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At least 325 records · Page 18Linked to original sources
PubMed1999

Mouse colitis induced by Escherichia coli producing Yersinia enterocolitica 60-kilodalton heat-shock protein: light and electron microscope study.

In patients with inflammatory bowel disease (IBD), including ulcerative colitis (UC), heat-shock protein (Hsp) 60 has been detected in serum and the intestinal tract. Our mouse colitis model was established using Escherichia coli transformed with Yersinia enterocolitica Hsp60 gene as an immunizing antigen, and examined light and electron microscopically as compared with lesions of UC. The large intestine of mice injected with Hsp60 antigen showed swollen goblet cells, glandular dilation, erosion, ulceration, and infiltration of inflammatory cells. The change like crypt abscesses was also found, and various phases of inflammation were observed simultaneously in individual mice. In addition, the reticulum fibers were absent ultrastructurally in the subepithelial reticular layer. Hyperplasia of the thymus was found in antigen-treated mice. These lesions were similar to those of UC. These results suggest that UC-like enteritis in mice was induced by using Hsp60, considered as one of the pathogens for UC.

Animals↗
PubMed1977

Cytomegalovirus inclusions in patients with ulcerative colitis and toxic dilation requiring colonic resection.

Microscopic examination of 50 colon resection specimens from 46 patients with ulcerative colitis revealed 6 patients whose colons contained intranuclear inclusions characteristic for cytomegalovirus (CMV). All patients were male, 47 years of age or older, and all had marked severe and fulminating courses. Five of the 6 patients had toxic dilation of the colon. Three of our patients had received no steroid therapy before their toxic dilation, however, all received steroids during attempts at medical management. Two other patients were found to have toxic dilation of the colon among our 46 patients, however, no evidence of CMV could be found in these 2 cases. There were 6 patients without toxic dilation whose colon specimens showed destructive inflammation and granulation tissue extending into the muscularis propria or transmurally. None of the colons from these 6 patients contained CMV inclusions. In our patients, the finding of CMV may be coincidental, but it is suggested that in our group of patients with ulcerative colitis, the CMV may play a role in altering the clinical course of these patients.

Aged↗
PubMed2002

Increased activity and expression of matrix metalloproteinase-9 in a rat model of distal colitis.

Matrix metalloproteinases may play a role in tissue remodelling and destruction associated with inflammation. We investigated activity and expression of matrix metalloproteinases in a rat model of colitis and tested the therapeutic potential of a synthetic inhibitor (CGS-27023-A). Colitis was induced by dextran sulphate sodium (at 5% in drinking water for 5 days) in a group of eight rats, whereas a matched control group received plain water. Activity and expression of matrix metalloproteinases were measured in colonic tissue homogenates using zymography and Western blot on days 3 and 5 after induction of colitis. In another set of experiments, two groups of colitic rats (20 per group) were treated with CGS-27023-A (20 mg/kg) or vehicle, respectively. On days 5 and 14, colonic mucosal lesions were blindly scored by microscopic examination. Induction of colitis led to a significant upregulation of matrix metalloproteinase-9 protein and its activity, but no change in matrix metalloproteinase-2 activity was observed. Treatment with CGS-27023-A significantly decreased the extent and severity of epithelial injury but did not influence mucosal repair. We conclude that increased activity of matrix metalloproteinases may contribute to epithelial damage in this model of colitis.

Animals↗
PubMed2005

Disseminated acute concomitant aspergillosis and mucormycosis in a pony.

A 6-year-old female pony died after 2 days of prostration. Clinical signs included hyperthermia and abnormal pulmonary auscultation sounds. Necropsy revealed diffuse severe necrohaemorrhagic colitis and splenitis, multiple visceral ecchymoses, petechial haemorrhages in the brain and lungs. Microscopical examination showed acute necrohaemorrhagic colitis, encephalitis, pneumonia and splenitis associated with fibrinoid vasculitis, thrombosis and fungal hyphae within and around vessels. Immunohistologically, concomitant aspergillosis (caused by Aspergillus fumigatus) and mucormycosis (causde by Absidia corymbifera) were identified in the colonic and pulmonary lesions, whereas pure mucormycosis was observed in cerebral and splenic lesions. Dual mycotic infections are very rarely described, and the present case emphasizes the need of immunohistochemistry in order to obtain a clear-cut diagnosis of mixed fungal infections.

Acute Disease↗
PubMed2006

Crohn's colitis perforation due to superimposed invasive amebic colitis: a case report.

The clinical and microscopic appearances of inflammatory bowel disease may be very similar to those of amebic colitis. The coexistence of invasive amebiasis with inflammatory bowel disease may have disastrous results. Patients with inflammatory bowel disease have a greater prevalence of amebiasis, but this association is more significant for ulcerative colitis. There have been very few reports in the literature presenting the superimposition of amebiasis on Crohn's disease. In this report, a rare case of Crohn's colitis with superimposed amebiasis resulting in colonic perforation is presented. Patients with inflammatory bowel disease traveling to endemic areas may benefit from receiving a course of prophylactic anti-amebic medication.

Abdominal Abscess↗
PubMed2002

Lymphocytic colitis treated with proctocolectomy and ileal J-pouch-anal anastomosis: report of a case.

PURPOSE: We present a case of severe diarrhea caused by lymphocytic colitis and concurrent celiac sprue in a patient who did not respond to maximal medical therapy and required surgery. METHODS: The patient was initially treated with fecal diversion via an end ileostomy. Six months later, she underwent colectomy and one-stage ileal J-pouch-anal anastomosis. RESULTS: Notably, the characteristic microscopic changes of lymphocytic colitis were still present at the time of colectomy despite diversion. CONCLUSION: Colectomy with continent reconstruction is an option for treatment of patients with lymphocytic colitis refractory to medical therapy.

Anal Canal↗
PubMed1989

[Transient ischemic colitis. Diagnostic value of patchy epithelial atrophy].

Microscopic findings, observed in 58 colonic biopsies, have been described by the authors during transient ischemic colitis. One of these lesions, closely associated with the diagnosis and named patchy tubular atrophy, was considered as a marker for ischemia. Patchy tubular atrophy was observed at the beginning of the disease, and was regularly associated with normal and necrotic areas. Three morphological aspects characterized this condition: --non secretory glandular crypts covered with rudimentary basophilic epithelium, --crypts regularly distributed in a geometrical pattern with intact connective spaces, --absence of interstitial inflammatory infiltrate, and presence of fibrinous thrombosis with extravasation of erythrocytes. This morphologic pattern was specific enough to rule ou the other inflammatory or trophic bowel diseases. Therefore patchy tubular atrophy, observed during transient ischemic colitis, was considered by authors as a distinct entity.

Aged↗
PubMed2003

Effects of intrarectal and intraperitoneal N(G)-nitro-L-arginine methyl ester treatment in 2,4,6-trinitrobenzenesulfonic acid induced colitis in rats.

Inflammatory bowel disease (IBD) has been associated with an increased generation of nitric oxide (NO). Different authors have shown that NO in IBD can be either harmful or protective. The aim of this study was to investigate the efficiency of intrarectal (i.r.) and intraperitoneal (i.p.) application of N(G)-nitro-L-arginine methyl ester (L-NAME), a non-specific nitric oxide synthase inhibitor, in experimental acute colitis in the rats. Acute colitis was induced in rats by 2,4,6-trinitrobenzenesulfonic acid (TNBS) and ethanol. Twenty-eight rats were divided into four groups. L-NAME (50 mg/kg/day) was administered i.p. (Group 1) and i.r. (Group 2) for 7 days following the day when colitis was induced. Group 3 rats were not given any treatment after induction of colitis. Control group rats were given saline solution i.r. instead of TNBS. The presence of hyperemia, inflammation and ulcer was evaluated to score of macroscopic morphologic damage. The severity of colitis was assessed by microscopic criteria including ulceration, mucus cell depletion, crypt abscesses, inflammatory cysts, mucosal atrophy, edema, inflammatory cell infiltration, and vascular dilatation. Rectal tissue myeloperoxidase (MPO) activity and serum-rectal tissue nitrite levels were measured. Serum and rectal tissue nitrite levels increased in Group 3 rats. Both i.p. and i.r. L-NAME treatment significantly reduced serum and rectal tissue nitrite levels, but no effect on MPO activity and histologic damage score was observed. Under the present conditions we concluded i.r. and i.p. L-NAME treatment, applied at the dosage of 50 mg/kg/day, does not have any protective effect on the colonic injury.

Acute Disease↗
PubMed1999

Chronic microscopic enterocolitis with severe hypokalemia responding to subtotal colectomy.

The authors present the first case report of a 50-year-old woman with a 33-year history of severe, chronic watery diarrhea and hypokalemia secondary to chronic active microscopic enterocolitis with patterns similar to lymphocytic colitis but with acute cryptitis and terminal ileum involvement microscopically. The progressive nature of her illness resulted in multiple hospital admissions secondary to hypokalemia with subsequent chronic renal failure. High continuous doses of oral potassium supplements failed to correct the hypokalemic episodes. After subtotal colon resection, the patient made a marked clinical improvement with normal serum potassium levels without receiving potassium supplementation.

Chronic Disease↗
PubMed2003

Pyoderma gangrenosum in a patient with collagenous colitis.

The association between pyoderma gangrenosum and inflammatory bowel disease is well established. Collagenous colitis is one of the microscopic colitides, which are thought to be on the same spectrum of disease as Crohn's disease and ulcerative colitis. Before this study there had been no reported cases of pyoderma gangrenosum in the setting of collagenous colitis. We report a case of a 79-year-old woman with symptomatic collagenous colitis and refractory pyoderma gangrenosum.

Administration, Oral↗
PubMed1993

Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1 beta by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn's disease.

The perpetuation of inflammation in ulcerative colitis and Crohn's disease may be regulated in part by an increased secretion of proinflammatory cytokines due to either an appropriate response to initial stimulating agents, and/or due to an impaired down-regulation of cytokine secretion. The aim of this study was to determine the secretion patterns of the proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha), IL-6 and IL-1 beta, from isolated lamina propria mononuclear cells (LPMNC) isolated from colonic biopsies from patients with untreated ulcerative colitis or Crohn's disease. LPMNC isolated from involved inflammatory bowel disease (IBD) mucosa spontaneously produced increased amounts of TNF-alpha, and IL-6, and IL-1 beta. The TNF-alpha secretion from IBD LPMNC could be further enhanced by pokeweed mitogen stimulation. The secretion patterns of TNF-alpha and IL-1 beta by LPMNC from patients with either ulcerative colitis or Crohn's disease demonstrated a close correlation with the degree of tissue involvement and mucosal inflammation. LPMNC from non-involved ulcerative colitis mucosa secreted markedly increased levels of IL-6 compared with non-involved Crohn's disease mucosa or control mucosa. The heightened IL-6 secretion from LPMNC from non-involved ulcerative colitis mucosa without visible or microscopic signs of inflammation indicates that the pathophysiologic mechanisms involved in the initiation of inflammation may differ between ulcerative colitis and Crohn's disease. The determination of proinflammatory cytokine secretion by isolated LPMNC from colonoscopic biopsies may be a sensitive method for monitoring the severity of mucosal inflammation in IBD patients.

Adult↗
PubMed2002

Variability in serotonin and enterochromaffin cells in patients with colonic inertia and idiopathic diarrhoea as compared to normal controls.

AIM: To evaluate differences in distribution, density and staining intensity of enterochromaffin cells (EC) and serotonin cells (SC) in the colonic mucosa of patients with colonic inertia (CI), idiopathic diarrhoea (ID) and a control group. METHODS: Three groups were studied: 19 patients' colons after subtotal colectomy for CI, and 17 patients' biopsies for diarrhoea (>3 bowel movements/day) with histological findings of normal mucosa (excluding microscopic, eosinophillic and collagenous colitis). The third group included 15 patients who underwent colonoscopy and biopsy for indications other than constipation, inflammatory bowel disease, diarrhoea or neoplasm (control group). Specimen blocks were obtained in each case from the right and left colon. Immunohistochemical staining for EC and SC were done on 4 micro m sections from Hollandes fixed, paraffin embedded tissues with primary rabbit antibody against chromagranin A or serotonin, and biotynylated secondary antibody and enzyme labelled streptavidin. RESULTS: The number of EC in the mucosa of the left colon in patients with CI (16.8 +/- 10.2) and ID (19.9 +/- 9.7) were significantly higher than they were on the right side (CI: 9.4 +/- 6.0, ID: 12.1 +/- 5.3). However, there were no significant differences between the left and right sides in the control group (L: 10.3 +/- 5.3; R: 13.4 +/- 7.6). Although the quantity of EC in the left colon in both patients with CI (P < 0.05) and ID (P < 0.01) were significantly higher than in the controls, there was no significant difference between CI and ID. In both the right and left colon, the percentage of EC with low positive density was significantly higher (P < 0.01) while those cells with moderate or low staining intensity were significantly lower in patients with CI than in either patients with ID or control group. In patients with CI, the quantity of SC in the mucosa of the left colon (12.1 +/- 6.4) was higher than in the right (CI: 7.9 +/- 3.6; control 4.6 +/- 3.3; ID 4.6 +/- 2.9) (P = 0.0057). In contrast there was no significant difference in SC in either the ID or control groups. The quantity of SC in both sides of the colon was significantly higher both in patients with CI as compared to the control group (P < 0.01) and patients with CI vs. patients with ID (L = P < 0.01; R = P < 0.05). There was a significantly positive correlation between the numbers of EC and SC in patients with CI (L: r = 0.5425, P < 0.05; R: r = 0.745, P < 0.01). CONCLUSION: In patients with CI, EC increases possibly due to an increase in SC. Conversely, in patients with ID, the EC increase results from peptides other than SC. Our results suggest that different aetiological factors contribute to ID and CI.

Journal Article↗
PubMed2000

[Digestive disorders and Legionnaires' lung disease. Accompanying signs or visceral location?].

Digestive disorders in Legionella pneumophila pneumonia such as nausea, vomiting, diarrhoea, are common; they are clinical arguments to suspect this bacteria to be responsible for this pneumonia. In this case-report, a patient with pneumonia due to Legionella pneumophila serogroup I presented in the follow-up with signs of enteritis with ascites. We looked ahead in literature who made us discover the multiple organ involvement that may happen in Legionnaires' disease. Diagnostic procedures consist in simple tests as ultrasonography, abdominal computerised tomography, that show inflammatory disease signs and sometimes ascites. Exceptionally, Legionella pneumophila has been demonstrated with direct immunofluorescent microscopic study, in inflammatory colitis pieces with haemorrhagic necrosis in different stage processes. Pathogenesis could be explained by the systemic spread of the organism and formation at distance of necrotising enteritis focus. It is initiated by necrotising factors of bacterial origin and hypersensitivity reactions (type I and III).

Adult↗
PubMed2000

[A case of ANCA positive idiopathic crescentic glomerulonephritis initiated with fever and liver dysfunction].

We studied a case of a 63 year old Japanese man who presented in October, 1994 with general fatigue, low grade fever, micro hematuria and leukocytosis, elevated CRP as well as liver dysfunction. A liver biopsy at that time revealed mild cholangiolitis. Six months later he was admitted because of weight loss, protein urea, and renal failure. At that time he was positive for antineutrophil cytoplasmic antibody(ANCA) with perinuclear staining patter(p-ANCA) done by indirect immunofluorescence. He was also positive for anti-myeloperoxidase antibody(MPO-ANCA) done by ELISA. A renal biopsy showed idiopathic crescentic glomerulonephritis with pauci-immune type(ICGN). Despite therapy with steroids and cyclophosphamide, which improved his subjective symptoms, his renal failure accelerated necessitating hemodialysis which he has been on for over four years. In conclusion, this patient has a rare case of ICGN that presented with liver dysfunction similar to autoimmune hepatitis. Since ANCA has been known to be associated with systemic vasculitides as well as chronic inflammatory diseases(e.g. ICGN, microscopic polyarteritis nodosa, ulcerative colitis or autoimmune liver diseases), both the crescent formation in this patient's glomeruli and cholangiolitis in his liver may have shared the common etiology related to ANCA.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed1991

[Malacoplakia of the vagina. Cytological, histological and ultrastructural study of a case].

A case of vaginal malakoplakia is reported in a 65 year old patient receiving prednisone for fifteen months for the treatment of collagen colitis. The macroscopic and microscopic appearance, cytological examination of the vaginal smear and ultrastructural examination were typical of malakoplakia. To our knowledge, this is the seventh detailed case of vaginal malakoplakia and the twenty-sixth case of malakoplakia of the female genital tract.

Aged↗