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PubMed2002

Protective role of appendicectomy on onset and severity of ulcerative colitis and Crohn's disease.

BACKGROUND AND AIMS: Recent studies on appendicectomy rates in ulcerative colitis and Crohn's disease have generally not addressed the effect of appendicectomy on disease characteristics. The aims of this study were to compare appendicectomy rates in Australian inflammatory bowel disease patients and matched controls, and to evaluate the effect of prior appendicectomy on disease characteristics. METHODS: Patients were ascertained from the Brisbane Inflammatory Bowel Disease database. Controls matched for age and sex were randomly selected from the Australian Twin Registry. Disease characteristics included age at diagnosis, disease site, need for immunosuppression, and intestinal resection. RESULTS: The study confirmed the significant negative association between appendicectomy and ulcerative colitis (odds ratio (OR) 0.23, 95% confidence interval (CI) 0.14-0.38; p<0.0001) and found a similar result for Crohn's disease once the bias of appendicectomy at diagnosis was addressed (OR 0.34, 95% CI 0.23-0.51; p<0.0001). Prior appendicectomy delayed age of presentation for both diseases and was statistically significant for Crohn's disease (p=0.02). In ulcerative colitis, patients with prior appendicectomy had clinically milder disease with reduced requirement for immunosuppression (OR 0.15, 95% CI 0.02-1.15; p=0.04) and proctocolectomy (p=0.02). CONCLUSIONS: Compared with patients without prior appendicectomy, appendicectomy before diagnosis delays disease onset in ulcerative colitis and Crohn's disease and gives rise to a milder disease phenotype in ulcerative colitis.

Adult↗

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↗

PubMedDate not supplied

Efficacy of cyclosporin with corticotropin for refractory ulcerative colitis.

BACKGROUND/AIMS: Cyclosporin was reported to be useful for steroid-resistant severe ulcerative colitis in the short term, but limited data are available on the long-term follow-up of such patients. Our aim was to assess the short- and long-term efficacy of combination therapy with cyclosporin and corticotropin for steroid-resistant ulcerative colitis. METHODOLOGY: Twenty-one patients with ulcerative colitis who did not respond to corticosteroid therapy, were treated with corticotropin, and 9 patients (43%) of them achieved complete remission. Twelve patients (57%) who did not achieve complete remission by corticotropin alone were given combination therapy with cyclosporin and corticotropin. RESULTS: In 12 patients who received combined therapy with cyclosporin and corticotropin, clinical severity was distinctly improved in 11 patients (92%) by combination therapy within 2 weeks and 7 patients (58.3%) entered into complete remission with salicylazosulfapyridine or 5-aminosalicylic acid alone. Two patients (16.7%) demonstrated insufficient effect and continue to receive a lower dosage of cyclosporin or corticosteroid. Three patients (25%) failed to respond to the combination therapy and required colectomy. Three of 7 patients who entered into remission relapsed 0.5, 5 and 5.5 months (average: 3.7 months) after cyclosporin withdrawal, but the clinical severity at the time of relapse was milder than that at the beginning of the treatment, namely, moderate in 2 patients, and mild in 1 patient. There were no significant adverse effects in our series. CONCLUSIONS: We demonstrated that oral cyclosporin in combination with corticotropin was highly effective for ulcerative colitis refractory to corticosteroid or corticotropin therapy and severe relapse was uncommon during several years of follow-up.

Adolescent↗

PubMed1999

[Appendiceal lesion in ulcerative colitis].

Recently, there has been a resurgence in the interest of the role of the appendix in ulcerative colitis. The lesion of appendix in ulcerative colitis is reviewed. Surgical studies were mainly reported in western countries and endoscopic studies were mainly reported in Japan. Epidemiological and experimental studies suggest a central role of the appendix in development of ulcerative colitis. It was considered that understanding of the significance of a skip lesion in the appendix would contribute to the elucidation of the pathogenesis of ulcerative colitis.

Animals↗

PubMed2005

Cyclosporine for severe ulcerative colitis.

OBJECTIVE: To evaluate evidence for the use of cyclosporine in treating patients with severe ulcerative colitis. DATA SOURCES: A literature search was performed using MEDLINE, EMBASE, Cochrane Database, and ISI Web of Knowledge (1966-November 2005) with the search terms cyclosporine, cyclosporin A, CsA, ulcerative colitis, UC, inflammatory bowel disease, IBD, steroid-refractory, and immunosuppression. Additional papers were located by hand-searching relevant references. Only human studies in adults and literature published in English were included. DATA SYNTHESIS: Intravenous cyclosporine has been evaluated for the treatment of severe ulcerative colitis in 4 randomized, controlled trials, as well as in many open-label and retrospective studies. Studies that evaluated cyclosporine for severe ulcerative colitis were reviewed. All 4 controlled trials showed an initial positive clinical response as defined by the Crohn's Activity Index when intravenous cyclosporine 4 mg/kg/day was administered as monotherapy or combined with intravenous corticosteroids. One of the 4 trials indicated that high-dose cyclosporine (4 mg/kg/day) has no additional clinical benefit over the low-dose (2 mg/kg/day) and that the lower dose may improve safety related to dose-dependent adverse effects. CONCLUSIONS: There is evidence to support the use of intravenous cyclosporine for patients with severe ulcerative colitis who are refractory to corticosteroid therapy. Because most of the adverse effects associated with cyclosporine are dose dependent, therapy should be initiated with the lower 2 mg/kg/day dose. Subsequent doses should be adjusted based on cyclosporine blood concentrations of 150-250 ng/mL. Cyclosporine should be used only to induce remission and serve as a "bridge" to azathioprine or 6-mercaptopurine maintenance therapy. At this time, there are insufficient data to support the long-term use of cyclosporine monotherapy for avoidance of surgery or maintenance of remission.

Colitis, Ulcerative↗

PubMed1992

[DNA ploidy and dysplasia in ulcerative colitis--interim analysis of a prospective study].

DNA ploidy and cell cycle phases were evaluated by flow cytometry in colonic biopsy specimens from 107 patients with ulcerative colitis in order to analyse the prevalence of DNA aneuploidy as an indicator of numerical chromosomal aberrations and the cell proliferation in all forms of ulcerative colitis. Whereas G2/M-phase fractions in ulcerative colitis and in controls were comparable (2.7 +/- 1.1% vs. 2.8 +/- 1.1%), S-phase fractions in ulcerative colitis exceeded those of controls (7.5 +/- 3.2% vs. 6.5 +/- 2.3%; p < 0.01). In 28 control patients, only diploid DNA histograms existed. Single or multiple aneuploid stem lines were detected in 10 patients with ulcerative colitis (9.3%). Aneuploidy was nearly exclusively associated with pancolitis. Dysplasia was present in 13 patients (indefinite: 8; low-grade: 5), of whom 5 patients also showed DNA aneuploidy. 5 patients with non-dysplastic mucosa exhibited DNA aneuploidy. Because dysplasia and DNA aneuploidy can be discordant and might therefore identify different subgroups at risk, flow cytometry might play a role as a valuable complement to histological examination in surveillance programs of ulcerative colitis.

Adult↗

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↗

PubMed2005

Solitary microcarcinoid of the rectal stump in ulcerative colitis.

A case of solitary microcarcinoid and chronic ulcerative colitis of the rectal stump is described. The association of intestinal carcinoid with ulcerative colitis has been reported previously in 26 patients. Pathogenic pathways are discussed according to the presence of multifocal carcinoid and/or gut endocrine cell hyperplasia.

Adult↗

PubMed1996

Evidence of genetic heterogeneity in IBD: 1. The interleukin-1 receptor antagonist in the predisposition to suffer from ulcerative colitis.

OBJECTIVE: To investigate a polymorphism within intron 2 of the interleukin-1 receptor antagonist (IL-1ra) gene in a Dutch white population of patients with ulcerative colitis and Crohn's disease. DESIGN: Genotype and allele frequencies of the polymorphic region in the IL-1ra gene were determined in 111 unrelated patients with ulcerative colitis, 92 patients with Crohn's disease, and 86 healthy controls. METHODS: The polymorphic region on the IL-1ra gene was amplified by the polymerase chain reaction (PCR). The resultant products were analyzed by electrophoresis on 2% agarose gels and stained with ethidium bromide. Amplification of the second exon of HLA-DRB1, HLA-DQA1, and HLA-DQB1 genes was performed by PCR, and Dot-blot analysis with biotin-labelled sequence-specific oligonucleotide probes was used for HLA typing. The standard perinuclear antineutrophil cytoplasmic antibodies (pANCA) indirect immunofluorescence assay was performed according to the protocol described by the First International Workshop on ANCA. RESULTS: The frequency of allele 2 of the IL-1ra gene in ulcerative colitis (27.0%) and Crohn's disease patients (25.5%) did not differ significantly from healthy controls (23.8%). However, the estimate of the relative risk for carriers of allele 2 for ulcerative colitis [odds ratio (OR): 1.35, 95%-confidence interval (CI) from 0.73 to 2.49] was in agreement with a previous British study. The exact test for homogeneity of odds ratios provided no evidence for heterogeneity between both populations (P = 0.35) and therefore confirmed the genetic associated between ulcerative colitis and the IL-1ra allele 2 in a different population. Our data confirm that, in ulcerative colitis, the presence of this allele is a genetic marker for severity of the disease. A significant association was demonstrated between the carriership of allele 2 of the IL-1ra gene and the trend over the three localizations in ulcerative colitis (P = 0.023). The same approach for Crohn's disease when compared with healthy controls did not provide evidence for a similar association. The meta-analysis, based on the British data and our data, yielded: OR = 1.06, 95%-CI from 0.71 to 1.59, and P = 0.767. No association between IL-1ra gene polymorphism, and pANCA and the HLA-DR2 allele was found in ulcerative colitis.

Alleles↗

PubMed1976

Anergy to dinitrochlorobenzene and depression of T-lymphocytes in Crohn's disease and ulcerative colitis.

Skin reactivity to dinitrochlorobenzene (DNCB) and levels of circulating T-lymphocytes were measured in 15 patients with ulcerative colitis, 15 patients with Crohn's disease, and 12 normal control subjects. Diminished reactivity to DNCB was demonstrated in 87% of patients with Crohn's disease (P less than 0-001) and in 53% with ulcerative colitis (P less than 0-02), as compared with only 8-5% of controls; anergy was more frequent in Crohn's disease than in ulcerative colitis (P less than 0-05). Levels of circulating T-lymphoctes were also depressed in both Crohn's disease and ulcerative colitis (P less than 0-001) as compared with controls, with the values lower in Crohn's disease than in ulcerative colitis (P less than 0-02). There were no correlations of DNCB response with extent, duration, or severity of disease nor with T-cell levels within any patient group. These data provide further support for the concept that there is impairment of cell-mediated immunity among many patients with chronic inflammatory bowel disease, including both Crohn's disease and ulcerative colitis.

Colitis, Ulcerative↗

PubMed1985

Experimental models for ulcerative colitis.

Animal model systems have been used extensively to study both experimental and naturally occurring ulcerative colitis syndromes. Interestingly, despite a variety of different animal species and a broad range of inducing agents, the response of the large intestine has been somewhat predictable. Although there is suggestive evidence for transmissible agents in several of these animal model systems, documentation of a bacterial or viral etiology has remained elusive. Perhaps the best evidence to suggest that bacteria play a role in the development of naturally occurring ulcerative colitis resides in the studies utilizing the rabbit-dinitrochlorobenzine model and the carrageenin-induced ulcerative colitis model in the guinea pig. The evidence for microbial involvement in these model systems includes the use of single bacterial species in the carrageenin model to produce an ulcerative colitis like disease and the use of antimicrobial agents to alter the experimental model system in the guinea pig and hamster with proliferative ileitis and evidence of transmissibility. Recent reports of transmissible agents for both ulcerative colitis and Crohn's disease in studies utilizing immunologically deficient mice also suggest that the search for the "agent" and mechanism should continue in model systems. The many differences between animal model systems and the human disease cannot be ignored. These differences make establishing what appears to be a complicated etiology even more difficult. Despite the difference in anatomy, physiology, and nutritional factors between animal model systems and the human disease process, the fact remains that one or more of these model systems may reflect the same mechanism or etiologic agent which occurs in the human disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1978

[Pathology of ulcerative colitis (author's transl)].

The macroscopic and histological appearance, and the local immune response in ulcerative colitis are discussed. The main criteria for the differentiation between ulcerative colitis and Crohn's disease of the large bowel are reviewed. The risk to develope carcinoma in the large bowel is greater in patients with total ulcerative colitis than in the general population. Precancerous changes in rectal and colonoscopical biopsies are a useful parameter in detecting early cancer in colitis. A description of the morphology of precancerous changes in ulcerative colitis is given.

Biopsy↗

PubMed2003

Resolution of immune thrombocytopenic purpura after colectomy for ulcerative colitis.

A number of different hematologic abnormalities are often encountered in patients with ulcerative colitis. Among them, thrombocytopenia is observed mostly as a side effect of therapy. Immune thrombocytopenic purpura is rarely reported in patients with ulcerative colitis, and various treatment modalities have been used for these two disorders. We report a case with ulcerative colitis and immune thrombocytopenic purpura which were cured after the colectomy. This result suggests that immune thrombocytopenic purpura is the extraintestinal manifestation of ulcerative colitis.

Colectomy↗

PubMed2005

Prevalence, detection rate and outcome of cytomegalovirus infection in ulcerative colitis patients requiring colonic resection.

OBJECTIVE: To determine the prevalence of cytomegalovirus infection in patients with steroid-refractory ulcerative colitis who required colonic resection, and to assess its possible association with the use of immunosuppressive and steroid treatment and outcome after colectomy. PATIENTS AND METHODS: The study included surgical specimens and related pre-operative endoscopic biopsy specimens of 77 consecutive ulcerative colitis patients (34 females) who underwent colectomy because of intractable steroid-refractory ulcerative colitis (55 patients), toxic megacolon (6 patients), dysplasia or cancer (7 patients) or loss of function of the colon (9 patients). Clinical features and current and past treatments were analysed. Haematoxylin and eosin and specific immunohistochemical staining for cytomegalovirus were used to detect inclusion bodies in all specimens. RESULTS: Cytomegalovirus infection was found in 15 of 55 steroid-refractory ulcerative colitis patients (27.3%) and in 2 of 22 non-refractory patients (9.1%) (p=0.123). Only six patients had positive staining for cytomegalovirus in pre-operative endoscopic biopsy specimens. Detection of cytomegalovirus inclusion in biopsy specimens was not related to the number of biopsies or to time that had elapsed since colonoscopy and index surgery. Cytomegalovirus-positive patients were more likely to be on systemic corticosteroids (p=0.03). In contrast, current use and duration of immunosuppressive treatment, number of steroid cycles since diagnosis and in the last year, as well as chronic use of steroid in the last year were not significantly related to cytomegalovirus infection. Cytomegalovirus-positive patients did not receive antiviral therapy following proctocolectomy but did not show endoscopic or histological cytomegalovirus reactivation in the ileo-anal pouch and in the remaining bowel. CONCLUSIONS: Cytomegalovirus infection is frequently found in surgical specimens of patients with steroid-refractory ulcerative colitis and is more likely in patients on corticosteroid treatment. Cytomegalovirus infection is frequently unrecognised in pre-operative biopsy specimens, thus raising concerns about the accuracy of the available diagnostic tools. Unrecognised and untreated cytomegalovirus infection does not affect the outcome of ulcerative colitis patients following proctocolectomy.

Adrenal Cortex Hormones↗

PubMed1999

Phospholipase A2 in serum and colonic mucosa in ulcerative colitis.

Group II phospholipase A2 is involved in the pathogenesis of various inflammatory diseases and in the host defence against bacteria. The enzyme is expressed in the epithelial cells of colonic mucosa in ulcerative colitis. In this study, we measured the concentration of group II phospholipase A2 in serum and colonic mucosa of patients with ulcerative colitis of different severity and of control patients without any inflammatory disease. The activity of ulcerative colitis was assessed by endoscopy. The concentration of group II phospholipase A2 was measured with an immunoassay. The concentrations of group II phospholipase A2 in serum and colonic mucosa were significantly higher in patients with active and inactive ulcerative colitis than in controls. However, the group II phospholipase A2 levels did not separate patients with different disease activity. The concentration of group II phospholipase A2 in colonic mucosa corresponded with the mucosal inflammatory activity (higher in active colonic areas) intra-individually, but not between different patients with ulcerative colitis. Serum group II phospholipase A2 values were above the normal reference range more often than the values of 11 standard laboratory blood tests widely used for the follow-up of inflammatory activity in ulcerative colitis. These results indicate that the concentration of group II phospholipase A2 is increased in serum and colonic mucosa of patients with ulcerative colitis. The clinical value of the measurement of group II phospholipase A2 in the follow-up of ulcerative colitis remains to be clarified.

Adult↗

PubMed1982

Survival with carcinoma arising in mucosal ulcerative colitis.

Adenocarcinoma of the colon is a well-recognized complication of total chronic ulcerative colitis. The incidence increases with time, and the carcinoma arising in chronic ulcerative colitis has developed a bad clinical reputation in terms of aggressive behavior. The survival statistics of patients with cancer arising in chronic ulcerative colitis are compared with statistics for a group of noncolitic patients with equivalent clinicopathologic staging treated at the same institution. When grouped by extended Duke's classification and compared with carcinoma arising without ulcerative colitis, there was no statistical difference in survival rates. The overall results are worse because of a higher percentage of patients with incurable disease at the time of operation. With improved surveillance and methods of detecting premalignant changes, the necessity for prophylactic proctocolectomy should decline.

Adenocarcinoma↗

PubMed2004

Therapy of ulcerative colitis.

PURPOSE OF REVIEW: The past year has brought forth several controversies regarding the treatment of ulcerative colitis along with several potentially important clinical advances. The aim of this review is to provide the practicing gastroenterologist with a summation of these recent developments, with particular emphasis on advances that have already moved toward acceptance into clinical practice. RECENT FINDINGS: Controversies remain regarding the optimal formulations and doses of aminosalicylates. At the same time, the potential for chemoprotective effects in patients using maintenance therapy with mesalamine derivatives has been expanded. In addition, advances in biologic therapy for Crohn disease are beginning to be formally evaluated in ulcerative colitis, although the benefits of anti-tumor necrosis factor therapy in this condition remain to be established. Biologic therapies are beginning to be explored as adjunctive therapy for steroid-refractory ulcerative colitis, where trials of calcineurin inhibitors are also advancing clinical practice for this poor prognostic subgroup of patients. Finally, after surgery for ulcerative colitis, the treatment and prevention of pouchitis has become the one established indication for probiotic therapy. SUMMARY: Despite some inroads into the medical therapy of ulcerative colitis, controversies remain regarding the optimal dosing and delivery systems of the most fundamental therapies, and how to optimize therapy for severe ulcerative colitis. Clinical research will continue to investigate new biologic agents that inhibit tumor necrosis factor and other pro-inflammatory cytokines, and ongoing trials with leukocyte apheresis are currently under way.

Journal Article↗

PubMed2006

Disruption of the p53-p53r2 DNA repair system in ulcerative colitis contributes to colon tumorigenesis.

With ulcerative colitis (UC)-associated tumorigenesis, p53 gene alteration is considered to be a key event. To clarify whether the p53-checkpoint is operating in foci of inflammation and that its disruption is a feature of UC-associated neoplasms, the present immunohistochemical study was conducted. Since accumulation of butyric acid with active UC is associated with apoptosis, effects of in vitro exposure of newly established UC-cancer derived cell lines to organic acids were also assessed. The regulatory subunit of ribonucleotide reductase, p53R2, was found to be localized with p53 in situ, and levels of p53, phospho-p53, p53R2 and inducible nitric oxide synthase were significantly intercorrelated. However, p53R2 expression was clearly reduced with progression through UC-associated dysplasia to carcinoma, demonstrating an inverse relation with p53 overexpression. In vitro treatment with butyrate or propionic acid, but not succinic acid, elicited a positive response in the p53-p53R2 system. Moreover, p53-dependent DNA repair, investigated by radioactive nucleotide incorporation, was induced by butyric acid and inhibited by short-interfering p53 and p53R2 RNAs. Therefore, it was concluded that the p53-p53R2-dependent DNA repair system is constitutively stimulated by butyric acid, which accumulates in UC inflammatory lesions. Since failure of the p53-G(1) checkpoint may cause dysfunction of repair under the influence of butyrate, gene alterations may increase and spread through the genome, leading to tumorigenesis.

Apoptosis↗