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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↗
PubMed2005

Patient defined dichotomous end points for remission and clinical improvement in ulcerative colitis.

BACKGROUND AND AIMS: Ulcerative colitis disease activity indices offer good statistical power but small changes in these indices may not be clinically important. There are no validated definitions of remission or of significant improvement for these indices. The use of clinically important end points would strengthen the validity of study outcomes. Our aims were to identify objective end points in standard disease activity indices for remission and for improvement in ulcerative colitis. METHODS: Sixty six consecutive patients with ulcerative colitis provided information about remission status and their disease activity. At a return visit 1-14 months later, these patients provided information about the change in their disease activity, and non-invasive indices were measured. RESULTS: Specific objective end points for determining remission with four standard indices and a quality of life instrument were determined (St Mark's <3.5, ulcerative colitis disease activity index <2.5, simple clinical colitis activity index (SCCAI) <2.5, Seo <120, and inflammatory bowel disease quality of life index (IBDQ) >205). These cut offs also identified patients who met a regulatory definition of remission. Specific objective end points for clinical improvement in two non-invasive indices and a quality of life instrument were determined with good sensitivity and specificity (SCCAI decrease >1.5, Seo decrease >30, IBDQ increase >20). CONCLUSIONS: We found specific cut off values for disease activity indices that identify patients who have significantly improved or achieved remission in an objective, sensitive, and specific manner. These cut offs should help in the interpretation of the outcomes of clinical trials in ulcerative colitis.

Adult↗
PubMed2006

Sporadic adenoma in ulcerative colitis: endoscopic resection is an adequate treatment.

BACKGROUND AND AIMS: In studies with small numbers of cases, it has been shown that endoscopic resection of adenomas in ulcerative colitis represents adequate treatment. In a larger study cohort with more prolonged follow up, we assessed the reliability of this finding. METHODS: Between 1988 and 2002, 148 consecutive patients, mainly from private gastroenterologists' practices, with ulcerative colitis were diagnosed as having an adenoma. In 60 patients, histological diagnosis was established in biopsies and in 87 patients in polypectomy specimens; one patient underwent proctocolectomy following diagnosis. The outcome of these patients was analysed after a mean follow up period of 6.0 (3.63) years. RESULTS: Among 60 patients, surprisingly without endoscopic treatment, 48.3% developed ulcerative colitis associated neoplasia in the same colon segment (23.3% low grade intraepithelial neoplasia; 8.3% high grade intraepithelial neoplasia; 16.7% carcinoma). Among 87 patients undergoing polypectomy of the adenoma, follow up revealed colitis associated neoplasia in other segments of colon in 4.6% of cases. CONCLUSION: Development of adenocarcinomas in a total of 6.7% of the overall patient group, and in 2.3% of those undergoing polypectomy, indicates that biopsy based diagnosis of an adenoma in ulcerative colitis must be considered to mandate endoscopic resection of the lesion; 40% of affected patients did not receive any form of endoscopic removal of the lesion. This shows that the most recent guidelines are not followed in a considerable number of patients with ulcerative colitis in private practice in Germany. Although polypectomy of the adenoma represents adequate therapy, further regular follow up examinations are nevertheless necessary.

Adenocarcinoma↗
PubMed2006

Angiogenesis blockade as a new therapeutic approach to experimental colitis.

BACKGROUND: Neoangiogenesis is a critical component of chronic inflammatory disorders. Inhibition of angiogenesis is an effective treatment in animal models of inflammation, but has not been tested in experimental colitis. AIM: To investigate the effect of ATN-161, an anti-angiogenic compound, on the course of experimental murine colitis. METHOD: Interleukin 10-deficient (IL10(-/-)) mice and wild-type mice were kept in ultra-barrier facilities (UBF) or conventional housing, and used for experimental conditions. Dextran sodium sulphate (DSS)-treated mice were used as a model of acute colitis. Mice were treated with ATN-161 or its scrambled peptide ATN-163. Mucosal neoangiogenesis and mean vascular density (MVD) were assessed by CD31 staining. A Disease Activity Index (DAI) was determined, and the severity of colitis was determined by a histological score. Colonic cytokine production was measured by ELISA, and lamina propria mononuclear cell proliferation by thymidine incorporation. RESULT: MVD increased in parallel with disease progression in IL10(-/-) mice kept in conventional housing, but not in IL10(-/-) mice kept in UBF. Angiogenesis also occurred in DSS-treated animals. IL10(-/-) mice with established disease treated with ATN-161, but not with ATN-163, showed a significant and progressive decrease in DAI. The histological colitis score was significantly lower in ATN-161-treated mice than in scrambled peptide-treated mice. Inhibition of angiogenesis was confirmed by a significant decrease of MVD in ATN-161-treated mice than in ATN-163-treated mice. No therapeutic effects were observed in the DSS model of colitis. ATN-161 showed no direct immunomodulatory activity in vitro. CONCLUSION: Active angiogenesis occurs in the gut of IL10(-/-) and DSS-treated colitic mice and parallels disease progression. ATN-161 effectively decreases angiogenesis as well as clinical severity and histological inflammation in IL10(-/-) mice but not in the DDS model of inflammatory bowel disease (IBD). The results provide the rational basis for considering anti-angiogenic strategies in the treatment of IBD in humans.

Acute Disease↗
PubMed1980

Abnormal gastrocolonic response in patients with ulcerative colitis.

The purpose of these studies is to determine the colonic myoelectrical and contractile response after eating a 1000 calorie meal in patients with active ulcerative colitis. During fasting, slow waves are identifiable significantly more in patients with ulcerative colitis than in normal subjects (p < 0 . 01). The predominant slow wave frequency is 6 . 1 +/- 0 . 2 cycles/min, which is similar to the normal subjects. The slow waves are not altered by eating in either group. Minimal spike or contractile activity occurs during the fasting period both in patients with ulcerative colitis and in normal subjects. In patients with ulcerative colitis, spike activity increases rapidly after eating the 1000 calorie meal (P < 0 . 01), but the maximal response is decreased and shorter in duration than in normal subjects. There is no simultaneous increase in colonic contractility above fasting levels after the meal in patients with ulcerative colitis. This is strikingly different from the simultaneous increase in contractile and spike activity (P < 0 . 01) that occurs after eating in normal subjects. These studies suggest that in ulcerative colitis (1) the colonic smooth muscle slow wave activity is intact; and (2) a disturbance in the normal colonic contractile response to eating is present despite an adequate spike response. This lack of colonic contractility may contribute to the increase in diarrhoea that occurs in these patients after eating.

Adult↗
PubMed1980

Ulcerative colitis and pregnancy.

A survey has been made of pregnancy occurring in patients who were attending the Ulcerative Colitis Clinic at Oxford during the 20-year period, 1960-79 inclusive. There were 256 married women of child-bearing age who attended during this period. Of these, 100 were excluded from the survey for various reasons, such as that they had completed their family before the onset of the ulcerative colitis, had already had an hysterectomy, or had a proctocolectomy before their first pregnancy. Of the remaining 156 patients, nine could not be traced. Full details were obtained from 147 patients, virtually all of whom were interviewed. The fertility of these patients was normal. Of the 147 women, 119 (81%) had conceived and only 10 (6.8%) were involuntarily infertile. The size of family approximated to that found in the general British population. The overall outcome of the pregnancies was similar to that in the general British population. The patients in whom the disease was quiescent at the start of pregnancy fared particularly well. Those with active disease had a somewhat lower chance of producing a normal live baby. The small group of patients in whom the disease was severe had a much lower chance of a normal outcome. Patients in whom the ulcerative colitis was quiescent at the beginning of pregnancy had a good chance of remaining symptom-free throughout the pregnancy and puerperium. Even if the colitis recurred, it was likely to be mild and responsive to medical treatment. By contrast, when the ulcerative colitis was active at the start of pregnancy, most patients continued to have symptoms in spite of medical treatment. Some patients had their first attack of ulcerative colitis during pregnancy or the puerperium. In contrast to previous experience the attacks were generally mild and responded to medical treatment. Medical treatment with corticosteroids or sulphasalazine appeared to have no obvious deleterious effects on the fetus or new-born child.

Adrenal Cortex Hormones↗
PubMed1981

Dinitrochlorobenzene-induced colitis in the guinea-pig: studies of colonic lamina propria lymphocytes.

Dinitrochlorobenzene-induced colitis in guinea-pigs may be immunologically mediated: animals must be presensitised to dinitrochlorobenzene to develop colitis, sensitivity can be passively transferred by lymphocytes and the injury can be mitigated by immunosuppression. In this study, we examined lamina propria lymphocytes isolated from colons of animals with dinitrochlorobenzene-induced colitis, and appropriate controls. Lamina propria lymphocytes from colitis animals have a greater percentage of rabbit erythrocyte-rosetting cells (T cells) (20.1 +/- 3.0 vs 2.3 +/- 0.8, p less than .01) and a greater capacity to mediate mitogen-induced cellular cytotoxicity with phytohaemagglutinin than lamina propria lymphocytes from normal colon (% specific cytoxicity = 29.4 +/- 8.7 vs 5.0 +/- 4.5, P less than .005). There was no difference in the percentage of rosetting cells or cytotoxicity index of spleen or mesenteric lymph node lymphocytes between the colitis animals and controls. These data suggest that there are changes in the distribution and functional characteristics of lamina propria lymphocytes which correlate with mucosal cell injury in the dinitrochlorobenzene-colitis model.

Animals↗
PubMed1982

Cancer morbidity in ulcerative colitis.

Cancer morbidity at all sites has been studied in a series of 676 patients with ulcerative colitis under long-term review, of whom more than two-thirds had extensive disease, and the level and pattern of risk over time examined. Age-, sex-, and site-specific incidence rates were used to compute the number of cancers that might have been expected to occur. A highly significant excess of cancers was observed overall but the excess was due entirely to cancers of the digestive system. In women there was no excess or deficit of cancers outside the digestive system. In men there was a small deficit of cancers of the respiratory system. An overall 11-fold excess colorectal cancer risk was found in the series compared with that in a relevant general population after patient-years at risk had been corrected for surgical resection and patients with colorectal cancer at their first referral had been corrected for surgical resection and patients with colorectal cancer at their first referral had been excluded. When these data were expressed in an actuarial form the cumulative probability of developing colorectal cancer in the series was 8% (3.5-13%) at 25 years, after the diagnosis of ulcerative colitis had been established. The relative risk of developing colorectal cancer was highest in those patients developing colitis before the age of 30 years, and the relative risk fell as the age at diagnosis of their colitis increased. The pattern of risk of colorectal cancer over time suggests that there is an association between cancer and colitis in susceptible individuals and that the level of risk is related to age at onset of colitis.

Adult↗
PubMed1987

Chronic ulcerative colitis: incidence and prevalence in a community.

Utilising the population based data resources of the Rochester Epidemiology Project, we determined the incidence and prevalence of chronic ulcerative colitis among Rochester, Minnesota, residents over the 20 year period, 1960-79. One hundred and thirty eight cases met diagnostic and residency criteria, for an overall age, and sex adjusted chronic ulcerative colitis incidence rate of 15.0 per 100,000 person years. The male:female ratio of age adjusted rates was 1.5:1. Age specific incidence was roughly bimodal in appearance but was not consistent in different patient subgroups. On 1-1-80, there were 120 Rochester residents with a history of chronic ulcerative colitis, corresponding to a prevalence rate of 225.2 per 100,000 population. Fifty three per cent of chronic ulcerative colitis incidence cases were 'definite' and 47% were 'probable', the former requiring consistent observations for at least six months. The definite group had proportionately more men and disease of greater extent and severity. Pancolitis comprised about one-third of all cases (4.6 per 100,000 person years). Proctitis and distal disease (7.1 and 2.0 per 100,000 person years) made up most of the rest. One-fourth of all patients had 'severe' or 'moderate' disease (3.8 per 100,000 person years), while the remainder had either 'mild' or 'transient' chronic ulcerative colitis (11.2 per 100,000 person years). In residents of Rochester, Minnesota, chronic ulcerative colitis is most often a mild disease. The over-representation of severe or complicated examples that results from selected referral to major centres probably distorts the natural clinical spectrum of the disease.

Adolescent↗
PubMed1988

Ulcerative colitis--a disease characterised by the abnormal colonic epithelial cell?

The leakiness of the cell membranes of colonic epithelial cells isolated by the collagenase/Dispase technique from normal or diseased colons was assessed in a 4 h 51Cr release assay. Cells from normal, adenoma bearing or cancer bearing colons showed 51Cr release of 8% or less in almost all of 46 cell populations tested. In contrast, cells from mucosa affected by ulcerative colitis [11.9 (4.3%) n = 23] or Crohn's disease [8.4 (2.7%) n = 18] released significantly more 51Cr than the non-inflamed groups. Values are expressed as mean (SD). Overall, release values were greater in ulcerative colitis than Crohn's disease (p less than 0.01). In Crohn's disease, cells obtained from histologically inflamed mucosa released significantly more 51Cr [9.7 (2.5%) n = 11] than those from non-inflamed mucosa [6.4 (1.5%) n = 7, p less than 0.02] whereas, in ulcerative colitis, abnormal release values were found in 8 of 13 cell populations isolated from mucosa showing no histological evidence of active disease. In five patients with distal ulcerative colitis, cells from mucosa not apparently involved demonstrated normal 51Cr release in four of five studies despite abnormal release from cells from involved mucosa suggesting that a diffuse abnormality of the colonic epithelial cell is not usually present. These data indicate that chronic mucosal inflammation per se is associated with abnormalities of the colonic epithelial cell but that, in ulcerative colitis, the abnormality remains in many patients with quiescent disease. Identification of the local factors responsible for such an abnormality may contribute to an understanding of the pathogenesis of ulcerative colitis.

Adolescent↗
PubMed1990

Ulcerative colitis: one disease or two? (Quantitative histological differences between distal and extensive disease).

Cell counts and measurements of mucosal architecture were made on rectal biopsies from nine patients with total colitis, eight with left sided colitis, 15 with distal colitis, and 11 with proctitis. The mean total lamina propria cell count in proctitis and distal colitis approached twice that of extensive left sided and total colitis (p less than 0.001) and in distal proctocolitis the cell numbers are further increased in the chronic over the acute phase. This difference was not explained by age, duration, activity, or treatment. The predominantly increased lymphoid and mononuclear cell infiltrate in distal proctocolitis indicates a different pattern of immune response, suggesting a separate process from extensive colitis or a more intense reaction resulting in localisation of disease.

Adolescent↗
PubMed1992

DNA aneuploidy in Crohn's disease and ulcerative colitis: results of a comparative flow cytometric study.

DNA ploidy and S-phase fractions were assessed by flow cytometry in colonic biopsy specimens from 28 patients with ulcerative colitis and 51 with Crohn's disease. Whereas only diploid DNA histograms were found in Crohn's disease and control subjects, three patients with ulcerative colitis exhibited DNA aneuploidy. In one case, aneuploidy was associated with low grade dysplasia. S-phase fractions were higher in ulcerative colitis (mean (SD) 17.8 (7.7)%) than in Crohn's disease (13.1 (4.6)%) or control subjects (14.2 (4.6)%), but did not correlate with either disease activity or duration in any group. In this study, aneuploidy was associated exclusively with ulcerative colitis, even in the absence of dysplasia. In view of the epidemiological differences in malignant colonic transformation between ulcerative colitis and Crohn's disease, this study suggests that flow cytometry may help to identify individuals with an increased cancer risk in ulcerative colitis.

Aneuploidy↗
PubMed1993

Failure of colonoscopic surveillance in ulcerative colitis.

A prospective surveillance programme for patients with longstanding (> = 8 years), extensive (> = splenic flexure) ulcerative colitis was undertaken between 1978 and 1990. It comprised annual colonoscopy with pancolonic biopsy. One hundred and sixty patients were entered into the programme and had 739 colonoscopies (4.6 colonoscopies per patient; 709 patient years follow up). Eight eight per cent of examinations reached the right colon. There was no procedure related death. One Dukes's A cancer was detected. Forty one patients (25%) defaulted. Of these 25 remain well; 13 are unaccounted for, and one died from colonic cancer. One patient had colectomy for medical reasons, and another died of carcinoma of the pancreas. Retrospectively an additional 16 eligible patients were identified who had not been recruited. Of these, 14 remain well, two are unaccounted for. None developed colonic cancer. Four patients refused colonoscopy. All remain well. Over the same period seven other cases of colonic cancer were found in association with ulcerative colitis, two in patients who had erroneously been diagnosed as having only proctitis and were therefore not entered into the programme, but were found at operation to have total colitis, one in a patient with colitis of seven years duration, and four patients who had previously attended the clinic but had been lost to follow up before 1978 and then had represented with new symptoms during the surveillance period. Thus, of the nine colitis related cancers diagnosed in this centre during the study period only one was detected by the surveillance programme. The results of this large study, a a review of published works, cast doubts on the effectiveness of colonoscopic surveillance programmes in detecting colorectal cancer in patients with ulcerative colitis.

Adult↗
PubMed1995

Enhanced colonic nitric oxide generation and nitric oxide synthase activity in ulcerative colitis and Crohn's disease.

Recent studies have suggested that nitric oxide (NO.), the product of nitric oxide synthase in inflammatory cells, may play a part in tissue injury and inflammation through its oxidative metabolism. In this study the colonic generation of oxides of nitrogen (NOx) and nitric oxide synthase activity was determined in ulcerative colitis and Crohn's disease. Colonic biopsy specimens were obtained from inflammatory bowel disease patients and from normal controls. Mucosal explants were cultured in vitro for 24 hours and NOx generation was determined. Nitric oxide synthase activity was monitored by the conversion of [3H]-L-arginine to citrulline. Median NOx generation by inflamed colonic mucosa of patients with active ulcerative colitis and Crohn's colitis was 4.2- and 8.1-fold respectively higher than that by normal human colonic mucosa. In ulcerative colitis and Crohn's colitis nitric oxide synthase activity was 10.0- and 3.8-fold respectively higher than in normal subjects. Colonic NOx generation is significantly decreased by methylprednisolone and ketotifen. The decrease in NOx generation by cultured colonic mucosa induced by methylprednisolone suggests that NO synthase activity is induced during the culture and the steroid effect may contribute to its therapeutic effect. Enhanced colonic NOx generation by stimulated nitric oxide synthase activity in ulcerative colitis and Crohn's disease may contribute to tissue injury.

Adult↗
PubMed1995

Collagenous colitis in Orebro, Sweden, an epidemiological study 1984-1993.

The incidence and prevalence of collagenous colitis are unknown. An epidemiological study was undertaken between 1984-93. All patients living in the immediate catchment area of Orebro Medical Center Hospital with the diagnosis collagenous colitis were identified. Biopsy specimens classified as unspecific intestinal fibrosis were re-examined to identify cases not correctly diagnosed at first. Medical records were scrutinised and colorectal biopsy specimens re-evaluated. Thirty patients with collagenous colitis were diagnosed during the study period. The female:male ratio was 9:1. The median age at diagnosis was 64 (28-78) years. The prevalence at 31 December 1993, was 15.7/10(5) inhabitants (95% CI; 9.8 to 21.6/10(5)). The mean annual incidence during the period 1984-93 was 1.8/10(5) inhabitants (95% CI; 1.2 to 2.4/10(5)). A peak incidence was found in women 70-79 years old. Collagenous colitis occurs mainly in middle aged women, and the frequency is higher than earlier anticipated. The prevalence and incidence is similar to primary biliary cirrhosis. In women 70-79 years of age, the incidence for collagenous colitis approaches the incidence for ulcerative colitis.

Adult↗
PubMed1995

Corticotropin releasing hormone in colonic mucosa in patients with ulcerative colitis.

Corticotropin releasing hormone (CRH) is a key hormone in integrated response to stress, acting as the major regulator of the hypothalamic-pituitary-adrenal axis. Recently, local production of CRH has been detected in normal human colonic enterochromaffin cells. CRH is locally secreted in granulomatous and arthritic tissues in rats and humans, where it seems to act as a local proinflammatory agent. To find out if CRH is present in colonic tissues of patients with ulcerative colitis, this study examined the expression of this peptide in the large bowel of patients with ulcerative colitis. Colonic tissues of patients with ulcerative colitis obtained by endoscopic biopsy were immunostained with anti-CRH antibody. CRH messenger (m) RNA was also examined in biopsy specimens of ulcerative colitis by the reverse transcribed polymerase chain reaction method and by in situ hybridisation. Considerably enhanced expression of immunoreactive CRH was found in mucosal inflammatory cells. Intense staining with anti-CRH antibody was also shown in mucosal macrophages. CRH mRNA was expressed in mucosal epithelial cells. The expression of immunoreactive CRH in colonic mucosal epithelial cells of ulcerative colitis slightly increased, but not significantly, compared with normal colonic mucosal epithelial cells. These results suggest that CRH may play a part in the modulation of intestinal immune and inflammatory system, and as a modulator in the pathogenesis of ulcerative colitis.

Adult↗
PubMed1996

Interchange between collagenous and lymphocytic colitis in severe disease with autoimmune associations requiring colectomy: a case report.

BACKGROUND: Collagenous colitis and lymphocytic colitis present with a similar clinical picture. Whether these conditions are separate entities or whether they represent different pathological stages of the same condition is an unresolved issue. PATIENT: This is a case of collagenous colitis following a fulminant course in which a colectomy was necessary. In the operative specimen the thickened collagen plate, which had been present only two weeks preoperatively had been lost and the pathology was of a lymphocytic colitis. Six months postoperatively this patient developed a CREST syndrome and primary biliary cirrhosis. CONCLUSIONS: This case shows the lability of the collagen plate and the common ground between collagenous and lymphocytic colitis, and presents evidence that these two conditions are different manifestations of the same disease. It also describes for the first time an association between collagenous colitis and CREST syndrome and primary biliary cirrhosis.

Autoimmune Diseases↗
PubMed1996

Promotion of colorectal neoplasia in experimental murine ulcerative colitis.

BACKGROUND: The mechanisms underlying the frequent development of colorectal carcinomas in patients with ulcerative colitis are still unknown. AIMS: To evaluate whether mucosal necrosis and regeneration act as enhancing or promoting factors in colorectal tumorigenesis, development of multiple colorectal tumours was studied in a murine model of ulcerative colitis with azoxymethane pretreatment. METHODS: Periods of chronic ulcerative colitis in mice were induced by three repeated administrations of 3% dextran sulphate sodium subsequent to a single azoxymethane pretreatment, to give conditions similar to the clinically observed active and remission phases. RESULTS: In the chronic colitis group with carcinogen exposure, multiple mucosal tumours (10.5/mouse) developed in the colorectum. This occurred primarily on the left side of the large intestine or transverse colon, the sites of the most severe colitic injury. The observed lesions were high grade dysplasias and invasive adenocarcinomas. Increased cell proliferation was evidenced by high uptake of bromodeoxyuridine, and increased activities of thymidylate synthetase and thymidine kinase. No tumours were induced in the control groups with azoxymethane pretreatment or chronic colitis alone. CONCLUSIONS: Repeated mucosal erosion with necrosis and regeneration is critical for the development of colorectal tumours in this experimental colitis system.

Animals↗