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At least 469 records · Page 26Linked to original sources
PubMed2006

Inhibition of Smad7 with a specific antisense oligonucleotide facilitates TGF-beta1-mediated suppression of colitis.

BACKGROUND & AIMS: Defective transforming growth factor (TGF)-beta1 signaling due to high levels of Smad7 is a feature of inflammatory bowel disease (IBD). In this study, we analyzed the effect of reducing Smad7 levels with antisense oligonucleotide on mouse models of colitis. METHODS: Mucosal samples taken from colitic tissue of mice with colitis due to either haptenating reagents (trinitrobenzene sulfonic acid [TNBS] or oxazolone) or to transfer of T cells (SCID transfer colitis) were analyzed for Smad3 and/or Smad7 expression by Western blotting and, in some cases, content of TGF-beta1 by enzyme-linked immunosorbent assay. The effect of oral Smad7 antisense oligonucleotide on mucosal inflammation was assessed. RESULTS: TGF-beta1 levels were increased in the inflamed tissues of mice with colitis induced by either TNBS or oxazolone. Nevertheless, TGF-beta1 did not exert a regulatory effect, probably because TGF-beta1 signaling was blocked, as indicated by the presence of reduced Smad3 phosphorylation and high levels of Smad7. Oral administration of Smad7 antisense oligonucleotide to colitic mice restored TGF-beta1 signaling via Smad3 and ameliorated inflammation in hapten-induced colitis. In addition, Smad7 antisense oligonucleotide had a therapeutic effect on relapsing TNBS-induced colitis but not on cell-transfer colitis. CONCLUSIONS: These data suggest that colitis models associated with high endogenous TGF-beta1 levels and defective TGF-beta1 signaling due to high levels of Smad7 can be ameliorated by down-regulation of Smad7 and by oral administration of Smad7 antisense oligonucleotide. This may represent a new approach to the control of IBD, particularly during active phases when its Smad7 profile resembles that of hapten-induced colitis.

Animals↗
PubMed2001

Familial occurrence of microscopic colitis: a report on five families.

BACKGROUND: The etiology and pathogenesis of microscopic colitis is unknown. Whether genetic predisposition is of importance, as in many other gastrointestinal diseases, is unknown. Familial occurrence of collagenous colitis has earlier been reported only in two families. METHODS: Familial occurrence of microscopic colitis was searched for in a Swedish national microscopic colitis register. RESULTS: Familial occurrence of microscopic colitis was identified in five families. In all families a sister-sister relationship was found. Two sisters with collagenous colitis had been living apart in different Nordic countries for many years before developing the disease. In one pair, the smoking sister had collagenous colitis and the never smoking sister had lymphocytic colitis. CONCLUSIONS: Considering the relative rarity of microscopic colitis, these findings indicate that a genetic predisposition may be of importance.

Adult↗
PubMed1998

The histopathology of nonsteroidal anti-inflammatory drug-associated colitis.

We describe the histologic findings of biopsies performed on specimens from 14 patients with nonsteroidal antiinflammatory drug (NSAID) associated colitis. Thirteen patients had endoscopially patchy colitis with small erosions in different parts of the colon. One patient had diffuse colitis extending from the rectum to the midtransverse colon. Histologically, 8 patients had a mixed inflammatory infiltrate, 4 had predominantly neutrophilic inflammation, and 2 had predominantly lymphocytic inflammation. Seven patients had erosions. Eight patients had crypt architectural disarray, but none had crypt architectural distortion or granulomas. The histology of NSAID-associated colitis is similar in our experience to that of Crohn disease and infectious-type colitis. It shares no features with ulcerative colitis. Given the widespread use of NSAIDs, pathologists should consider NSAID-associated colitis along with Crohn disease and infectious-type colitis in the histologic differential diagnosis of focal active colitis.

Adolescent↗
PubMed1975

Mucosal-cell counts in ulcerative and granulomatous colitis.

Epithelial and connective-tissue cells were counted in rectal mucosal biopsies from 215 patients with ulcerative colitis, 98 patients with granulomatous colitis, and 50 controls. The results were analyzed statistically. Significantly decreased mucous goblet cells were found both in sigmoidoscopically abnormal ulcerative colitis and in granulomatous colitis, and they increased during the healing process. More pyknotic and karyorrhectic epithelial cells occurred in active ulcerative colitis than in granulomatous colitis. Inactive ulcerative colitis still manifested histologic evidence of acute and chronic inflammation, while sigmoidoscopically normal granulomatous colitis biopsies after previous gross rectal disease showed significantly increased macrophages in the lamina propria. Cell counts were valuable for differential diagnosis after the sigmoidoscopic appearance became normal. The acute inflammation of ulcerative colitis, as indicated by neutrophils, was decreased most notably following therapy with prednisone or 6-mercaptopurine. Chronic inflammation associated with fewer plasma cells was decreased after salicylazosulfapyridine as well as either of the other two drugs; macrophages, indicators of healing, increased most after 6-mercaptopurine combined with another anti-inflammatory agent.

Biopsy↗
PubMed1997

Crohn's-like complications in patients with ulcerative colitis after total proctocolectomy and ileal pouch-anal anastomosis.

Total proctocolectomy with ileal pouch-anal anastomosis (IPAA) has become an established surgical procedure for ulcerative colitis. Occasional patients who have undergone IPAA develop persistent or recurrent episodes of pouchitis (chronic pouchitis), from which a subset also develop gastrointestinal and systemic complications that are identical to those seen in Crohn's disease. These complications include enteric stenoses or fistulas in the pouch or pouch inlet segment, perianal fistulas or abscesses, pouch fistulas, arthritis, iridocyclitis, and pyoderma gangrenosum. The development of Crohn's-like gastrointestinal complications in a patient with chronic pouchitis frequently engenders concern that the pathologist misinterpreted the proctocolectomy specimen as ulcerative colitis instead of Crohn's disease. We describe eight patients who developed chronic pouchitis and Crohn's-like complications after IPAA and total proctocolectomy. In each case, concern was voiced about misinterpretation of the proctocolectomy specimen as ulcerative colitis instead of Crohn's disease after the development of the Crohn's-like complications. Preoperatively, all eight patients had characteristic clinical, radiographic, and pathologic features of ulcerative colitis. Review of the pathology specimens indicated that all eight had ulcerative colitis. Crohn's-like complications are most likely related to chronic pouchitis, which probably is a form of recrudescent ulcerative colitis within the novel environment of the pouch. A diagnosis of Crohn's disease after IPAA surgery should only be made when reexamination of the original proctocolectomy specimen shows typical pathologic features of Crohn's disease, Crohn's disease arises in parts of the gastrointestinal tract distant from the pouch, pouch biopsies contain active enteritis with granulomas, or excised pouches show the characteristic features of Crohn's disease, including granulomas. There were no histologic differences in the total colectomy specimens between the eight ulcerative colitis study patients and 16 control ulcerative colitis patients who had a favorable clinical outcome after IPAA surgery groups. Crohn's-like complications and chronic pouchitis does not necessarily imply an incorrect original interpretation of ulcerative colitis by the pathologist.

Adolescent↗
PubMed2001

T cells of the colonic mucosa in patients with infantile colitis.

BACKGROUND: Infantile colitis is a heterogeneous group of disorders, including enterocolitis complicating Hirschsprung disease, allergic colitis, inflammatory bowel disease, and Behçet syndrome. There are limited data concerning the immune responses induced by the inflammation of the intestine in young infants. METHODS: Twenty-four colonic biopsy specimens from 12 infantile colitis patients and 12 age-matched control patients were studied by immunohistologic methods. The authors compared the T cells, their subsets expressing the surface antigens CD8 and CD4, and T-cell receptors alphabeta and deltagamma, and densities of mononuclear and epithelial cells expressing human leukocyte antigen class II antigens. RESULTS: The density of CD3+ intraepithelial lymphocytes (IELs) in the large intestinal specimens was significantly higher (P = 0.036) in colitis patients than in the control group. The majority of the CD3+ IELs were CD8+-expressing cells, and only a minority were CD4+ cells in both groups. T-cell receptors alphabeta+ (P = 0.023) and deltagamma+ (P = 0.027) IELs were observed significantly more frequently in colitis patients than in the control group. In surface epithelium, delta non-disulphide-linked type T-cell receptor (deltaTCS1) IELs were found strikingly more frequently (P = 0.001) in the specimens taken from the colitis patients. Also, the density of the deltaTCS1+ cells in crypts of the large intestine was significantly higher in colitis patients than in the control patients (P = 0.047). CONCLUSIONS: A significant increase of CD3+ lymphocytes in the colonic epithelium of the patients with infantile colitis was noted. This increase involved both T-cell receptor alphabeta-positive and deltagamma-positive IELs. The finding of this study supports the proposal that intraluminal antigens, either microbial or food derived, are important in the pathogenesis of colitis in young infants.

Antibodies, Monoclonal↗
PubMed1992

Colorectal carcinoma in Indian patients with idiopathic ulcerative colitis.

In contrast to reports from Western countries, the incidence of colorectal carcinoma among patients with idiopathic ulcerative colitis is considered to be low in the Indian subcontinent. In order to assess the risk of carcinoma in Indian patients, a retrospective analysis of 436 cases of idiopathic ulcerative colitis seen by us over a period of 12 years was carried out. Eight cases of colitis carcinoma (1.8%) were encountered during the study period. Pancolitis was present in six of them while colitis was of limited extent in two cases. The mean duration of colitis prior to development of carcinoma was 12.1 (range 7-25) years. While four of these patients were on our follow-up list and were diagnosed to have carcinoma at the time of a medical or surgical complication, four others first presented to us with a surgical complication of colitis carcinoma. We conclude that colitis carcinoma is not a rare entity among Indian patients with idiopathic ulcerative colitis. We feel that until proved otherwise, patients with idiopathic ulcerative colitis from the Indian subcontinent should not be denied the benefits of a cancer surveillance programme.

Adult↗
PubMed2001

Characterization of antigen-presenting dendritic cells in the peripheral blood and colonic mucosa of patients with ulcerative colitis.

OBJECTIVE: Increased lymphocyte activation and production of inflammatory cytokines are implicated in the pathogenesis of ulcerative colitis. Because antigen-presenting dendritic cells play a cardinal role in the activation and survival of activated lymphocytes, the aim of the present study was to characterize dendritic cells in ulcerative colitis. DESIGN: This study was designed to compare the phenotypes and functions of peripheral blood dendritic cells among healthy normal volunteers and patients with ulcerative colitis or Crohn's disease. Activated dendritic cells were also localized at the colonic mucosa. METHODS: Peripheral blood dendritic cells were generated from 15 patients with ulcerative colitis, 10 patients with Crohn's disease and 15 healthy control volunteers. The stimulatory capacities of dendritic cells were analysed in an allogenic mixed lymphocyte reaction. Nitric oxide was detected by the Griess method. Single- and dual-colour flow cytometry was employed to study the levels of maturation of dendritic cells. Activated dendritic cells were localized immunohistochemically in the colonic mucosa. RESULTS: In comparison to normal controls, peripheral blood dendritic cells from patients with ulcerative colitis showed significantly increased stimulatory capacities (P < 0.05) and produced significantly higher levels of nitric oxide (P < 0.05). The numbers of activated dendritic cells were also significantly higher in ulcerative colitis (P < 0.05). Mature and activated dendritic cells expressing the CD83 antigen were detected at the inflamed colonic mucosa in patients with ulcerative colitis and Crohn's disease. CONCLUSIONS: Activated and mature dendritic cells may have a role in the induction of an exacerbated immune response in ulcerative colitis. This study provides the scientific and logical basis for blocking the maturation and activation of dendritic cells in ulcerative colitis as a new therapeutic intervention.

Adult↗
PubMed2002

The role of CD40 in ulcerative colitis: histochemical analysis and clinical correlation.

OBJECTIVES: CD40 co-stimulator seems to be implicated in the loss of tolerance against self-antigens in many autoimmune diseases. The evidence suggests that in the pathogenesis of ulcerative colitis there is an activity state against self-antigens of the gut wall and flora. The aim of this study was to analyse the expression of CD40 in ulcerative colitis, comparing it with Crohn's disease and nonspecific inflammation of the colon and to determine whether there is a relationship between its expression and the activity stage of the disease. METHODS: The expression of CD40 in the colonic samples of 51 patients (30 ulcerative colitis, 9 Crohn's disease and 12 nonspecific inflammation) was analysed by immunohistochemistry. Twenty-four patients with ulcerative colitis were scored according to clinical, endoscopic and histological classification. RESULTS: The mean percentage of CD40+ cells per field in the colonic mucosa was: ulcerative colitis 21 +/- 11%, Crohn's disease 24 +/- 9%, nonspecific inflammation 7 +/- 7%. The ulcerative colitis patients were statistically significantly different compared to the patients with nonspecific inflammation (P < 0.005), even when comparing the patients in remission (P < 0.05). The expression in Crohn's disease was similar to that in ulcerative colitis. The expression of CD40 in ulcerative colitis was directly proportional to the state of activity of the disease according to the clinical (P < 0.02), endoscopic (P < 0.01) and histological (P < 0.02) criteria. CONCLUSIONS: The expression of CD40 in the colonic mucosae of patients with ulcerative colitis is significantly increased and is proportional to the state of activity. The results seem to confirm the hypothesis that a loss of tolerance could be involved in the pathogenesis of this disease.

B-Lymphocytes↗
PubMed1999

Cancer risk in collagenous colitis.

Collagenous colitis is a recently described form of chronic inflammatory bowel disease. Other inflammatory bowel disorders are associated with increased risk of colorectal and extracolonic malignancies, but this has not been evaluated in collagenous colitis. Colorectal and extracolonic malignancies were identified in 117 patients with collagenous colitis from the Johns Hopkins Registry. The incidence rates of identified tumors, overall incidence rate of tumors, and overall mortality were then compared with general population through person year analysis with adjustment for population. No cases of colorectal cancer were found in collagenous colitis patients during a mean follow-up period of 7.0 years (range 2-12 years) after the diagnosis of colitis. Two patients developed colorectal cancer prior to the diagnosis of colitis, but no increase in life-time relative risk of colorectal cancer was found (relative risk 0.52; 95% confidence limits 0.05-1.5). An increased relative risk of lung cancer in women (relative risk 3.7; 95% confidence limits 1.0-9.6; p = 0.048) was noted. The relative risk of overall malignancy and overall mortality was not different than the general population. In collagenous colitis patients the life-time relative risk of colorectal cancer and the relative risk after the diagnosis of colitis with a mean observation period of 7 years was not increased. An increase in relative risk of lung cancer in women with collagenous colitis argues for further investigation of the role of smoking and other factors in this disorder.

Age Distribution↗
PubMed2003

Role of NK1.1+ and AsGm-1+ cells in oral immunoregulation of experimental colitis.

NK1.1 and AsGm-1 expressing cells play a role in immunomodulation. Our purpose was to determine the role of NK1.1+ and AsGm-1+ expressing cells in the inflammatory/tolerance paradigm in experimental colitis. Oral tolerance towards colitis-extracted proteins had previously been shown to alleviate experimental colitis. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Oral tolerance was induced via five oral doses of proteins extracted from TNBS-colitis colonic wall. Clinical, macroscopic, and microscopic scores were used for colitis assessment. To evaluate the putative role of AsGm-1 in tolerance induction, depletion of AsGm-1 expressing cells was performed. To evaluate the mechanism of tolerance induction, liver-associated NKT lymphocytes were harvested 14 days following tolerance induction, and cultured with concanavalin A (con A) and colitis-extracted proteins. T cell subsets were measured by flow cytometry. Cytokine expression was measured by intracellular staining and enzyme-linked immunosorbent assay (ELISA). Orally tolerized mice exhibited significant alleviation of the clinical, macroscopic, and microscopic parameters of colitis, with increased CD4+ILA+/CD4+IFNgamma+ lymphocyte ratio, increased IL-4, and decreased IFNgamma and IL-12 serum levels. In contrast, orally fed mice that were AsGm-1 depleted showed evidence of severe colitis. These mice exhibited significant decreased CD4 +IL4+/CD4+IFNgamma+ ratios, and an increase in IFNgamma and IL-12, with decreased IL-4 levels. NKT cells harvested from tolerized mice secreted high levels of antiinflammatory cytokines. In contrast, in nontolerized mice, NKT cells mainly secreted proinflammatory cytokines. In a tolerized environment, both NK1.1 and AsGm-1 expressing cells are essential for disease alleviation. In contrast, in a nontolerized environment, AsGm-1 expressing cells support an antiinflammatory immune paradigm, while NKT lymphocytes support a proinflammatory shift.

Animals↗
PubMed2003

Intractable ulcerative colitis caused by cytomegalovirus infection: a prospective study on prevalence, diagnosis, and treatment.

PURPOSE: Cytomegalovirus infection has been known to complicate ulcerative colitis. This study was designed to elucidate the prevalence and clinical features of ulcerative colitis that might point efficiently to the diagnosis of complicating cytomegalovirus infection in cases of ulcerative colitis. METHODS: The study included 47 consecutive patients diagnosed to have moderate-to-severe ulcerative colitis who were treated on an inpatient basis at our department during a two-year period. A prospective examination for cytomegalovirus antigenemia was conducted in all patients with moderate-to-severe ulcerative colitis to determine the prevalence of cytomegalovirus infection among these patients. Then, the characteristic clinical and endoscopic features of ulcerative colitis complicated by cytomegalovirus infection were investigated by comparison of the cytomegalovirus-infected group with the non-cytomegalovirus-infected group. The therapeutic effects of antiviral drugs also were assessed. RESULTS: Cytomegalovirus infection was detected in 16 of 47 patients (34 percent). Proportion of female patients, age at the time of determination, and proportion of patients showing corticosteroid resistance was significantly higher in the cytomegalovirus-infected group (59.1 percent) than in the non-cytomegalovirus-infected group (13.6 percent). The prevalence of endoscopically severe ulcerative colitis was higher in patients with cytomegalovirus antigenemia than in those without cytomegalovirus antigenemia (P = 0.016). Ganciclovir was administered to 12 of 16 ulcerative colitis patients with complicating cytomegalovirus infection, and was found to be effective in 8 (66.7 percent). CONCLUSIONS: It is not easy to make a diagnosis of cytomegalovirus infection complicating ulcerative colitis based on clinical features, including endoscopic biopsy. On the other hand, blood examination for the detection of cytomegalovirus antigenemia in corticosteroid-resistant patients, particularly in relatively elderly patients, may enable diagnosis of cytomegalovirus infection with a high sensitivity and allow effective treatment to be administered in these patients.

Adult↗
PubMedDate not supplied

Microscopic colitis: pathologic considerations, changing dogma.

Microscopic colitis as an entity was first recognized in 1976, and has become one of the most frequent diseases to exclude on colonic mucosal biopsies. In some pathology practices, up to 30% of colonic biopsies received are from patients in whom microscopic colitis is the clinical question. In this review, the evolution of the terminology and early studies describing the pathology of microscopic colitis are discussed. The pathology of lymphocytic and collagenous colitis is reviewed in detail, including common diagnostic pitfalls, and what is currently known about the pathogenesis of these diseases. The differential diagnosis of microscopic colitis includes other idiopathic inflammatory bowel diseases (Crohn's and ulcerative colitis), infections, and drug reactions. The distinction between these entities and microscopic colitis is discussed in detail. Finally, recent studies have revealed new histopathologic changes in microscopic colitis that challenge the currently held concepts of how microscopic colitis fits into the spectrum of inflammatory bowel diseases.

Colitis↗
PubMedDate not supplied

Seasonal pattern of onset in lymphocytic colitis.

BACKGROUND: The etiology of lymphocytic colitis, a microscopic colitis syndrome, has remained elusive. Because 1) many infectious enteritides exhibit seasonal variability in incidence and 2) a few investigators have proposed some infectious mechanism in lymphocytic colitis, our aim was to determine if any variability in symptom onset existed among lymphocytic colitis patients diagnosed at our institution. STUDY: We identified 71 nonduplicated, consecutive patients with lymphocytic colitis over a 4-year period using rigorous clinicopathologic inclusion criteria: 1) chronic watery diarrhea, 2) endoscopically normal colon, 3) no evidence for celiac sprue or drug-induced colitis, 4) diffuse colitis with increased intraepithelial lymphocytes of at least 10 lymphocytes per 100 epithelial cells, 5) evidence of surface epithelial damage, and 6) no significant neutrophilic infiltrates, architectural distortion of the mucosa, or subepithelial collagen deposits. The date of diagnosis was corrected for month of onset of symptoms. RESULTS: The distribution of month of onset of symptoms showed a statistically significant (chi test of homogeneity, P = 0.0008) temporal variability and seasonal incidence pattern with excess cases during summer and fall and a paucity of cases during colder months. CONCLUSIONS: To our knowledge, this is the first study to examine systematically and report a significant seasonal incidence pattern of lymphocytic colitis. Our observations may support a potential link to an infectious source in lymphocytic colitis.

Adult↗
PubMed2006

Basiliximab for the treatment of steroid-resistant ulcerative colitis: further experience in moderate and severe disease.

BACKGROUND: Preliminary data have suggested that interleukin-2 receptor blockade with basiliximab may increase steroid sensitivity. We have previously reported a small case series demonstrating the potential of basiliximab as a novel agent for the treatment of steroid-resistant ulcerative colitis. AIM: To report further experience of the efficacy and safety of treatment with the interleukin-2 receptor blocking monoclonal antibody basiliximab, in addition to steroids, for the treatment of severe and moderate steroid-resistant ulcerative colitis. METHODS: Twenty patients were enrolled - 13 patients with moderate steroid-resistant ulcerative colitis (Ulcerative Colitis Symptom Score: >or=6) and seven patients with severe steroid-resistant ulcerative colitis. All were given a single dose of 40 mg basiliximab plus standard steroid therapy in an open-label, uncontrolled trial. Primary end point was clinical remission within 8 weeks (Ulcerative Colitis Symptom Score: <or=2). RESULTS: Within 8 weeks, 10 of 20 (50%) patients achieved clinical remission (seven of 13 moderate, and three of seven severe). At 24 weeks, 13 of 20 (65%) patients were in clinical remission. Five patients required colectomy (four severe, one moderate ulcerative colitis) and one required rescue ciclosporin (moderate ulcerative colitis). Two patients developed herpes zoster, but treatment was generally well tolerated. CONCLUSIONS: Basiliximab appears to promote prolonged remission after a single treatment. Taken in combination with previously reported data, basiliximab shows particular promise in moderate steroid-resistant ulcerative colitis.

Adolescent↗
PubMed1999

Ischemic colitis associated with pseudoephedrine: four cases.

OBJECTIVE: There is one previously reported case linking ischemic colitis and orally administered nasal decongestants containing pseudoephedrine (MEDLINE 1974-1998). We aimed to document an association between pseudoephedrine ingestion and ischemic colitis. METHODS: We reviewed the cases of four women (ages, 37-50 yr) who presented with the sudden onset of colicky abdominal pain followed by hematochezia. Three patients had used medicine containing pseudoephedrine daily for approximately 1 wk before admission. The fourth patient had used pseudoephedrine chronically for 6 months. Two patients had no significant past medical history. One woman had presented 6 months earlier with ischemic colitis while taking both pseudoephedrine and hormone replacement therapy. This time she presented with ischemic colitis while not taking hormone replacement therapy, but still taking decongestants. Another woman had a history of ulcerative colitis, which had been quiescent for 10 yr. One patient had been a smoker; however, like the other patients she had no evidence of systemic vascular disease. On colonoscopy, all four patients had colitis, primarily affecting the splenic flexure in the anatomical watershed area. Other causes of segmental colitis, including infectious colitides, pseudomembranous colitis, and Crohn's disease, were not evident. Colonoscopic biopsies were consistent with ischemic injury. RESULTS: All cases responded to abstinence from pseudoephedrine and medical supportive therapy. None has had a relapse since discontinuing the pseudoephedrine (8-12 months). CONCLUSIONS: The vasoconstrictive action of pseudoephedrine may predispose susceptible patients to develop ischemic colitis in the watershed area of the splenic flexure. Perimenopausal women may be especially susceptible because of irregular ovulation. This may result in relative vasoconstriction when estrogen levels are low or a hypercoagulable state when estrogen levels are excessive.

Adult↗
PubMed2002

Appendectomy protects against the development of ulcerative colitis but does not affect its course.

OBJECTIVES: Appendectomy has been shown to protect against the development of ulcerative colitis. The objective of this study was to examine the effect of appendectomy on the clinical features and natural history of colitis. METHODS: A total of 259 consecutive adults patients with ulcerative colitis were studied. Of the patients, 20 had undergone appendectomy (12 before onset of colitis and eight after diagnosis). RESULTS: The frequency of appendectomy was significantly less than in a group of 280 controls, which comprised partners of the patients and a group from the community (OR = 0.25; 95% CI = 0.14-0.44). This was even more significant if only the 12 patients who underwent surgery before the onset of colitis were considered (OR = 0.15; 95% CI = 0.07-0.28). Patients with prior appendectomy developed symptoms of ulcerative colitis for the first time at a significantly later age than those without appendectomy (42.5 +/- 6.5 vs 32.1 +/- 0.8 yr; p < 0.01) or those who had appendectomy after the onset of colitis (24.6 +/- 3.4 yr; p < 0.05). Appendectomy did not influence disease extent, need for immunosuppressive treatment with azathioprine or 6-mercaptopurine (as a marker of resistant disease), or the likelihood of colectomy. Five patients in the appendectomy group had clinical evidence of primary sclerosing cholangitis (25%). This was more common than in those without appendectomy (8%; OR = 4.09; 95% CI = 1.04-13.60). CONCLUSIONS: These results indicate that although appendectomy may delay onset of colitis, it does not influence its course. However, it is associated with the development of primary sclerosing cholangitis. Appendectomy is unlikely to be of benefit in established ulcerative colitis.

Adolescent↗
PubMed2004

Appendicectomy has no beneficial effect on admission rates in patients with ulcerative colitis.

BACKGROUND AND AIMS: Those who have had an appendicectomy have a reduced risk of developing ulcerative colitis. However, the effect of appendicectomy on disease activity in patients with ulcerative colitis has not been established. METHODS: We used the Danish National Patient Registry to identify all incident cases of ulcerative colitis in Denmark during the period 1981 to 1999. Of these, 202 had an appendicectomy after their first admission with ulcerative colitis. In these patients, we compared the incidence rate of hospitalisations with ulcerative colitis as first diagnosis during the period between the onset of ulcerative colitis and appendicectomy, with the rate of such hospitalisations after appendicectomy. To adjust for the clinical course of ulcerative colitis unrelated to appendicectomy, we extracted a reference cohort (n = 808), matched to the index subjects with respect to age, sex, and year of first admission, but with an intact appendix. RESULTS: The rate of admission with ulcerative colitis as first diagnosis decreased by 47% after appendicectomy (rate ratio 0.53 (95% confidence interval (CI) 0.36-0.80)). However, the reference cohort showed a similar decline in admission rate (rate ratio 0.51). Thus appendicectomy had no apparent beneficial effect on admission rate after adjustment for the clinical course of disease unrelated to appendicectomy (adjusted rate ratio 1.05 (95% CI 0.67-1.67)). CONCLUSIONS: Appendicectomy had no significant beneficial effect on admission rates in patients with ulcerative colitis.

Adult↗