7 days at the same doses, before or after colitis induction. Significant reductions in wet weight, macroscopic injury, polymorphonuclear infiltration and wall thickness were observed in colonic mucosa of D-002-treated animals compared with controls in both protective and therapeutic alternatives. It is concluded that D-002 was effective to protect or prevent the damage associated to acetic acid-induced colitis.

Acetates↗
PubMed1992

Development of ulcerative colitis under the immunosuppressive effect of cyclosporine.

In recent studies, cyclosporine has been used for the treatment of both ulcerative colitis and Crohn's disease. The results of these studies were variable. We report on a patient who was treated for 6 years with cyclosporine after kidney transplantation. He developed chronic distal colitis with all the features of ulcerative colitis. An infectious etiology of the colitis was carefully excluded. High-dose treatment with methylprednisolone was required to induce remission. This report shows that immunosuppressive therapy with cyclosporine did not prevent the development of ulcerative colitis in this patient.

Colitis, Ulcerative↗
PubMed1993

Ischaemic colitis and colorectal cancer: some problems and pitfalls.

Four cases out of 204 new cases of colorectal carcinoma seen in a 24 month period were proven to have concomitant proximal ischaemic colitis. Ischaemic colitis associated with obstructing carcinoma of the colorectum may present dramatically with gangrene or colonic perforation if the acute vascular insufficiency is severe. Less severe degrees of ischaemic insult must be recognised intra-operatively as the incorporation of ischaemic colon in a colonic anastomosis may result in an anastomotic leak. Two other patients with ischaemic colitis were wrongly diagnosed as colorectal carcinoma on colonoscopy. Endoscopic features of ischaemic colitis may mimic colonic carcinoma and endoscopic biopsy is essential where any doubt exist as to the possibility of ischaemic colitis so that unnecessary surgery may be avoided.

Aged↗
PubMed1993

Smoking and ulcerative colitis: a community study.

Smoking habits of patients with ulcerative colitis, diagnosed in the City of Cardiff between the 1st of January 1978 and the 31st of December 1987 were examined. There was a significant deficit of current smokers, an excess of life-long non-smokers and ex-smokers compared with the general population. Men who had previously smoked presented with colitis later than life long non-smokers (mean age difference 16.1 years). The proportion of ex-smokers in this group of patients with colitis was more than twice that expected in the general population. The interval between cessation of smoking and subsequent onset of colitis in ex-smokers was relatively short and in more than half of them occurred within 8 years. There was no significant difference in the frequency of colectomy or the extent of disease among smokers, ex-smokers or life-long non-smokers with ulcerative colitis.

Adult↗