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PubMed2006

Visceral pain perception is determined by the duration of colitis and associated neuropeptide expression in the mouse.

BACKGROUND: Even though inflammation is a traditional tool for the induction of hyperalgesia in many tissues, recent observations suggest that not all inflammatory processes produce this change. Tolerance to colorectal distension (CRD) is reduced in patients with acute ulcerative colitis but is increased in patients with chronic inflammatory bowel disease. This suggests that the nature of the inflammatory infiltrate influences visceral perception. AIM: To test this hypothesis by assessing responses to CRD in mice with mild, acute or chronic colitis. METHODS: CRD responses were measured in mice with mild non-specific colitis, and dextran sodium sulphate (DSS)-induced acute and chronic colitis. Responses were compared with tissue infiltrate and damage, interleukin (IL)1beta and myeloperoxidase (MPO) activity and substance P, beta-endorphin and micro opioid receptor (MOR) expression. RESULTS: Mild and acute colitis were associated with increased responsiveness to CRD. In contrast, CRD responses were not increased in mice with chronic colitis and this difference was not due to altered colonic wall compliance. MPO and IL1beta levels were greater in acute than in chronic colitis. Larger increases in tissue substance P were seen in acute than in chronic DSS, whereas CD4 T cells, beta-endorphin and MOR expression were evident only in chronic colitis. An inverse correlation was seen between substance P and MOR in these tissues. CONCLUSIONS: Acute colitis increased responsiveness to CRD and is accompanied by an acute inflammatory infiltrate and increased tissue substance P. Chronic DSS is accompanied by an increase in beta-endorphin and MOR expression, and CD4 T cells, but no change in compliance or CRD responses. We conclude that acute inflammation generates hyperalgesia, whereas chronic inflammation involves infiltration by lymphocytes accompanied by MOR and beta-endorphin up regulation, and this provides an antinociceptive input that restores normal visceral perception.

Acute Disease↗
PubMed1990

Circulating antibodies against human colonic extract enriched with a 40 kDa protein in patients with ulcerative colitis.

We have previously described a 40 kDa colonic protein(s) which is specifically recognised by tissue-bound immunoglobulin G obtained from the colon of patients with ulcerative colitis. We now report the presence of circulating antibodies against this antigen using an enzyme-linked immunosorbent assay with a highly enriched preparation of the 40 kDa protein from normal colon extracts. Serum was collected from 79 patients with ulcerative colitis, 36 with Crohn's disease, 16 with specific diarrhoeal syndromes, and from 19 normal subjects. Twenty nine of 79 patients with ulcerative colitis, 21 of 36 with Crohn's disease, and all patients with diarrhoea were symptomatic during the collection of sera. The difference in optical density values between patients with symptomatic ulcerative colitis and each of the other groups, including patients with ulcerative colitis in remission, was highly significant (p less than 0.01). Seventy nine per cent of patients with symptomatic ulcerative colitis had optical density values above the means for all other groups. Fifty five per cent of sera from patients with symptomatic ulcerative colitis had optical densities beyond two SDs of the values for all other groups and only two of 71 sera from non-ulcerative colitis patients (one Crohn's disease and one normal subject) had values in this range. These results show the presence of anti-colon antibodies against the 40 kDa protein(s) in the sera of many patients with symptomatic ulcerative colitis.

Adolescent↗
PubMed1992

Immunoglobulin G (IgG), IgG1, and IgG2 determinations from endoscopic biopsy specimens in control, Crohn's disease, and ulcerative colitis subjects.

Acute exacerbations of chronic inflammatory bowel disease (ulcerative colitis and Crohn's disease) are characterised by an increase in immunoglobulin G (IgG) positive cells in the mucosa, whereas uninflamed mucosa of inflammatory bowel disease patients displays only moderately increased or normal numbers of these cells. Previous data suggest that acute exacerbations of ulcerative colitis and Crohn's disease can be distinguished by different IgG subclass expression of mucosal immunocytes and a different IgG subclass production pattern of lamina propria lymphocytes. A procedure to obtain enough intestinal mononuclear cells from biopsy specimens to measure in vitro IgG and IgG1 production in control subjects and various patient groups has been established. IgG2 could be measured in Crohn's disease and ulcerative colitis only, as the concentrations in control subjects were below the sensitivity of the ELISA method. We found that IgG and IgG1 production correlated with the degree of local inflammation in both diseases, even in slightly inflamed mucosa, compared with control subjects. The proportion of IgG1 subclass was significantly increased in severely inflamed mucosa of both ulcerative colitis and Crohn's disease patients. A major difference between Crohn's disease and ulcerative colitis mucosa is apparent in mild or no inflammation. In Crohn's disease mucosa in remission, the IgG1/IgG ratio is comparable with that in controls, yet ulcerative colitis mucosa still displays significantly increased proportions of IgG1. In addition, the IgG2/IgG ratio is 0.12 in ulcerative colitis and 0.19 in Crohn's disease patients. The results show the dependence of local IgG and IgG1 production on the degree of inflammation and that an increase in subclass IgG1 in ulcerative colitis is present at all stages, including remission. These findings support the hypothesis that different immunoregulatory mechanisms are involved in Crohn's disease and ulcerative colitis. Environmental stimuli or genetic background may be responsible for the observed differences.

Biopsy↗
PubMed1993

Prevalence and family risk of ulcerative colitis and Crohn's disease: an epidemiological study among Europeans and south Asians in Leicestershire.

The family history of patients identified during incidence studies in Leicestershire were investigated and the prevalence and comparative risks calculated; 1254 patients aged 15 to 80 years were sent a questionnaire about their family history. All cases with a positive family history were reviewed and confirmed cases included in the study. In Europeans the standardised prevalence of Crohn's disease was 75.8/10(5) and that of ulcerative colitis 90.8/10(5). The prevalence of Crohn's disease among South Asians was 33.2/10(5) and that of ulcerative colitis 135/10(5). The prevalence of Crohn's disease in Europeans was significantly greater than that in Hindus (chi 2 = 16, p < 0.001), while the prevalence of ulcerative colitis was significantly lower in Europeans than Hindus (chi 2 = 27, p < 0.001) and Sikhs (chi 2 = 4.4, p < 0.05). The comparative risk of developing ulcerative colitis in first degree relatives of Europeans patients with ulcerative colitis was increased by approximately 15, but the risk of Crohn's disease was not increased. The comparative risk of developing Crohn's disease among first degree relatives of patients with Crohn's disease was increased by up to 35, the comparative risk of ulcerative colitis was approximately 3. The risk among relatives of South Asian patients with Crohn's disease was not increased, but the risk of ulcerative colitis to relatives of patients with ulcerative colitis was. This study supports the view that Crohn's disease and ulcerative colitis arise in people with a genetic predisposition and exposed to some, as yet unknown, environmental factor.

Adolescent↗
PubMed1993

Ulcerative colitis disease activity following treatment of associated primary sclerosing cholangitis with cyclosporin.

Thirty five adult patients with precirrhotic primary sclerosing cholangitis were randomly allocated to treatment for at least one year with low dose (4.1 mg/kg/day) cyclosporin or placebo in a double blind trial. Thirty patients had coexisting ulcerative colitis, including three who had previously undergone colectomy and one who discontinued treatment after three months. Of the remaining 26 patients, 16 received cyclosporin and 10 received placebo. Endoscopy was performed at entry to confirm the diagnosis of inflammatory bowel disease. The ulcerative colitis disease activity was prospectively classified annually as remission/mild, moderate, or severe using the Truelove and Witt's criteria. Before treatment there were no differences between the cyclosporin and placebo groups in the number of patients with remission/mild colitis, 14/16 (88%) v 9/10 (90%), and moderate colitis, 2/16 (12%) v 1/10 (10%). During treatment, a remission/mild disease course was present in 15/16 (94%) v 6/10 (60%), p = 0.05 and a moderate disease course in 1/16 (6%) v 4/10 (40%), p = 0.05. It is concluded that patients treated with cyclosporin for primary sclerosing cholangitis who have coexisting ulcerative colitis have a more benign course of colitis resulting both from improvement of moderately active colitis and from fewer flares of remission/mildly active colitis. These findings suggest that cyclosporin may be of benefit to the colon in patients with ulcerative colitis who are being treated with cyclosporin for primary sclerosing cholangitis.

Adult↗
PubMed1999

Mesenteric blood flow is related to disease activity and risk of relapse in ulcerative colitis: a prospective follow up study.

BACKGROUND: The diagnostic significance of increased splanchnic blood flow in ulcerative colitis is unclear. This prospective study was therefore undertaken to define the role of Doppler sonography in the assessment of disease activity and in the prediction of early relapse. SUBJECTS/METHODS: Splanchnic flowmetry was performed in 76 patients with ulcerative colitis (47 with active disease and 29 in remission), six with infectious colitis, and 13 healthy controls during fasting and 30 minutes after ingestion of a standardised meal. Twenty seven of the patients with ulcerative colitis and all patients with infectious colitis were investigated during the active state as well as in clinical remission and followed up for six months. Flow velocity and pulsatility index (PI) of the superior (SMA) and inferior (IMA) mesenteric arteries and the portal vein were related to clinical (Truelove index), laboratory (C-reactive protein), and endoscopic (Sutherland index) parameters of disease activity. RESULTS: The mean flow velocity of the IMA correlated closest with clinical activity (Truelove, r = 0.41, p<0.005), the PI with C-reactive protein (r = 0.30, p<0.05), and endoscopic activity (r = 0.45, p<0.001). All patients in remission after six months (14/14) or with infectious colitis (6/6) showed an increase in PI of the IMA compared with the initial measurement during active disease (mean increase for ulcerative colitis +36% and for infectious colitis +77%). In contrast, most patients with later relapse or surgery (11/13) had decreased PI during initial remission (mean decrease -12%). The positive predictive value of this index for maintenance of remission was 0.77. Flow variables of the SMA and portal vein displayed weaker correlations. CONCLUSIONS: Flow measurements in the IMA are closely related to clinical and endoscopic disease activity in patients with ulcerative colitis. Repeated measurement of the PI allows estimation of the risk of recurrence.

Adolescent↗
PubMed2003

Lactobacillus GG prevents recurrence of colitis in HLA-B27 transgenic rats after antibiotic treatment.

BACKGROUND AND AIMS: Bacteroides vulgatus induces colitis in gnotobiotic HLA-B27 transgenic (TG) rats while broad spectrum antibiotics prevent and treat colitis in specific pathogen free (SPF) TG rats although disease recurs after treatment ends. Lactobacilli treat human pouchitis and experimental colitis. We investigated if Lactobacillus rhamnosus GG (L GG) can prevent colitis in TG rats monoassociated with B vulgatus and if L GG or Lactobacillus plantarum 299v (LP 299v) can treat established colitis in SPF TG rats and prevent recurrent disease after antibiotics were stopped. METHODS: Germfree B27 TG rats were monoassociated with B vulgatus for four weeks following two weeks of colonisation with L GG or no bacteria. SPF B27 TG rats received oral vancomycin and imipenem for two weeks, or water alone, followed by four weeks of treatment with oral L GG, LP 299v, or water only. Disease activity was quantified by blinded gross and histological scores, caecal myeloperoxidase (MPO) activity, and levels of interleukin (IL)-1 beta, tumour necrosis factor (TNF), transforming growth factor beta, and IL-10. RESULTS: L GG did not prevent colitis in B vulgatus co-associated TG rats or treat established disease in SPF rats. However, L GG but not LP 299v prevented colitis relapse in antibiotic treated rats with reduced gross and histological scores, caecal MPO, IL-1 beta, and TNF whereas caecal IL-10 was increased. CONCLUSIONS: L GG does not prevent colitis in gnotobiotic TG rats or treat established disease in SPF rats, but is superior to LP 299v in the prevention of recurrent colitis. These studies suggest that antibiotics and probiotic agents provide synergistic therapeutic effects, perhaps mediated by altered immunomodulation with selective activity of different lactobacillus species.

Animals↗
PubMed2004

Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity.

The role of nitric oxide (NO) in inflammatory bowel diseases has traditionally focused on the inducible form of NO synthase (iNOS). However, the constitutive endothelial (eNOS) and neuronal (nNOS) isoforms may also impact on colitis, either by contributing to the inflammation or by regulating mucosal integrity in response to noxious stimuli. To date, studies examining the roles of the NOS isoforms in experimental colitis have been conflicting, and the mechanisms by which these enzymes exert their effects remain unclear. To investigate and clarify the roles of the NOS isoforms in gut inflammation, we induced trinitrobenzenesulfonic acid colitis in eNOS, nNOS, and iNOS knockout (KO) mice, assessing the course of colitis at early and late times. Both eNOS and iNOS KO mice developed a more severe colitis compared with wild-type mice. During colitis, iNOS expression dramatically increased on epithelial and lamina propria mononuclear cells, whereas eNOS expression remained localized to endothelial cells. Electron and fluorescence microscopy identified bacteria in the ulcerated colonic mucosa of eNOS KO mice, but not in wild-type, iNOS, or nNOS KO mice. Furthermore, eNOS KO mice had fewer colonic goblet cells, impaired mucin production, and exhibited increased susceptibility to an inflammatory stimulus that was subthreshold to other mice. This susceptibility was reversible, because the NO donor isosorbide dinitrate normalized goblet cell numbers and ameliorated subsequent colitis in eNOS KO mice. These results identify a protective role for both iNOS and eNOS during colitis, with eNOS deficiency resulting in impaired intestinal defense against lumenal bacteria and increased susceptibility to colitis.

Animals↗
PubMed1993

Attenuation of colitis in the cotton-top tamarin by anti-alpha 4 integrin monoclonal antibody.

Recent studies have demonstrated the induced expression of endothelial adhesion molecules including E-selectin (also called endothelial leukocyte adhesion molecule-1), vascular cell adhesion molecule and intercellular adhesion molecule in actively involved mucosa of patients with ulcerative colitis and Crohn's disease. Similar induction has been demonstrated in the colon of the Cotton-top tamarin (CTT), a New World primate that experiences a spontaneous acute and chronic colitis resembling ulcerative colitis. To assess the potential importance of leukocyte adhesion as a necessary step in acute colitis, the effect of parenteral mAb directed against adhesion molecules on CTT colitis was evaluated in placebo-controlled blinded trials. Serial administration of either of two anti-E-selectin mAb designated BB11 and EH8 effectively coated endothelial surfaces expressing this vascular adhesion molecule. Although colitis activity was slightly diminished after the 10-d treatment period in CTT receiving either BB11 or EH8, this reduction was not significantly different than that seen in animals given a placebo control when assessed by a previously validated standardized scale of inflammatory activity: mean histologic activity grade 2.2 +/- 0.2 pretreatment vs 1.5 +/- 0.5 posttreatment in group receiving mAb and 2.1 +/- 0.1 pretreatment vs 1.3 +/- 0.5 posttreatment in the placebo group (P > 0.2). In contrast, administration of an anti-alpha 4 integrin mAb designated HP1/2 that binds VLA4 (alpha 4 beta 1) and presumably alpha 4 beta 7 integrins resulted in significant attenuation of acute colitis when compared to both pretreatment activity index (P = 0.005) and the placebo control group (P < 0.01): mean histologic activity grade 1.6 +/- 0.3 pretreatment vs 0.2 +/- 0.1 posttreatment in the group receiving HP1/2 and 1.8 +/- 0.5 pretreatment and 1.2 +/- 0.2 posttreatment in the placebo control group. These studies using a model of spontaneous colitis in the CTT demonstrate the feasibility of modulation of leukocyte-vascular adhesion and/or other integrin-mediated events possibly including T cell aggregation and T cell-stromal interactions, as well as lymphocyte homing. These results suggest both that these processes are important and possibly essential elements in sustaining acute colitis and that their disruption may result in therapeutic benefit.

Animals↗
PubMed1997

Antiinflammatory effects of human milk on chemically induced colitis in rats.

We examined the effects of a human milk diet on rats with chemical colitis induced with a 4% acetic acid enema. Colonic myeloperoxidase activity was used as a surrogate marker for neutrophil infiltration. Control rats fed rat chow had little colonic myeloperoxidase activity; geometric mean, 0.27 U/g of tissue. Rats with colitis fed rat chow had significantly increased colonic myeloperoxidase activity (geometric mean, 6.76 U/g, p < 0.01 versus no colitis), as did rats with colitis fed infant formula or Pedialyte (geometric mean, 6.92 and 8.13 U/g, respectively, both p < 0.01 versus no colitis). Animals with colitis fed human milk had significantly lower colonic myeloperoxidase activity (geometric mean, 2.34 U/g) than did animals with colitis fed either chow or infant formula (p < 0.001). Similar effects were seen in rats with colitis fed infant formula supplemented with recombinant human IL-1 receptor antagonist (geometric mean, 1.95 U/g). These data show that orally administered human milk has an antiinflammatory effect on chemically induced colitis in rats, which may be mediated in part by IL-1 receptor antagonist contained in human milk.

Acetic Acid↗
PubMed2001

Dextran sodium sulfate-induced colitis in germ-free IQI/Jic mice.

This study presents a histological examination of dextran sodium sulfate (DSS)-induced colitis in germ-free (GF) mice. A comparison of the pathology between GF and conventionalized mice (CVz) was made to determine the role that intestinal microflora play in DSS-induced colitis. To induce colitis, GF and CVz IQI/Jic mice were given either 5% or 1% DSS orally. Administration of 5% DSS, a common concentration used to induce colitis in mice, caused gross rectal bleeding and a marked decrease in hematocrit as early as day one in GF mice. These mice died on day three due to massive bleeding into the intestinal lumen. In contrast, CVz mice did not die during the seven-day experimental period. Histopathological examination three days after administration of 5% DSS did not reveal any colitis lesions in GF mice, but CVz mice had developed moderate colitis in the large intestine. Administration of a low concentration of DSS (1%), which only induces mild basal crypt loss in CVz mice, caused severe colitis in the distal colon in GF mice, and they died on day 14. These data suggest that intestinal microflora are not necessary for the induction of colitis. Furthermore, DSS may be highly toxic to GF mice, and when given at a concentration of 5% it causes massive bleeding into the intestinal lumen resulting in death prior to development of colitis.

Administration, Oral↗
PubMed2005

Beneficial effects of N-acetylcysteine on acetic acid-induced colitis in rats.

Ulcerative colitis is a chronic recurrent inflammatory bowel disease in which oxidative stress has been implicated. The aim of the present study was to evaluate possible protective effects of N-acetylcysteine against acetic acid-induced colitis in a rat model. Rats were administered intrarectal saline (control group) or acetic acid (colitis model group). Rats with acetic acid-induced colitis were treated by intraperitoneal or intrarectal administration of N-acetylcysteine (500 mg/kg) (treated group). Another series of rats were pre-treated by intraperitoneal or intrarectal administration of N-acetylcysteine, then administered intrarectal acetic acid (pre-treated group). The degree of tissue injuries was assessed by macroscopical and histopathological scores of the colonic mucosa. Malondialdehyde, myeloperoxidase, reduced glutathione, superoxide dismutase, and catalase levels were measured in tissue extracts of the dissected colon. Administration of N-acetylcysteine intraperitoneally or intrarectally ameliorated macroscopic score alterations produced by acetic acid in treated groups. In addition, microscopical improvement was observed in all N-acetylcysteine-treated rats compared to untreated animals with colitis. In the colonic tissues of the acetic acid-induced colitis, myeloperoxidase activity and malondialdehyde levels were elevated, while the reduced glutathione levels and superoxide dismutase and catalase activities were decreased. However, intraperitoneal or intrarectal treatment with N-acetylcysteine reversed these parameters, compared to the untreated colitis group. Notably, intrarectal administration of N-acetylcysteine elevated the reduced glutathione levels more markedly compared to the other treatment groups. Superoxide dismutase levels were increased in intraperitoneally or intrarectally N-acetylcysteine-treated groups significantly compared to the control, colitis and pre-treated groups. But there was no significant increase in catalase activity. In conclusion, N-acetylcysteine could be beneficial as a complementary agent in treatment of ulcerative colitis.

Acetic Acid↗
PubMed1997

Serum aminoterminal propeptide of type III procollagen (S-PIIINP) and hepatobiliary dysfunction in patients with ulcerative colitis.

The aim of the study was to estimate the usefulness of measuring the circulating concentration of serum aminoterminal propeptide of type III collagen (S-PIIINP) in screening for hepatobiliary diseases in patients with ulcerative colitis. S-PIIINP was measured in 69 patients with ulcerative colitis and normal liver biochemistry, in 14 patients with ulcerative colitis and elevated catalytic concentration of alkaline phosphatases in serum (S-ALP, EC 3.1.3.1) but without primary sclerosing cholangitis (PSC), and in 20 patients with ulcerative colitis and PSC. The median S-PIIINP was 3.1 micrograms l-1 in patients with ulcerative colitis and normal liver biochemistry, 4.3 micrograms l-1 in patients with ulcerative colitis and hepatobiliary disorder other than PSC and 8.9 micrograms l-1 in those with ulcerative colitis and PSC. When the S-PIIINP cut-off level was set at 5.0 micrograms l-1, 1% of the patients with ulcerative colitis and normal liver biochemistry, 21% of those with hepatobiliary disorder, not PSC, and 90% of the patients with PSC had S-PIIINP values above that concentration. In conclusion, S-PIIINP above 5.0 micrograms l-1 in a patient with ulcerative colitis strongly suggests concomitant PSC.

Adolescent↗
PubMed1991

Temporal changes in the clinical type or diagnosis of Behçet's colitis in patients with aphthoid or punched-out colonic ulcerations.

The intestinal lesion of Behçet's colitis shows aphthoid or punched-out ulceration. However, the diagnosis of Behçet's colitis should be based on the presence of other stigmata of Behçet's syndrome, since these morphological characteristics are not pathognomonic by themselves. Furthermore, the stigmata of Behçet's syndrome could appear simultaneously or separately with intervals of several months to years. Besides, when a physician first meets patients with intestinal ulcerations of aphthoid or punched-out shape, if they do not have any stigma of Behçet's syndrome, the physician has some difficulty in making a diagnosis of Behçet's colitis. The purpose of this retrospective study was to investigate the followings: 1) The upgrade in clinical type of Behçet's colitis with the advance of time. 2) What portion of the patients with aphthoid or punched-out ulcerations, but without any other clinical feature of Behçet's syndrome, could be diagnosed as Behçet's colitis with the advance of time? During the mean follow-up period of 38.2 months, 4 (22.2%) out of 18 patients with Behçet's colitis upgraded their clinical types. In the nonspecific ileocolitis group, who had no major stigma of Behçet's syndrome on their initial visit, 3 (30%) out of 10 patients were subsequently diagnosed as Behçet's colitis during the mean follow-up period of 33.3 months. From these results, we could conclude that in possible or suspicious cases of Behçet's colitis, a more confident diagnosis could be made by close observations for new developments of major stigma of Behçet's syndrome. Even in cases of nonspecific ileocolitis, the diagnosis of Behçet's colitis could be made in a significant number of cases as time goes by.

Adolescent↗
PubMed1996

Association of antineutrophil cytoplasmic antibodies with resistance to treatment of left-sided ulcerative colitis: results of a pilot study.

OBJECTIVE: To determine the frequency of antineutrophil cytoplasmic antibodies with perinuclear staining in patients with treatment-resistant left-sided ulcerative colitis. METHODS: We studied four groups: treatment-resistant left-sided ulcerative colitis, treatment-responsive left-sided ulcerative colitis, ulcerative colitis historical controls, and healthy control subjects. Antineutrophil cytoplasmic antibodies were detected by enzyme-linked immunosorbent assay, and positive results were confirmed by demonstration of a perinuclear staining pattern by indirect immunofluorescence assay. RESULTS: The frequency of perinuclear antineutrophil cytoplasmic antibodies was significantly greater in treatment-resistant left-sided ulcerative colitis (90%) than in treatment-responsive left-sided ulcerative colitis (62%) (P = 0.03) or in ulcerative colitis historical controls (60%). CONCLUSION: The increased frequency of perinuclear antineutrophil cytoplasmic antibodies in treatment-resistant left-sided ulcerative colitis suggests a possible association between these antibodies and relative resistance to medical therapy in patients with ulcerative colitis.

Adolescent↗
PubMed1999

[Tenascin: a simple tool in the diagnosis of collagenous colitis].

BACKGROUND: Collagenous colitis is characterised clinically by chronic, voluminous, watery diarrhoea, and histopathologically by a thickened subepithelial collagen layer and infiltration of the lamina propria with inflammatory cells. In practice, the exact measurement of this subepithelial collagen layer is complicated by its blunt limit, a nonorthogradely affected cell layer and often only focal findings. Immunohistochemically, the subepithelial collagen layer stains positively with the glycoprotein tenascin, a marker for extracellular matrix remodeling. AIM: To assess if immunohistochemical staining with tenascin could be used as a simple and practical tool in the diagnosis of collagenous colitis. METHODS: 86 of the routinely examined colon biopsy specimens with the following initial diagnosis: 33 collagenous colitis, 21 lymphocytic colitis, 15 inflammatory bowel disease (ulcerative colitis or Crohn's disease), 8 unspecific inflammation and 9 without histopathological findings, were incubated with tenascin. They were then evaluated blindly by 5 different investigators (2 senior pathologists, 2 assistant doctors and 1 chief assistant of the laboratory experienced in immunohistochemistry). Each specimen was evaluated semiquantitatively from 0 (for no tenascin-positive subepithelial collagen layer) to 3 (wide, clearly tenascin-positive collagen layer). RESULTS: In specimens with the initial diagnosis "collagenous colitis" the semiquantitatively assessed subepithelial collagen layer was significantly wider than in specimens with other initial diagnosis. Experience and educational level of the investigators did not influence the results. CONCLUSIONS: Immunohistochemical incubation with tenascin is a simple, economical and rapid tool in the diagnosis of collagenous colitis. With the aid of tenascin staining collagenous colitis can be differentiated histopathologically with sufficient accuracy from other colitis.

Biomarkers↗
PubMed2001

[Protective effect of appendectomy on the development of ulcerative colitis. A case-control study].

AIMS: To examine by a case-control study the relationship between appendectomy and subsequent ulcerative colitis development in a French population. METHODS: A total of 150 patients with ulcerative colitis were matched for age (+/- 5 years) and sex, with 150 controls recruited in a preventive medicine center. The following data were collected from medical records and by standardised questionnaire in consultation or by phone: appendectomy and tonsillectomy before the onset of ulcerative colitis, smoking habits and area of residence. RESULTS: The rate of previous appendectomy in patients with ulcerative colitis was 8% (12/150) compared with 30.6% (46/150) in the control group (P=0.001). There was no significant association between ulcerative colitis and tonsillectomy (25.3 and 27.3% in the control and the ulcerative colitis groups, respectively). Smoking was more frequent in the control group (36%) than in the ulcerative colitis group (25.3%) but the difference was not significant (P=0.07). In multivariate analysis, the risk of developing ulcerative colitis was significantly lower after previous appendectomy (odds ratio=0.26; 95% confidence interval: 0.13-0.55; P=7 x 10(-4)). CONCLUSION: Our study confirms the inverse association between appendectomy and subsequent ulcerative colitis, in a French population, after adjusting on smoking.

Adult↗
PubMedDate not supplied

Expression of the Kp43 (CD 94) receptor by natural killer (NK) cells in ulcerative colitis.

BACKGROUND/AIMS: The presence of natural killer cells in the colon mucosa of patients with ulcerative colitis has not been studied, therefore, the study was designed to investigate the densities of cells expressing CD3+, CD4+, CD8+, CD56+ and the new CD94+ in colon mucosa of active and inactive ulcerative colitis patients. METHODOLOGY: Twenty ulcerative colitis patients, 10 with active disease and 10 with inactive disease, and 10 subjects with a histologically normal rectal mucosa were used as patients and controls. Additionally, a subgroup of 6 patients with active proctitis has been studied. Two biopsy specimens from rectal mucosa were taken for all patients and controls. Two biopsy specimens of proximal colon mucosa of the subgroup of 6 patients were also taken. One biopsy was processed for immunohistochemical studies and another for histologic study. RESULTS: The densities of CD3+, CD16+, CD56+ and CD 94+ were significantly increased in active ulcerative colitis patients compared to inactive subjects (P < 0.001). The increase in the CD4+ and CD8+ was not statistically significant. Patients with inactive ulcerative colitis also presented increased numbers of CD3+, CD56+ and CD94+ cells compared to controls (P < 0.001). In the subgroup of proctitis, the densities of cells expressing all the antigens were significantly lower in the normal mucosa compared to the affected colon (P < 0.001). No differences in the number of lamina propria DC1a+ cells between patients and controls were found. CONCLUSIONS: These findings suggest that natural killer cells are increased in active ulcerative colitis subjects and that the affected mucosa of ulcerative colitis patients with inactive disease is in state of "latent" inflammation. On the other hand, the normal looking mucosa from active ulcerative colitis patients does not differ from the mucosa of control subjects. Therefore, it seems that in ulcerative colitis the immunological alterations are limited to the affected mucosa.

Adult↗