[Microscopical colitides as a cause for chronic diarrhea].
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Chronic Disease↗
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[Microscopic and macroscopic fungi in the colon].
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Actinomycosis↗
Proctitis and colitis following diversion of the fecal stream.
Inflammation limited to excluded segments of the colon was observed in 10 patients without prior inflammatory bowel disease who had undergone colostomy or ileostomy for various indications. With the exception of 1 patient who complained of mucoid rectal discharge, the patients were asymptomatic when the lesion was discovered; 2 others subsequently developed mild symptoms. The proctoscopic findings were similar in appearance to those of mild ulcerative colitis. In 8 of 10 patients the inflammatory changes were confined to the distal few centimeters of the rectum, while in the remaining 2 patients the entire excluded segment was affected. Microscopic alterations were focal and included crypt abscesses, epithelial cell degeneration, acute and chronic inflammation in the lamina propria, and regenerative changes in the crypts. The inflammation persisted for as long as 8 yr in the 5 patients who did not have restoration of intestinal continuity, but subsided in the 5 patients whose colostomies were closed. The prior as subsequent clinical courses of these patients, together with the focal, nonspecific microscopic features, strongly suggest that the inflammation in these patients resulted from diversion of the fecal stream and was not a recognized form of specific or idiopathic colitis. Diversion-related colitis must not be confused with other forms of inflammation since this may result in improper therapy and/or delay in treatment of the condition for which the fecal diversion was performed.
Adult↗
Dextran sulfate sodium (DSS) colitis in rats: clinical, structural, and ultrastructural aspects.
Aim of this study was to assess the structural, ultrastructural, immunohistochemical, and clinical aspects in Sprague-Dawley rats with dextrane sulfate sodium (DSS)-induced colitis. Colitis was induced in Sprague-Dawley rats by seven days of DSS oral administration followed by seven days of tap water only (for one, two and three cycles). Controls were fed with water only. Segments of proximal, mid-, and distal colon of each animal were adequately prepared for light and scanning electron microscope observations. The severity of the lesions was scored histologically. For immunohistochemical study, a cocktail of S-100, NSE, and antineurofilament antibodies was used. Symptoms such as weight, feces consistency, diarrhea, hematochezia were recorded daily. From a clinical point of view symptoms appeared significantly later after the first cycle than after the second and third cycles and lasted significantly longer in the second and third cycles. Treated rats showed a slower weight gain rate by 20% compared to controls, and the whole colon length appeared to be significantly shorter after colitis induction compared to controls. Structural observations by light microscopy showed prominent involvement of the distal colon. Immunohistochemical study of both submucosal and myoenteric nerve plexuses was similar to controls. Scanning electron microscope observations of the colonic mucosal surface in colitis rats showed a complete subversion of its architecture, characterized by dilatations of gland crypt openings, dropout of goblet cells, and inhomogeneous distribution or lack of microvilli. These were most evident after the third cycle. In conclusion, experimental DSS colitis in SD rats appeared to be highly reproducible and shared most features with human UC, not only from a structural and clinical but also from an ultrastructural point of view.
Animals↗
Distribution and anti-inflammatory effect of mesalazine on carrageenan-induced colitis in the rabbit.
1. A controlled-release preparation of mesalazine microgranules (PentasaR; Ferring AS, Vanlose, Denmark) releases the active ingredient over a wide area from the small intestine to the rectum and is consequently expected to bring about therapeutic benefits to patients with ulcerative colitis and Crohn's disease. 2. Mesalazine microgranules (50 or 150 mg/kg per day) were administered orally to each rabbit with carrageenan-induced colitis for six weeks. Its inhibitory effect on colonic mucosal damage was assessed in terms of the microscopic damage scores, leukotriene B4 concentrations and concentrations of mesalazine derivatives. 3. At the end of the experiment, the mesalazine 150 mg group had gained a significantly greater bodyweight than the control group. Microscopic damage was significantly lower in the 150 mg group than in the untreated control group. Tissue concentrations of 5-aminosalicylic acid and acetyl-5-amino-salicylic acid in the small and large intestine were higher in the 150 mg group than in the 50 mg group. Mucosal leukotriene B4 levels tended to be lower in rabbits receiving the larger dose of mesalazine. 4. The present study indicates that slow release 5-amino-salicylic acid at the larger dose reaches the large bowel in sufficiently high concentrations following oral administration and significantly reduces carrageenan-induced colitis in the rabbit.
Aminosalicylic Acids↗
Lymphocytes endowed with colon-selective homing and engineered to produce TGF-beta1 prevent the development of dinitrobenzene sulphonic acid colitis.
BACKGROUND: Gene therapy is an attractive approach to the treatment of inflammatory diseases. However, the lack of tissue targeting of available vectors jeopardizes their clinical use. AIMS: Since alpha4beta7 integrin mediates lymphocyte homing to the intestinal mucosa, we tested the possibility of in-vitro engineering alpha4beta7-bearing lymphocytes to restrict the production of a therapeutic cytokine, transforming growth factor (TGF)-beta1, to within the colonic mucosa. METHODS: Lymphocytes were isolated from colonic lamina propria or spleen and transfected with either pC1 or pC1/TGF-beta1. RESULTS: Transfected spleen and lamina propria cells released TGF-beta1 for up to 5 days in vitro and administration of 107 spleen cells, but not 106 lamina propria or spleen cells, to normal mice caused a significant rise in circulating TGF-beta1. Following intrarectal injection of dinitrobenzene sulphonic acid, intraperitoneal administration of lamina propria or spleen cells transfected with pC1/TGF-beta1, but not pC1, significantly reduced colitis-associated body weight loss, colonic myeloperoxidase (MPO) activity, interleukin-1beta levels, and macroscopic and microscopic inflammatory damage. Vector-specific TGF-beta1 mRNA transcripts were detectable in the colon and liver following injection of lamina propria lymphocytes, and in the spleen, liver and colon following administration of spleen lymphocytes. Incubation of pC1/TGF-beta1-transfected lamina propria lymphocytes with anti-alpha4beta7 integrin antibody blocked their protective effects and caused the disappearance of vector-specific TGF-beta1 transcripts from the colonic mucosa. CONCLUSION: We conclude that lymphocytes are an efficient vehicle for transient gene therapy and that cells bearing alpha4beta7 integrins preferentially deliver therapeutic genes to the colonic mucosa.
Animals↗
The effect of nitric oxide synthases inhibitors on inflammatory bowel disease in a rat model.
BACKGROUND/AIMS: Overexpression of nitric oxide (NO) has been implicated in the pathogenesis of experimental and clinical inflammatory bowel disease (IBD). NO is produced by two types of enzymes: constitutively expressed and inducible NO synthases (NOS). This study assessed N(W)-nitro-L-arginine methyl ester (L-NAME) and aminoguanidine (AMG), the most studied inhibitors of nitric oxide synthases, with regard to their effectiveness as modulators of inflammation in trinitrobenzene sulfonic acid (TNBS)-induced colitis in the rat. MATERIALS AND METHODS: Colitis was induced in Wistar rats. The colitis was treated everyday for 10 days with L-NAME and AMG. To assess the severity of the colitis, clinical (body weight), hematological (hematocrit and erythrocytes sedimentation rate-ESR) and morphological (gross and microscopic) criteria were used. RESULTS: The administration of both nitric oxide synthases inhibitors L-NAME and AMG proved to be beneficial in all the examined parameters compared with the control group. A statistically significant difference between the L-NAME and the AMG groups was observed only in macroscopic and histological grading. CONCLUSION: NOS inhibitors may be promising agents in preventing the onset, or mediating the symptoms, of inflammatory bowel disease.
Animals↗
Molecular screening of patients with long standing extensive ulcerative colitis: detection of p53 and Ki-ras mutations by single strand conformation polymorphism analysis and differential hybridisation in colonic lavage fluid.
BACKGROUND: In patients with long standing ulcerative colitis at risk of developing malignancy, mutations of the p53 and Ki-ras gene were investigated in lavage solution obtained at surveillance colonoscopy. METHODS: DNA was isolated from 31 consecutive patients with total or subtotal ulcerative colitis and a disease duration of between seven and 26 years. Twenty seven control patients showed no macroscopic or microscopic inflammation on colonoscopy. Exons 5-8 of the p53 gene and exon 1 of the Ki-ras gene were amplified by polymerase chain reaction. Mutations of the p53 gene were detected by single strand conformation polymorphism analysis. Point mutations of the Ki-ras gene were hybridised on dot blots with oligonucleotides marked with digoxigenin. RESULTS: In all cases of ulcerative colitis and in all of the 27 control patients, wild type p53 and wild type Ki-ras could be detected. In four patients with ulcerative colitis, a mutation in exon 5 to 7 of the p53 gene was found, and two patients had a mutation of the Ki-ras gene (Gly to Asp-12, Gly to Val-12). None of these patients had dysplasia in serial biopsy specimens, and all but one had had the disease for more than 10 years. One control patient had a mutation. CONCLUSIONS: Mutations were more frequent in patients with long standing ulcerative colitis (19%) than in control patients (3%, p = 0.07). The technique may be useful for screening for early malignancy in ulcerative colitis.
Adult↗
[Immunologic methods in diagnosis of inflammatory bowel disease].
Chronic inflammatory bowel disease is included into autoimmune diseases, which is proved by presence of inflammatory lesions, circulating autoantibodies and the deposits of immune complexes in tissues. Coeliac disease (classic and atypical form), Crohn's Disease and ulcerative colitis are considered as chronic autoimmune bowel diseases. The auto-antibodies can be detected with indirect immunofluorescence, ELISA and immunoblotting methods. In coeliac disease the autoantibodies against endomysium (tissue transglutaminase) and antibodies against gliadin are found in patient's sera. The auto-antibody detecting is helpful in establishing diagnosis, controlling gluten-free diet effectiveness and during gluten challenge. In Crohn's disease and ulcerative colitis immunological laboratory tests are helpful to confirm the clinical diagnosis. The following auto-antibodies are tested: against cytoplasm of exocrinal pancreatic cells, and products of these cells, against the neutrophile cytoplasm and against goblet cells. The antibodies against Saccharomyces cerevisiae are also investigated. The clinical relevance of above autoantibodies is not clear, but it is suggested that their presence correlates with exacerbations and severe clinical outcome. In the present study the pictures of autoantibodies from fluorescent microscope were shown.
Autoantibodies↗
A prospective evaluation of diversion colitis.
Numerous case reports suggest that diversion of the fecal stream results in nonspecific colitis, with abnormalities ranging from minimal friability to gross ulceration. Published reports consist largely of patients with symptomatic colitis, and there are scant data suggesting at what frequency diversion colitis actually occurs. In an attempt to identify the frequency of diversion colitis and any associated etiologic factors, 20 patients scheduled for colostomy closure at Grady Memorial Hospital between 8/1/88 and 6/15/89 underwent colonoscopy, including the excluded segment, to evaluate for diversion colitis. Colostomies were performed for the management of diverticulitis, trauma, cancer, protection of an anastomosis, and diversion of fecal fistula. Patients with ulcerative colitis or Crohn's disease were excluded. The colon was classified grossly as normal or colitis (including easy friability, edema, inflammation, and ulceration as colitis). Fourteen of the 20 patients (70%) had findings of diversion colitis (DC), while six had a normal exam (NL). Nine biopsies were performed in the DC group and all revealed microscopic abnormalities. One of the normal patients was also biopsied, revealing mild, nonspecific changes. There was no difference in mean age (DC 49.3, NL 48.2), interval from formation of colostomy (DC 9.21 +/- 7.27 months, NL 2.83 +/- 1.94 months), type of colostomy, or reason for colostomy in the two groups. None of the DC patients had symptoms of colitis (mucous or bloody discharge, tenesmus, or pain), and one of the DC patients manifested symptoms of colitis after colostomy closure. We conclude that diversion colitis is a common subclinical problem in patients with a diverting colostomy.(ABSTRACT TRUNCATED AT 250 WORDS)
Biopsy↗
Immunomodulatory therapeutic effect of glatiramer acetate on several murine models of inflammatory bowel disease.
Inflammatory bowel disease (IBD) is characterized by detrimental immune reactivity in the gut and imbalance between proinflammatory and anti-inflammatory reactivity. In an attempt to down-regulate colitis, we investigated the effect of the immunomodulator glatiramer acetate (GA, Copaxone, copolymer 1) on two murine models of IBD, chemically induced and spontaneous. Acute experimental colitis of different levels of severity was induced in C57BL/6 mice by dextran sulfate sodium (DSS) administered orally at different concentrations and frequencies. It was manifested in weight loss, intestinal bleeding, and diarrhea, as well as by macroscopic and microscopic colon damage. GA treatment led to amelioration of all of these pathological manifestations, resulting in improved long-term survival. Moreover, even when colitis was induced by three cycles of DSS in this highly susceptible mouse strain, as well as in BALB/c mice that exhibit a chronic disease pattern, a substantial reduction in disease activity and mortality was obtained. GA treatment induced a beneficial effect also in a spontaneous model of colitis developed in the C3H/HeJBir IL-10-deficient mice. The detrimental proinflammatory response manifested by proliferation, tumor necrosis factor-alpha, and interferon-gamma expression was modulated by GA, whereas the regulatory anti-inflammatory transforming growth factor-beta and IL-10 cytokines response was elevated. This was demonstrated on the level of protein secretion in splenocytes and local mesenteric lymphocytes in response to syngeneic colon extract and in the overall response to anti-CD3, as well as on the level of mRNA expression in the colon.
Adjuvants, Immunologic↗
Selective uptake of intraluminal dextran sulfate sodium and senna by macrophages in the cecal mucosa of the guinea pig.
The involvement of macrophages in the passage of intraluminal substances into the lamina propria was examined in the large intestine of the guinea pig. Dextran sulfate sodium (DSS) and senna, which, experimentally, induce ulcerative colitis and melanosis coli, respectively, were chosen for examination, since these substances are visible under the microscope without any special treatment. DSS (MW 50,000) and senna were orally administered to guinea pigs. In tissue sections of the intestine, the presence of DSS was demonstrated by toluidine blue staining, while senna was visible under the light microscope as brown pigment. In the large intestine of guinea pigs, macrophages were most numerous in the cecum, decreasing in number towards the rectum. Metachromatic reaction due to DSS was first recognized in the epithelium of the cecum, and was subsequently incorporated by macrophages. The presence of DSS, either in the epithelium or in macrophages, was not recognized in the small intestine or the distal colon. Senna pigmentation was also limited to the cecum and proximal colon, in which pigmented macrophages aggregated in the lamina propria. The two different substances administered orally were taken up in the cecum, and partly also in the proximal colon; the substances passed through the epithelium and were incorporated by macrophages. This finding suggests the existence of a weak point in the intestinal barrier in this particular portion of the intestine.
Animals↗
Piroxicam decreases postirradiation colonic neoplasia in the rat.
This study evaluated the effects of the nonsteroidal antiinflammatory agent piroxicam on chronic radiation proctitis in the rat. Forty female Wistar rats received a 2250-cGy dose of irradiation to the distal 2 cm of the colon. Twenty received piroxicam 8.0 mg/kg orally 30 minutes before exposure and 24 hours after exposure; 20 rats served as irradiated controls. All animals were evaluated by colonoscopy 1 and 3 weeks postexposure and every third week until death or killing at 1 year. At killing, colons were removed for light microscopic examination. One year postirradiation results showed no differences in mortality, vascular changes, acute inflammation, colitis cystica profunda, or rectal stricture between the control and piroxicam-treated groups. However, at 1 year postirradiation the control group demonstrated neoplasia in 15 of 19 animals compared with eight of 20 animals in the piroxicam-treated group. The first endoscopic appearance of colonic neoplasm occurred at 15 weeks postirradiation in one control irradiated rat whereas the first evidence of endoscopic neoplasm in the piroxicam-treated group did not occur until 36 weeks postirradiation. Histologic examination documented a tendency toward a greater presence of adenocarcinomas in the control group compared with the piroxicam-treated group. The authors conclude that piroxicam treatment significantly decreased the incidence of colonic neoplasia in general as well as delayed the endoscopic appearance of colonic neoplasia in rats after pelvic irradiation.
Adenocarcinoma↗
A patient with improvement of ulcerative colitis after appendectomy.
Recently, several retrospective studies have shown an inverse association between appendectomy and development of ulcerative colitis. We describe a 21-year-old man with distal ulcerative colitis and appendiceal involvement. The patient passed bloody stools continually during the 3 years before admission. Macroscopic and microscopic findings showed chronic moderate inflammation of the appendix and rectum. The ratio of CD4 to CD8 lymphocytes isolated from rectal and appendiceal mucosa was increased (4.3 and 3.8, respectively) compared with controls (n = 11; 1.0 in the rectum and 1.4 in the appendix). Clinical symptoms and colonoscopic and microscopic findings improved significantly after appendectomy. In addition, the amount of interferon gamma secreted from rectal lymphocytes was reduced to 89 pg/mL after surgery (before appendectomy, 254 pg/mL). However, interleukin 4 production was below detectable levels both before and after appendectomy. These findings suggest that appendectomy resulted in altered T-helper (Th)1/Th2 balance in this patient. In the 3 years since surgery, the patient has been in good condition without recurrence of symptoms. This is the first report demonstrating therapeutic benefit of appendectomy in a patient with ulcerative colitis and potential mechanistic relationship.
Adult↗
Liver damage in juvenile inflammatory bowel disease.
During a 12-year period, 46 children and adolescents with inflammatory bowel disease were followed from the time of diagnosis with regular biochemical tests of liver function. Thirty-four patients had ulcerative colitis and 12 had Crohn's disease. Mean age at the time of diagnosis was 10.2 years (range 7 months-17 years) and the mean follow-up period was 5.2 years (range 1-11 years). Pathological liver function tests were found in 60% of the 34 patients with ulcerative colitis: 9 of these 20 patients demonstrated more severe disturbance, usually at the time of diagnosis. Liver damage was most frequent in patients with total colitis. Liver biopsy was performed in eight patients, demonstrating "pericholangitis", fibrosis and in one case cirrhosis. Morphometry of electron microscopical pictures revealed a significantly increased number of lysosomes and dilated cisternae of the rough endoplasmic reticulum. ERCP was performed in two patients, verifying primary sclerosing cholangitis in one. Four of the 12 patients with Crohn's disease had mildly pathological liver function tests. No correlation was found to the extent, duration or treatment of bowel disease. In our series of juvenile inflammatory bowel disease, liver damage occurred frequently, especially in ulcerative colitis. The more severe changes tended to coincide with the onset of bowel disease.
Biopsy↗
Colitis cystica profunda simulating rectal carcinoma.
Localized colitis cystica profunda is a rare, benign disease of the lower gastro-intestinal tract, usually presenting as a rectal mass and characterized microscopically by the presence of mucus-filled cysts in the submucosa. Knowledge of this particular pathological entity is important as it can mimic a well differentiated adenocarcinoma of the rectum and therefore could lead to unnecessary surgical resection. We present a case of colitis cystica profunda misdiagnosed as adenocarcinoma based on their similar clinical picture and histological features.
Adenocarcinoma↗
Pneumomediastinum during relapse of ulcerative colitis.
Pneumomediastinum can be caused by gas dissecting along fascial tissue planes into the mediastinum from remote locations, including the retroperitoneum. One potential source of retroperitoneal gas is the colon. We present the third reported case of pneumomediastinum (plus pneumothorax and subcutaneous emphysema) without free intraperitoneal gas developing during an attack of ulcerative colitis. Because there was no colonic perforation noted at colectomy, the extracolonic gas was presumed to originate from a microscopic or partial thickness perforation of the colon. GI perforation must be considered not only in patients who have free intraperitoneal gas but also in those who present with symptoms, signs, or studies consistent with retroperitoneal gas, such as subcutaneous emphysema, pneumomediastinum, or pneumothorax.
Adult↗
DISSECTING MICROSCOPE APPEARANCES OF THE GASTRIC MUCOSA.
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Biopsy↗