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PubMed1997

Elevated serum levels and reduced immunohistochemical expression of thrombomodulin in active ulcerative colitis.

BACKGROUND & AIMS: The pathogenesis of ulcerative colitis and Crohn's disease is still unclear. Vascular injury has been suggested as a potential pathogenetic mechanism. Serum thrombomodulin is a marker of endothelial cell injury. The aim of this study was to determine the relevance of increased serum thrombomodulin levels for assessing disease activity in inflammatory bowel disease. As a potential cause of serum thrombomodulin level increase, the loss of local vascular thrombomodulin expression was investigated immunohistochemically. METHODS: Thrombomodulin levels were determined by enzyme-linked immunosorbent assay in sera from patients with ulcerative colitis, Crohn's disease, Schistosoma mansoni infection, and infectious diarrhea and controls. The vascular expression of thrombomodulin was investigated immunohistochemically in fresh frozen transmural specimens of normal, Crohn's, and ulcerative colitis bowel samples. RESULTS: Significantly elevated serum thrombomodulin levels were only detected in active ulcerative colitis and infectious diarrhea complicated by septicemia. A marked and general loss of vascular endothelial cell thrombomodulin expression was found immunohistochemically in inflamed bowel tissues. Graded by a newly established thrombomodulin staining index, this was significantly more marked in ulcerative colitis than Crohn's disease. CONCLUSIONS: Serum thrombomodulin proved to be a novel marker of disease activity in ulcerative colitis closely related to local vascular endothelial cell damage, which might be a relevant pathophysiological feature of ulcerative colitis.

Adult↗
PubMed1999

Anti-interleukin 12 treatment regulates apoptosis of Th1 T cells in experimental colitis in mice.

BACKGROUND & AIMS: Trinitrobenzene sulfonic acid (TNBS)-induced colitis is a T-helper 1 (Th1) T cell-mediated inflammation that is rapidly reversed by administration of anti-interleukin (IL) 12. This study sought to define the mechanism of this curative effect. METHODS: Cells and tissue from mice with TNBS colitis receiving treatment with anticytokines were analyzed for phenotype, cytokine production, and apoptosis. RESULTS: In initial studies, we found that treatment of mice with TNBS-induced colitis with anti-IL-12 was more effective than with anti-interferon (IFN)-gamma, and that anti-IL-12 led to complete normalization of IFN-gamma production by lamina propria T cells ex vivo, whereas anti-IFN-gamma did not. These data suggesting that anti-IL-12 leads to reversal of colitis by elimination of the Th1 T cells were substantiated by studies showing that anti-IL-12 treatment led to increased numbers of apoptotic cells in the lamina propria and spleen by both TUNEL staining of tissues and dispersed spleen cell populations. Finally, we found that the observed apoptosis was mediated by the Fas pathway because (1) MRL/MpJ-lpr(fas) mice lacking Fas function develop colitis that responds poorly to treatment with anti-IL-12; and (2) SJL/J mice with TNBS colitis that received Fas-Fc to block the Fas pathway were resistant to anti-IL-12 treatment. CONCLUSIONS: These studies show that a main mechanism of action of anti-IL-12 in TNBS-induced colitis is the induction of Fas-mediated apoptosis of the Th1 T cells, causing inflammation.

Animals↗
PubMed1994

Anti-neutrophil cytoplasmic antibodies in children with ulcerative colitis.

Tests that positively identify individuals with ulcerative colitis, distinguishing them from patients with Crohn disease or other causes of colitis, have not been reliable. Genetic predisposition to inflammatory bowel diseases and genetic influence on immune regulation resulted in the clinical evaluation of potential serologic markers. In adults the presence of anti-neutrophil cytoplasmic antibody (ANCA) in serum identifies patients with ulcerative colitis. In this study we demonstrated that high levels of ANCA are present in 83% of children and adolescents with ulcerative colitis. Furthermore, the majority of patients with ulcerative colitis had a perinuclear pattern of these antibodies by indirect immunofluorescence. The combination of a positive ANCA and perinuclear indirect immunofluorescence pattern was 97% specific for ulcerative colitis. We conclude that determination of ANCA is a sensitive and specific clinical test for identification of children and adolescents with ulcerative colitis.

Adolescent↗
PubMed2002

Endothelin in human inflammatory bowel disease: comparison to rat trinitrobenzenesulphonic acid-induced colitis.

There have been suggestions that endothelins (ET-1, ET-2, ET-3) are involved in the pathogenesis of human inflammatory bowel disease (IBD). Furthermore, the non-selective endothelin receptor antagonist, bosentan, ameliorates colonic inflammation in TNBS colitis in rats. However, no studies have measured the tissue expression and release of endothelins in human IBD in direct comparison to experimental TNBS colitis. Mucosal biopsies were obtained from 114 patients (42 Crohn's colitis, 35 ulcerative colitis and 37 normal) and compared to whole colonic segments from rats with TNBS colitis. ET-1/2 levels were reduced in human IBD but greatly increased in experimental TNBS colitis. RT-PCR indicated ET-2 was the predominant endothelin isoform in human IBD whereas ET-1 prevailed in the TNBS model. No associations were found between human IBD and tissue expression, content or release of ET-1/2. Our study shows, therefore, that unlike TNBS colitis in rats, in which ET-1/2 levels are greatly elevated and ET receptor antagonists are efficacious, there is no significant link between endothelins and human IBD.

Animals↗
PubMed1994

Cigarette smoking and ulcerative colitis: a case-control study.

OBJECTIVE: To determine whether the previously reported decreased risk of ulcerative colitis in current smokers and increased risk in former smokers are explained by age, sex, race, ethnicity, or socioeconomic status. DESIGN: We conducted a case-control study at a university hospital gastroenterology clinic. MATERIAL AND METHODS: One hundred patients with ulcerative colitis and 100 age- and sex-matched community control subjects were randomly selected for a telephone interview to collect information on smoking habits, race, religion, income, education, and occupation. Smoking habits at the onset of symptoms were analyzed with use of conditional logistic regression for matched data to obtain adjusted odds ratios and 95% confidence intervals for current or former smokers. RESULTS: In comparison with those who had never smoked, current smokers were less likely to have ulcerative colitis: odds ratio = 0.13; 95% confidence interval = 0.05 to 0.38. Former smokers had no increased risk for ulcerative colitis: odds ratio = 1.24; 95% confidence interval = 0.52 to 2.95. No dose-response effect was noted on the basis of pack-years of cigarette smoking, and among former smokers, the interval since quitting smoking was not significantly associated with the relative risk of ulcerative colitis. No confounding effect was detected from race, religion, income, education, or occupation. CONCLUSION: An association seems to exist between ulcerative colitis and nonsmoking; perhaps patients with ulcerative colitis who smoke are less likely to experience symptoms than are nonsmokers because of the effects of nicotine.

Adult↗
PubMedDate not supplied

Outcome of patients undergoing ileal pouch-anal anastomosis for left-sided chronic ulcerative colitis.

Chronic ulcerative colitis is not a uniform disease entity because the clinical pattern and disease characteristics differ on the basis of the anatomic location of the inflammation. The aim of this study was to compare the preoperative characteristics, postoperative complications, and long-term functional outcome of ileal pouch-anal anastomosis (IPAA) in patients with left-sided colitis to those same characteristics in patients with pancolitis. Between 1990 and 1996, a total of 565 patients underwent IPAA for chronic ulcerative colitis at our institution. Of these, 111 patients were determined to have left-sided involvement, whereas 283 patients had pancolitis. The mean age at surgery was greater in the patients with left-sided colitis (37 years vs. 34 years, P = 0.01), and the mean duration of disease (8.7 years vs. 7.7 years, P = 0.05) tended toward a significant difference between the left-sided colitis and pancolitis groups. The complication rates were similar with the exception of small bowel obstructions, for which there was a higher incidence in the group with left-sided colitis (27% vs. 13%, P = 0.002) at 5 years. The incidence of pouchitis (43% vs. 39%) at 5 years was comparable. Long-term functional results and quality-of-life assessment did not show any significant differences between the two groups. We were unable to detect any correlation between the extent of colon involvement and the subsequent incidence of pouchitis, long-term pouch function, and quality of life. Patients with left-sided colitis were older, had a relatively longer duration of disease, and were at increased risk for postoperative small bowel obstruction as compared to patients with pancolitis.

Adult↗
PubMed2001

Evidence of Epstein-Barr virus infection in ulcerative colitis.

BACKGROUND AND AIM: The aetiology of ulcerative colitis is still controversial, however, recent studies have emphasised the possible role of infectious agents or ingested substances and their breakdown products, which might activate immune-mediated mechanisms eventually leading to tissue damage. Aim of this investigation was to ascertain the occurrence and the potential role of Epstein-Barr virus infection in large bowel mucosa of ulcerative colitis patients. PATIENTS AND METHODS: Twenty-three biopsies and six total colectomies from 17 patients were analysed for the expression of Epstein-Barr virus proteins and RNAs. Polymerase chain reaction experiments were also carried out to detect Epstein-Barr virus DNA. For comparison, ten biopsies from patients with Crohn's disease, ten biopsies from patients with different types of colitis, seven biopsies and five surgical margins of normal colonic mucosa from the small and large bowels were studied (controls). RESULTS: Six biopsies and four colectomies from seven ulcerative colitis patients showed scattered lymphocytes expressing nuclear EBER 1-2 and harbouring polymerase chain reaction-amplifiable Epstein-Barr virus-DNA. In some cases, linear viral DNA (typical of lytic Epstein-Barr virus infection) was also found. Epithelial cells were invariably negative in all cases. All control tissues from non-ulcerative colitis patients were also invariably non-reactive. CONCLUSION: Evidence of Epstein-Barr virus infection in the mucosal inflammatory cells of ulcerative colitis patients suggests a possible role of this virus in the chronicity of ulcerative colitis.

Adult↗
PubMed2000

Total antioxidant capacity of colon in patients with chronic ulcerative colitis.

It has been proposed that oxidative stress is involved in the pathophysiology of ulcerative colitis. We have reported the depletion of the nonenzymatic antioxidant, glutathione, in colon from active and inactive ulcerative colitis. The colon contains several biochemically linked antioxidant systems. We hypothesized that diminished total antioxidant capacity in active ulcerative colitis would be associated with increased colonic lipid peroxidation. This study was designed to determine total antioxidant capacity and lipid hydroperoxide levels using colon obtained at surgery from controls (N = 16; 4 females, 12 males; mean age 70 years), and active and inactive ulcerative colitis (N = 15; 3 females, 12 males; mean age 39). Total antioxidant capacity of control colon was higher in muscularis externa compared to the mucosal-submucosal layer (P < 0.05). There were no differences in colonic total antioxidant capacity or lipid hydroperoxide levels comparing control colon to inactive and active ulcerative colitis. The results did not support depletion of tissue total antioxidant capacity by free radicals. Depletion of glutathione in ulcerative colitis may be a specific disorder rather than a secondary defect attributable to global oxidative stress. Nonspecific antioxidant supplements appear unlikely to be beneficial in the treatment of ulcerative colitis.

Adult↗
PubMed2000

Rebamipide, an antiulcer drug, prevents DSS-induced colitis formation in rats.

This study was conducted to investigate the efficacy of rebamipide against experimental colitis induced by dextran sulfate sodium (DSS) in a rat model of inflammatory bowel disease. Experimental colitis was induced in male Wistar rats by oral administration of 3% DSS solution for one week. The rats were provided with standard diet containing 0.105% rebamipide (160 mg/kg/day) for 1 week. In rats treated with rebamipide, clinical (body weight loss, bloody diarrhea, reduced physical activity, severe anemia, shortened colonic length, and perianal injury) and histopathological (pathological lesion score) findings of DSS colitis were significantly less than in rats with DSS colitis not treated with rebamipide. Rebamipide thus inhibited the induction of colitis. Rebamipide significantly reduced concentrations of both interleukin-1alpha and GRO/CINC-1 (IL-8-like substance) and cell infiltrates in colonic wall, in parallel with decreased activity of myeloperoxidase. It also reduced expression of IL-1 mRNA but did not influence expression of GRO/CINC-1 mRNA. The attenuation of colonic indices of colitis by rebamipide in this rat model suggests that this drug might have beneficial effects in the treatment of human ulcerative colitis. These effects of rebamipide are attributable to its inhibition of inflammatory cytokine-mediated granulocyte (neutrophil) infiltration into the colon.

Alanine↗
PubMed2000

Effects of free radicals and leukocytes on increases in blood-brain barrier permeability during colitis.

This study examined the role of leukocytes and free radicals on increases in permeability of the blood-brain barrier (BBB) in rabbits with acute colitis. Trinitrobenzene sulfonic acid (TNBS) was used to induce colitis in male New Zealand White rabbits. The extraction ratio of fluorescein was used as an index of the permeability of the BBB. The extraction ratio for fluorescein was 1.0 x 10(-3) +/- 2 x 10(-4) ml/g and 1.1 x 10(-3) +/- 3 x 10(-4)ml/g (mean +/- SE) for saline (N = 7) and ascorbic acid-treated (N = 8) rabbits with sham colitis. Conversely, TNBS-induced acute colitis increased the extraction ratio over 70% in saline (N = 8) and ascorbic acid-treated (N = 8) animals. Vinblastine significantly reduced the number of circulating leukocytes, whereas the permeability of the BBB was augmented by 54% in rabbits with TNBS-induced acute colitis (N = 8). Vinblastine had no effect on the permeability of the BBB in rabbits with sham colitis (N = 8). These data suggest that free radicals are not responsible for BBB disruption, and leukocytes may protect the BBB during acute colitis.

Acute Disease↗
PubMed2001

Diagnostic value of DNA image cytometry in ulcerative colitis.

The increased risk of colorectal cancer in patients with extensive, long-standing ulcerative colitis is well established. The interpretation of dysplasia as the common precursor lesion of colorectal cancer in ulcerative colitis is, however, subject to inter- and intraobserver variation. The histologic diagnosis is particularly difficult in the presence of acute inflammation. Therefore, the analysis of ploidy patterns might be a more objective diagnostic tool. In the present study, the correlation of ploidy and dysplasia of the colonic mucosa was evaluated in the absence and presence of inflammation. Image cytometry was performed on 561 fixed, paraffin-embedded tissue specimens from 67 patients with ulcerative colitis. Twenty patients had long-standing and extensive disease, including eight patients in whom the colitis was associated with colorectal cancer. Dysplasia was only found in patients with long-standing colitis or with colorectal cancer and was significantly more often diagnosed in the case of concomitant inflammation. On the other hand, aneuploid patterns were shown to occur independent of inflammatory activity. Aneuploidy was present in all colorectal carcinomas associated with ulcerative colitis and in 46.2% of specimens with dysplasia. Moreover, aneuploidy was detectable in four of 12 samples with low-grade dysplasia as well as in one case devoid of any dysplastic alteration. Ulcerative colitis patients with low-grade dysplasia plus aneuploidy probably represent a subgroup that might be at higher risk of developing colorectal cancer than patients with low-grade dysplasia alone. All in all, image cytometry analysis might be instrumental in identifying neoplastic lesions even in cases of increased inflammatory activity or regenerative change.

Adolescent↗
PubMed1998

Effect of heparin on dextran sulfate sodium-induced colitis.

Heparin has been shown to ameliorate inflammatory bowel disease in several series. In addition to its anticoagulant properties, heparin has numerous other effects that may be beneficial in inflammatory bowel disease. Other sulfated polysaccharides, such as dextran sulfate, cause colitis in mice through unknown mechanisms. We postulate that dextran sulfate and heparin may act via similar pathways with opposite effects. To examine this thesis, the effect of heparin on dextran sulfate-induced colitis was studied. Swiss-Webster mice were given 5% dextran sulfate in their drinking water for five days to induce colitis. Heparin was given both therapeutically after the induction of colitis and prophylactically by subcutaneous injections, with saline injections given in controls. Histologic sections of colon were randomized and graded for colitis. Heparinized animals showed no significant difference in the pattern or severity of colitis when compared to control animals. It is concluded that heparin does not ameliorate the murine colitis induced by dextran sulfate in the doses given.

Animals↗
PubMed1998

Glutathione content of colonic mucosa: evidence for oxidative damage in active ulcerative colitis.

Oxidative stress appears to play a role in the tissue damage of active ulcerative colitis, and it has been suggested that a defect in mucosal antioxidant defenses is a etiological factor in the disease. This study was undertaken to investigate the mucosal content and oxidation state of glutathione in ulcerative colitis in the active and inactive states and to examine the relationship between glutathione content and disease activity in this patient population. Endoscopic biopsies of colon mucosa were collected from normal subjects, from macroscopically normal tissue of patients with inactive and active ulcerative colitis, and from inflamed tissue of patients with active ulcerative colitis. The mucosal contents of GSH and GSSG were determined by liquid chromatography. We found no significant differences in tissue contents of reduced glutathione among the four groups. The median tissue level of oxidized glutathione in inflamed mucosa from patients with active ulcerative colitis was increased 1.7-fold (P = 0.017) over that of patients with inactive disease. The oxidized glutathione content of the mucosa also showed significant positive correlations with clinical and histological indices of disease severity among ulcerative colitis patients. In conclusion, a change in the redox status of mucosal glutathione is associated with inflammation and disease activity in ulcerative colitis. This change appears to be a consequence of inflammation rather than a pathogenic factor for the disease.

Colitis, Ulcerative↗
PubMed2002

In vivo detection of morphological and microvascular changes of the colon in association with colitis using fiberoptic confocal imaging (FOCI).

Using a well-established rodent model of inflammatory bowel disease (IBD), the present study examined changes in the microvasculature of the colonic mucosa in association with ulcerative colitis (UC). The results were compared to microscopic alterations in tissue morphology to establish a temporal relationship between microcirculatory dysfunction and IBD pathology. Mild colitis was induced in rats by the oral consumption of 5% dextran sulfate sodium (DSS) in drinking water. Control animals were provided with water ad libitum. After 3, 5, and 7 days of oral ingestion of DSS, anesthetized rats were laparotomized. The mucosal surface of the distal colon was then examined using fiber optic confocal imaging (FOCI; excitation 488 nm argon ion laser, detection above 515 nm). Changes in the mucosal architecture were examined following the topical application of the fluorescent dye, tetracycline hydrochloride. Tetracycline hydrochloride, an antibiotic used widely in clinical medicine, enabled imaging of the crypts at the surface of the mucosa. Spatial changes in the microvascular structure were assessed following the intravenous administration of fluorescein isothiocyanate dextran (FITC-dextran). Confocal images were correlated with clinical parameters, including weight loss, occult blood, and stool consistency. Attenuation of the colonic epithelium was detected on day 3 colitis. Morphological changes including crypt loss, crypt distortion, and inflammatory cell infiltrate were detected on day 5 and day 7 colitis. Dual channel imaging showed the mucosal capillary network outlining the stromal confines of the mucus-secreting glands in control tissue. Experimental colitis resulted in diffuse hypervascularity and tortuosity of the capillary vessels. Evidence of increased vessel leakiness (leakage of FITC-dextran from the lumen) was first detected on day 5 colitis. Complete disruption of the normal honeycomb pattern of the vessels and capillary dilation was evident after 7 days of DSS ingestion. These findings suggest that the pathogenesis of ulcerative colitis is associated with changes in the vascular architecture as demonstrated in vivo using confocal microscopy.

Animals↗
PubMed1997

South Asians with ulcerative colitis exhibit altered lectin binding compared with matched European cases.

Ulcerative colitis is associated with abnormalities of mucin synthesis and secretion, features that may also be associated with malignant change. It has been shown that South Asians in Britain have a high incidence of ulcerative colitis but a low incidence of colorectal carcinoma compared with their European counterparts. Previous studies have demonstrated changes in colonic mucin sialylation and sulphation in both South Asian and European cases with ulcerative colitis. This was related to disease severity, but changes were also found in quiescent disease. The aim of the present study was to determine glycoconjugate expression in the colon from South Asian cases and to compare results with those from a group of affected Europeans. Glycans were identified in formalin-fixed, paraffin-embedded tissue from 17 South Asian patients with ulcerative colitis and from 11 European patients with a similar degree of colitis, by the application of 10 biotinylated lectins. These were directed against a range of sialyl, fucosyl and 2-deoxy, 2-acetamido-galactosyl sequences, using an avidin-peroxidase revealing system and semiquantitative assessment. The South Asian group showed a reduction in the binding of agglutinins from Sambucus nigra in the apical-membranous region of enterocytes, and a decrease in apical Maackia amurensis agglutinin binding. These results suggest that South Asians with ulcerative colitis show a different distribution of terminal N-acetyl neuraminyl residues, either in their alpha-2,6 or alpha-2,3 linkage, compared with their European counterparts. The changes in sialylation observed in European cases compared with normal disease-free control subjects were present in quiescent disease, but were also related to disease activity. Their absence in Asians with ulcerative colitis may imply an inherent, genetically determined variation in this group, which may also play a part in their reduced risk of subsequent malignancy.

Asia, Southeastern↗
PubMed2004

IL-10 gene therapy is therapeutic for dextran sodium sulfate-induced murine colitis.

The transfer of genes encoding immunoregulatory proteins is a promising new strategy in the treatment of intestinal inflammation. Previous work has demonstrated that daily systemic interleukin (IL)-10 therapy is able to prevent disease onset in animal models of colitis but is not sufficient to treat established disease. This study investigates the therapeutic efficacy of an adenovirus encoding IL-10 (AdvmuIL-10) in the treatment of experimental colitis. Colitis was induced in BALB/c mice by the addition of dextran sodium sulfate to the drinking water for 7 days. A single systemic injection of AdvmuIL-10, empty cassette vector (Adv0), or saline vehicle was administered on day 4 after the onset of colitis. The addition of DSS to the drinking water led to an acute, dose-dependent colitis. A single injection of AdvmuIL-10 led to a marked reduction in both stool markers of inflammation (IL-1beta, IL-6, and TNFRII) and serum IL-6. Furthermore, the histological colitis score was significantly reduced in mice receiving AdvmuIL-10 compared to controls (4.9 +/- 1.1 Vs 9.1 +/- 1.2, respectively; P < 0.05). A single systemic injection of AdvmuIL-10 is therapeutic in mice with established DSS colitis. Gene therapy strategies using adenoviral vectors encoding IL-10 may prove to be a potent therapy for chronic inflammation of the colon such as Crohn's disease.

Adenoviridae↗
PubMed2002

Review article: Immunosuppressants in distal ulcerative colitis.

BACKGROUND: Distal ulcerative colitis may prove to be resistant to steroids and aminosalicylates, but total colectomy is more difficult to justify than in severe extensive colitis. Immunosuppression is of established benefit in generalized colitis, but there are no data available specific to distal disease. AIM: To determine whether the protocol-driven use of immunosuppressants in resistant distal ulcerative colitis is of similar efficacy and safety to that in extensive disease. METHODS: Two hundred and twenty-eight patients with distal ulcerative colitis seen in a 5-year period were identified from a prospective database. Details of 52 who had received immunosuppression were analysed. RESULTS: The 52 patients received 68 courses of therapy (53 azathioprine, five mercaptopurine, 10 ciclosporin). The thiopurines yielded clinically valuable responses in only 43% of courses, with failure of response in 16% and toxicity in 34%. Ciclosporin was helpful on only two of 10 occasions. Eight patients required total colectomy. Adverse events were typical of those normally associated with immunosuppressants, with potential risk to life in seven patients; treatment was discontinued because of toxicity on a total of 31% of occasions. CONCLUSIONS: Immunosuppression appears to be of lower efficacy and higher toxicity in resistant distal colitis than when used in more extensive colitis.

Adult↗
PubMed2003

Non-steroidal anti-inflammatory drugs, aspirin and newly diagnosed colitis: a case-control study.

BACKGROUND: There have been a number of reports of colitis following exposure to non-steroidal anti-inflammatory drugs (NSAIDs) and salicylates. AIM: To conduct a case-control analysis of new cases of colitis, with particular reference to the usage of NSAIDs and salicylates prior to the development of the disease. METHODS: One hundred and five consecutive new cases of colitis presenting to a single gastroenterologist were questioned about their recent usage of NSAIDs and salicylates. For comparison, the frequency of usage of these compounds was studied in two groups of 105 age- and sex-matched controls taken from hospital in-patients and community cases attending the Accident and Emergency Department. RESULTS: Of the 105 cases of colitis studied, 78 patients (74%) had been taking NSAIDs or salicylates prior to or during the development of their disease. By comparison, 20% of community controls were using NSAIDs or salicylates (P < 0.001) and 30% of hospital in-patients were taking these compounds (P < 0.001). Comparison of these frequencies with those of the colitis group gave odds ratios of 9.1 (4.5, 21.9) with the community controls and 6.2 (3.2, 13.5) with the hospital controls. CONCLUSIONS: In new patients presenting with colitis, there is a significantly high frequency of antecedent exposure to NSAIDs or salicylates, supporting the concept that these agents may be important in the pathogenesis of colitis.

Adult↗