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Colonic Biopsies (colonic + biopsy)
Selected AbstractsRibosomal DNA sequence analysis of mucosa-associated bacteria in Crohn's diseaseINFLAMMATORY BOWEL DISEASES, Issue 6 2004Tom Prindiville MD Abstract Background: Enteric bacteria are implicated in the pathogenesis of Crohn's disease (CD); however, no specific causative organisms have been identified. Aims: This study was undertaken to correlate disease activity with changes in intestinal biota in patients with CD. Subjects: Ribosomal DNA analysis was used to explore the composition of the intestinal biota in patients with (1) CD undergoing colonoscopy, (2) CD undergoing surgical resection, and (3) no inflammatory bowel disease. Methods: Primers targeting bacterial 16S ribosomal DNA (rDNA) were used to amplify bacterial DNA associated with active CD lesions, comparable normal tissue from patients with CD, and normal control tissue. Each amplicon was cloned. Seven hundred thirty-nine rDNA clones were sequenced from 16 biopsies from CD patients, 15 surgical samples, and 10 biopsies from normal control patients. Results: Known extracellular or intracellular pathogens were not found. No rDNA sequence, phylogenetic group, or subgroup was consistently associated with CD lesions compared with normal tissues from the same patients. Colonic biopsies from CD-afflicted patients compared with biopsies from normal control subjects had an increase in facultative bacteria; in small bowel, CD patients had an increase in the Ruminococcus gnavus subgroup with a decrease in the Clostridium leptum and Prevotella nigrescens subgroups. However, differences in small bowel may have reflected individual variation rather than disease association. Surgical samples showed differences when compared with biopsy-derived samples. Conclusions: These findings suggest that CD is not caused by invasive pathogens associated specifically with the sites of lesions but that dysbiosis exists in this condition. [source] Differential expression of CCR5 and CRTH2 on infiltrated cells in colonic mucosa of patients with ulcerative colitisJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 9 2003KOJI MATSUZAKI Abstract Background and Aim:, The pathogenesis of ulcerative colitis (UC) is unclear, but abnormal infiltration of T lymphocytes in the colonic mucosa has been implicated in the mucosal tissue damage. The abnormal cytokine production because of a T helper (h)1/Th2 imbalance may play an important role in continuing inflammation in the colonic mucosa. In the present study, the expression of chemokine receptor 5 (CCR5) as a Th1 marker and a chemoattractant receptor-homologs molecule expressed on Th2 cells (CRTH2) were investigated in order to analyze impaired Th1/Th2 responses in the colonic mucosa of UC patients. Methods:, Tissue samples were obtained by colonic biopsies from patients with UC or colonic polyps, with informed consent. Immunohistochemical analysis was performed on periodate, lysine-paraformaldehyde-fixed serial cryostat sections using the labeled streptavidin biotin method. Monoclonal antibodies against CD4, CCR5 or CRTH2 were used as primary antibodies. The number of cells expressing CD4, CCR5 or CRTH2 per unit area was calculated by using an image analyzer. Results:, In the patients with UC, the numbers of CD4- and CCR5-positive cells were significantly increased in inflamed mucosa, and appeared to be correlated with the disease activity. The infiltration of CRTH2-positive cells was predominantly observed in the mildly inflamed or the margin of inflamed mucosa of UC patients. Conclusion:, There is a possibility that Th1 responses significantly occur in colonic mucosa with severe inflammation, while Th2 responses mainly occur with mild inflammation in UC patients. The Th1/Th2 imbalance in colonic mucosa may be related to the disease progression of UC. [source] Routine colonic mucosal biopsy and ileoscopy increases diagnostic yield in patients undergoing colonoscopy for diarrheaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 3 2002IAN F YUSOFF Abstract Background and Aims: In patients undergoing colonoscopy for diarrhea, when the examination is normal, the role of routine mucosal biopsy remains controversial, particularly in the open-access setting. It is uncertain whether routine ileoscopy adds anything to colonoscopy alone. We aimed to assess the yield of mucosal biopsy and ileoscopy in patients with diarrhea. Methods: We retrospectively reviewed all colonoscopies performed for diarrhea over a 9-year period in a tertiary referral center with an open-access service. We then selected cases where the examination was normal and biopsies were performed. The histopathology reports of these selected cases were then reviewed. Results There were 1131 cases identified. The mucosal examination was normal in 465 cases (41%); 362 of these had colonic biopsies performed. Histology was normal in 316 cases (87%) and was non-specific in 28 cases (8%). Significant histopathology was present in 18 cases (5%) with a significantly higher prevalence of microscopic colitis in patients above 60 years old. Ileoscopy was performed in 508 cases and was abnormal in 26 cases (5%). The abnormality on ileoscopy was the sole abnormality in 13 cases (3%). Conclusions Routine colonic mucosal biopsy and ileoscopy each identify significant additional pathology in 5% of cases when investigating patients with diarrhea, and are recommended as routine practice in this setting. We found ileal biopsy unhelpful when ileoscopy was normal. © 2002 Blackwell Science Asia Pty Ltd [source] Association between anal furunculosis and colitis in the dog: preliminary observationsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2002P. M. Jamieson Treatment of anal furunculosis in dogs is often unsatisfactory and may be associated with significant recurrence and complications. This may be compounded by the simultaneous presence of colitis in affected animals. Clinical signs associated with colitis and anal furunculosis may be similar, including faecal tenesmus, dyschezia and haematochezia. To examine the incidence of concurrent anal furunculosis and colitis, colonic biopsies were collected from 18 dogs referred for treatment of anal furunculosis. Nine dogs (50 per cent) had a histopathological diagnosis of colitis. Clinical signs more indicative of colitis than anal furunculosis (increased frequency of defecation, mucus in faeces and diarrhoea) were not observed more frequently in dogs with confirmed colitis compared with those with furunculosis alone. Therefore, while an association between colitis and anal furunculosis may exist, clinical signs alone cannot be used as an indicator of the presence of colitis in cases of anal furunculosis. The authors recommend that colonic biopsies should be undertaken in all dogs presented with anal furunculosis. Whether specific treatment of colitis in dogs with histopathological evidence of colitis improves the outcome of treatment for anal furunculosis awaits further study. [source] In vivo effects of mesalazine or E. coli Nissle 1917 on microsatellite instability in ulcerative colitisALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 6 2009A. GOEL Summary Background, Microsatellite instability (MSI) occurs in chronically inflamed colorectal tissue and may evolve to colitis-associated cancer. In vitro data suggest that mesalazine (5-ASA) improves MSI. Aim, To analyse the changes in MSI in 156 distal colonic biopsies of 39 patients with ulcerative colitis that had been treated within a randomized, double-blind trial comparing 5-ASA with E. coli Nissle (EcN). Methods, Two biopsies had been collected before and after 1 year of treatment. MSI testing was performed using a panel of eight markers, including 3 dinucleotide and 5 mononucleotide repeats. Results, No MSI was observed with any of the mono-repeats, and among dinucleotide repeats, only D5S346 (maps to APC) and D17S250 (p53) were consistently informative. Overall, 31/156 (20%) biopsies displayed MSI. After 1 year, 3/11 patients displayed MSI improvement [change to microsatellite stability (MSS); 1 on 5-ASA, 2 on EcN] at D5S346 and 4/11 showed MSI worsening (change from MSS to MSI; all 5-ASA). For D17S250, the corresponding data were for 3/9 patients (2 on 5-ASA, 1 on EcN) and 2/9 (both on 5-ASA), respectively. Conclusions, In the set of biopsies taken from patients treated with 1.5 g 5-ASA for 1 year, there was no improvement in the prevalence of MSI in the distal colon. [source] 111Indium-labelled human gut-derived T cells from healthy subjects with strong in vitro adhesion to MAdCAM-1 show no detectable homing to the gut in vivoCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2004J. KELSEN SUMMARY Integrin ,4,,7 is the principal gut-homing receptor, and it is assumed that expression of this specific integrin directs lymphocytes to the gut in vivo. Adoptive cellular immunotherapy against inflammatory bowel disease (IBD) may depend on the expression of integrin ,4,,7 to accomplish local delivery of intravenously injected regulatory T cells in inflamed gut mucosa. The present study aimed to investigate whether in vitro expanded human T cells from the colonic mucosa maintain integrin expression, show in vitro adhesion and retain in vivo gut-homing properties during cultivation. Whole colonic biopsies from healthy subjects were cultured in the presence of interleukin-2 (IL-2) and IL-4. The integrin expression of the cultured T cells was determined by flow cytometry and in vitro adhesion was assessed in a mucosal addressin cell adhesion molecule 1 (MAdCAM-1) adhesion assay. We studied the homing pattern after autologous infusion of 3 × 108 111Indium (111In)-labelled T cells in five healthy subjects using scintigraphic imaging. The cultured CD4+CD45RO+ gut-derived T cells express higher levels of integrin ,4,,7 than peripheral blood lymphocytes (PBLs) and show strong adhesion to MAdCAM-1 in vitro, even after 111In-labelling. Scintigraphic imaging, however, showed no gut-homing in vivo. After prolonged transit through the lungs, the T cells migrated preferentially to the spleen, liver and bone marrow. In conclusion, it is feasible to infuse autologous T cells cultured from the gut mucosa, which may be of interest in adoptive immunotherapy. Despite high expression of the gut-homing integrin ,4,,7 and adhesion to MAdCAM-1 in vitro, evaluation by 111In-scintigraphy demonstrated no gut-homing in healthy individuals. [source] Increased levels of insulin-like growth factor binding protein-2 in sera and tumours from patients with colonic neoplasia with and without acromegalyCLINICAL ENDOCRINOLOGY, Issue 4 2001F. Miraki-Moud OBJECTIVE Patients with acromegaly are at increased risk of developing colorectal carcinoma and premalignant tubulovillous adenoma. The pathogenesis of these neoplasms could involve a stimulatory effect of serum growth factors on colonic epithelial cell proliferation. The aim of this study was to evaluate changes in (1) serum IGF-I, IGF-II, IGFBP-3 and IGFBP-2 and (2) changes in local expression of IGFBPs and p53 in colonic epithelium in patients with colonic neoplasia with and without acromegaly. DESIGN A cross-sectional retrospective study was performed. Fasting serum samples were obtained at the time of colonoscopy for patients with acromegaly and at the time of surgery for patients with colonic neoplasia without acromegaly. MEASUREMENTS Serum IGF-I, IGF-II, IGFBP-2 and IGFBP,3 were measured using specific immunoassays. Tissue expression of IGFBP-2, IGFBP-3 and p53 status were determined by immunohistochemistry. PATIENTS Group 1: 26 age- and sex-matched control subjects (range 40,69 years); group 2: 18 patients with acromegaly without colonic neoplasia (range 39,68 years); group 3: 18 patients with acromegaly and colonic neoplasia (range 41,74 years, 11 = adenoma, seven = carcinoma); group 4: 19 patients with colonic neoplasia without endocrine disease (range 43,91 years, four = adenoma, 15 = carcinoma). Immunohistochemical staining of colonic biopsies was performed for IGFBP-2, IGFBP-3 and p53 in groups 3 and 4. RESULTS Mean serum IGF-I and IGFBP-3 levels were significantly elevated in group 2 (371 ± 131 µg/l and 6·5 ± 1·8 mg/l, respectively) and group 3 (379 ± 174 µg/l and 5·8 ± 1·6 mg/l, respectively), and significantly reduced in group 4 (103 ± 36 µg/l and 2·4 ± 1 mg/l) compared to controls (165 ± 40 µg/l and 4·7 ± 1 mg/l; P < 0·0001, P < 0·001, respectively). However, median serum IGFBP-2 levels were significantly elevated in group 3 (P < 0·01) and group 4 (P < 0·0001). Immunostaining for IGFBP-2 showed strong areas of immunoreactivity in the cytoplasm of malignant colonic epithelium compared to benign epithelium. IGFBP-3 immunostaining showed strong areas of immunoreactivity in the cytoplasm and in the nucleus of malignant and benign colonic epithelium compared to the normal epithelium. Nuclear staining for p53 was observed in three patients from group 3 (two carcinoma, one adenoma) and four patients from group 4 (all carcinoma). CONCLUSION Our results describe changes in IGFBP-2 expression in colonic neoplasia in patients with and without acromegaly, which suggest that this binding protein may regulate local bioavailability of IGF, which in turn could modulate colonic cell proliferation and/or differentiation. [source] | ||||||||||