DIGESTIVE ENDOSCOPY, Issue 4 2010
Takashi Hisabe
Background and Aim:, Ulcerative colitis (UC) is not only characterized by pathological lesions localized to colonic mucosa, but also to various complications involving other organs, including postoperative pouchitis. Among these complications, diffuse gastroduodenitis with lesions resembling colonic lesions has been reported, albeit rarely. The aim of the present study was to attempt to characterize the lesions of the upper gastrointestinal tract occurring as a complication of UC, and to assess the frequency and clinical course of these lesions. Methods:, A total of 322 UC patients who had undergone upper gastrointestinal endoscopy were retrospectively analyzed. We assessed the frequency of endoscopic findings, including diffuse gastroduodenal lesions resembling colonic lesions. Ulcerative gastroduodenal lesion (UGDL) associated with UC was diagnosed if lesions satisfied the following criteria: (i) improvement of the lesions with treatment of UC; and/or (ii) resemblance to UC in pathological findings. Results:, UGDL satisfying the aforementioned criteria was found in 15 (4.7%) of 322 patients. All the 15 patients had UGDL accompanied by pancolitis or after proctocolectomy. Frequency in 146 patients with pancolitis was 6.2% (nine patients) and that in 81 patients who had undergone proctocolectomy was 7.4% (six patients). Four patients with diffuse ulcerative upper-gastrointestinal mucosal inflammation (DUMI) had pouchitis. In all patients except one, the lesions resolved easily with medical treatment. Conclusions:, In more than half of the post-proctocolectomy patients, UGDL was related to the occurrence of pouchitis. The existence of characteristic UGDL must be taken into account in the diagnosis and treatment of UC, and UGDL is possibly related to the occurrence of pouchitis. [source]

REFRACTORY DIVERTICULAR COLITIS WITH PROGRESSIVE ULCERATIVE COLITIS-LIKE CHANGES EXTENDING TO THE RECTUM

DIGESTIVE ENDOSCOPY, Issue 3 2009
Tateki Yamane
A 68-year-old man visited our department because of diarrhea and bloody stools. Colonoscopy revealed diverticula scattered in the sigmoid colon with localized mucosal edema and reddening. The mucosa became somewhat rough 9 months later, and had an erosive, ulcerative colitis (UC)-like appearance after a further 6 months, with these changes extending to the rectum. These findings led to a diagnosis of diverticular colitis (DC) with UC-like changes. The condition was refractory to treatment including drug therapy and was thus surgically treated. No cases of DC have been reported in Japan, and a refractory case of DC with progressive UC-like changes extending to the rectum is rare even in Europe and the USA. [source]

MAGNIFYING COLONOSCOPY FOR THE DIAGNOSIS OF INFLAMMATORY CHANGES IN ULCERATIVE COLITIS

DIGESTIVE ENDOSCOPY, Issue 3 2006
Satoshi Sugano
Background:, Endoscopic observation is the most effective method for the evaluation of staging in ulcerative colitis (UC). However, in cases with very mild inflammatory activity, histopathological diagnosis may also be required. Unfortunately, biopsy-related accidents are not uncommon. As an alternative, we have used a magnifying colonoscope commonly used for tumor diagnosis to examine in detail the colon mucosa of UC patients in clinical remission, and then compared these findings relative to conventional endoscopy using histopathological diagnosis. Subjects and Methods:, Among UC cases examined by colonoscopy between April 2000 and April 2005, 27 cases without hematochezia for at least 1 month were enrolled in this study. Following observations of inflammatory changes using conventional colonoscopy, magnifying observation and biopsies at a total of 144 sites were evaluated. Using histopathological standards, acute-phase inflammation was indicated by the presence of neutrophil infiltration, whereas chronic-phase inflammation was indicated by infiltration of lymphocytes, plasma cells and eosinophils. Results:, Indicators of significant inflammation by conventional observation was erosion. Under magnification, inflammation appears as superficial defects in mucosa and small whitish spots. When the presence of infiltrating neutrophils was used as a positive histological marker for inflammation, there was no difference in the accuracy of diagnosis by conventional observation (95.1%) versus magnifying observation (97.2%). In contrast, when lymphocyte infiltration was used as a marker, the accuracy of diagnosis increased significantly (88.2%) using magnifying observation relative to conventional observation (61.1%). Conclusions:, Magnifying endoscopy can be used effectively in the evaluation of minute mucosal changes in cases of UC remission. [source]

WEGENER'S GRANULOMATOSIS COMPLICATED WITH APHTHOID COLITIS

DIGESTIVE ENDOSCOPY, Issue 3 2006
Yasushi Umehara
A 58-year-old man was admitted with upper abdominal pain and high fever. There was no abnormality on chest X-ray, abdominal ultrasonography, abdominal CT and upper gastrointestinal endoscopy. Antineutrophil cytoplasmic antibodies (C-ANCA) titers were high and a chest CT scan depicted multiple nodules in the bilateral lungs. A diagnosis of Wegener's granulomatosis was therefore made. Three weeks after admission, diarrhea and bloody stool developed. Colonoscopy revealed many aphthoid lesions surrounded by redness in the entire colon. Although the biopsy from aphtha did not show vasculitis or granuloma, the aphthoid lesions were suspected as a complication of Wegener's granulomatosis. As a result of predonisolone medication (60 mg/day), the plasma C-reactive protein (CRP) and high fever improved promptly. In conclusion, although colonic involvement in a patient with Wegener's granulomatosis is extremely rare, it is important to keep in mind that colonic lesions might be due to vasculitis in ANCA-positive disease, such as Wegener's granulomatosis. [source]

ILEITIS AS A MAIN RECURRENT LESION IN A PATIENT WITH ULCERATIVE COLITIS: REPORT OF A CASE

DIGESTIVE ENDOSCOPY, Issue 2 2000
Shuichi Sano
We report a case of ulcerative colitis complicating ileitis that endoscopically and histologically resembled a colonic lesion. Eight years prior to the time of writing, the patient had undergone proctosigmoidectomy and ileocecal resection because of severe hemorrhagic lesions of ulcerative colitis. A month prior to the time of writing, bleeding from the stoma occurred. Endoscopy revealed erosions on easy-bleeding mucosa in the ileum but no active inflammatory lesions in colonic mucosa except for small erosions in the descending colon beneath the stoma. Histologic findings of biopsy specimens from the ileal mucosa showed marked inflammation including neutrophile infiltration and crypt abscesses. This is a rare case of ulcerative colitis showing ileitis as a main recurrent lesion, suggesting that careful observation of the small intestine will be required after ileocecal resection in ulcerative colitis patients. [source]

RECURRENT COLITIS WITH DIFFERENT CAUSES

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 5 2003
Article first published online: 29 APR 200
No abstract is available for this article. [source]

5-HT1B/1D Agonists, Oral Contraceptives, and Ischemic Colitis,A Response

HEADACHE, Issue 6 2006
James A. Charles MD
No abstract is available for this article. [source]

Regulatory T cells and intestinal homeostasis

IMMUNOLOGICAL REVIEWS, Issue 1 2005
Janine L. Coombes
Summary:, Murine models of inflammatory bowel disease (IBD) are useful tools for the study of the pathogenesis and regulation of intestinal inflammation. Colitis can be induced in immune-deficient mice following transfer of populations of T cells or following infection with Helicobacter hepaticus and other intestinal pathogens. In these situations, colitis occurs as a result of the absence of a specialized population of regulatory cells, as transfer of CD4+CD25+ T cells prevents disease. Importantly, from a clinical perspective, CD4+CD25+ T cells can also reverse an established colitis. CD4+CD25+ T cells proliferate both in the secondary lymphoid organs and at the site of inflammation, suggesting that regulation occurs both locally and systemically. CD4+CD25+ T cells are not only capable of regulating other T cells but are also capable of suppressing components of the innate immune system. Control of colitis is dependent on the presence of the immunosuppressive cytokines interleukin-10 and transforming growth factor-,, although their roles are divergent and complex. Regulatory T cells represent one of the host's mechanisms to prevent immune pathology during chronic immune stimulation. Enhancement of regulatory T-cell activity may be useful to control autoreactive T-cell responses and inhibit harmful inflammatory diseases such as asthma and IBD. [source]

Patients' attitudes to medicines and adherence to maintenance treatment in inflammatory bowel disease

INFLAMMATORY BOWEL DISEASES, Issue 6 2009
Rob Horne PhD
Abstract Background: Nonadherence has been reported in over 40% of patients taking maintenance therapies (MT) for inflammatory bowel disease (IBD). Studies in other illness groups have shown that nonadherence is related to negative attitudes to treatment. The aim of this study was to assess patients' attitudes to MT for IBD (beliefs about personal need for MT and potential adverse effects) and to identify whether such beliefs are associated with adherence to MT. Methods: A cross-sectional survey was conducted in which 1871 members of the National Association for Colitis and Crohn's Disease (NACC) completed validated questionnaires assessing beliefs about MT and adherence to MT. Results: Low adherence to MT was reported by 29% of participants and was associated with doubts about personal need for MT (odds ratio [OR] = 0.56; 95% confidence interval [CI]: 0.48,0.64; P < 0.001) and concerns about potential adverse effects (OR = 1.66; 95% CI: 1.42,1.94; P < 0.001). Attitudinal analysis showed that while almost half (48%) of the participants were "accepting" of MT (high necessity, low concerns), a large proportion of the sample (42%) were "ambivalent" about MT (high necessity, high concerns), 6% were "sceptical" (low necessity, high concerns) and 4% were "indifferent" (low necessity, low concerns). Compared to those who were "accepting" of MT, participants in all 3 other attitudinal groups were significantly more likely to be nonadherent. Conclusions: The way in which patients judge their personal need for MT relative to their concerns about MT can be a significant barrier to adherence. Interventions to facilitate optimal adherence to MT for IBD should address such perceptual barriers. (Inflamm Bowel Dis 2008) [source]

Effect of extended MMX mesalamine therapy for acute, mild-to-moderate Ulcerative Colitis

INFLAMMATORY BOWEL DISEASES, Issue 1 2009
Michael A. Kamm MD
Abstract Background: Many patients with ulcerative colitis (UC) respond to mesalamine therapy within 8 weeks. Those not achieving remission after 8 weeks are often treated with steroids or other immunosuppressive therapies. This study aimed to determine the effect of 8 weeks' high-dose MMX mesalamine extension therapy in patients with active, mild-to-moderate UC who had previously failed to achieve complete remission in 2 phase III, double-blind, placebo-controlled studies of MMX mesalamine (SPD476-301 and -302). Methods: Patients with active, mild-to-moderate UC who did not achieve clinical and endoscopic remission after ,8 weeks' treatment with MMX mesalamine (2.4 or 4.8 g/day), ASACOL® (mesalamine) delayed-release tablets 2.4 g/day, or placebo in the phase III studies received MMX mesalamine 4.8 g/day for 8 weeks. The aim was to assess remission at week 8, defined as a total modified UC Disease Activity Index score of ,1, calculated as: scores of 0 for rectal bleeding and stool frequency, a combined Physician's Global Assessment score and sigmoidoscopy score of ,1, no mucosal friability, and a ,1 point reduction from baseline in sigmoidoscopy score. Results: Overall, 304 patients who entered this acute extension study were evaluated; 59.5% achieved remission at week 8. Remission rates were similar irrespective of prior treatment in the initial acute phase III studies. Conclusions: Most patients with mild-to-moderate UC who fail to achieve remission with up to 8 weeks' initial mesalamine therapy can achieve clinical and endoscopic remission following a further 8 weeks' treatment with high-dose MMX mesalamine therapy, thereby avoiding step-up therapy. (Inflamm Bowel Dis 2008) [source]

Therapeutic benefit of pentostatin in severe IL-10,/, Colitis

INFLAMMATORY BOWEL DISEASES, Issue 7 2008
Jeffrey B. Brown MD
Abstract Background: Pentostatin, an adenosine deaminase (ADA) inhibitor, is a purine antimetabolite used for the treatment of leukemias. ADA inhibition blunts expansion of proliferating lymphocytes and increases adenosine release, a potent anti-inflammatory molecule. Human inflammatory bowel disease (IBD) is driven by expansion of effector T cells (Teff) that overwhelm reulatory T cells (Treg) and propagate innate immune reponses. Here we study the therapeutic benefits of ADA inhibition to impair Teff cell expansion and reduce inflammatory cytokine release in IL-10-deficient (IL-10 -/- ) mice. Methods: Colitis was induced in IL-10 -/- mice by administering piroxicam for two weeks. Mice were treated with daily pentostatin or phosphate-buffered saline for 1 week and effects on tissue inflammation, lymphocyte numbers and cytokine production examined. Results: Pentostatin reduced inflammation by >50% and nearly normalized serum amyloid A levels. Lymphocyte expansions in the colon and mesenteric lymph node (MLN) (3.5-fold and >5-fold respectively) dropped by >50-90%. Pro-inflammatory factors in the colon and MLN (IL-1,, IFN-,, IL-6, CXCL10, TNF) dropped whereas FoxP3 and TGF-, were unchanged. Reductions in cytokine production from equivalent numbers of T cells from pentostatin-treated mice after in vitro (36h) or in vivo (3h) activation suggested anti-inflammatory effects of pentostatin independent of lymphodepletion contributed to its therapeutic benefit. Analysis of mucosal lymphocyte subsets suggested pentostatin reduced numbers of effector CD4+ CD69+ T cells, while sparing CD4+ CD62L+ T cells. Conclusions: Pentostatin dosages that avoid severe lymphocyte depletion effectively treat colitis by impairing Teff cell expansion and reducing pro-inflammatory cytokine production while preserving regulatory Treg populations and function. (Inflamm Bowel Dis 2008) [source]

Mode of delivery and risk of fecal incontinence in women with or without inflammatory bowel disease: Questionnaire survey,

INFLAMMATORY BOWEL DISEASES, Issue 11 2007
J.P.L. Ong MRCP
Abstract Background: Elective cesarean section (CS) may be recommended for patients with Crohn's disease and perineal involvement. Little is known about CS rates in parous women with inflammatory bowel disease (IBD), nor the possible long-term impact of vaginal delivery and episiotomy on continence in women with IBD. Methods: Questionnaires were sent to all 777 regional members of a Colitis and Crohn's Disease patient association. Male members were asked to request their unaffected female spouse/partner to complete the forms in order to give a "control" group for comparison. Results: Forms were returned by 491 members (response rate 63%). CS had been undertaken for 37 of the 229 parous women with IBD (16%) versus 15 of the 116 without IBD (13%) (,2 = 0.62, P = NS). Only 2 women had undergone CS due to IBD. Of the parous women with IBD, 75 (33%) had persisting problems with fecal incontinence, of whom 21 (28%) dated this back to the time of vaginal delivery. By contrast, only 2 (2%) of the parous control group had suffered persisting fecal incontinence following vaginal delivery (,2 = 8.27, P < 0.01). Conclusions: Persisting fecal incontinence is reported by a significant minority of parous women with IBD, of whom over one-quarter date this back to vaginal delivery. CS is rarely recommended due to IBD alone. If our findings are confirmed in prospective studies, the threshold for recommending CS may need to be lowered for patients with IBD. (Inflamm Bowel Dis 2007) [source]

Plant sterol guggulsterone inhibits nuclear factor-,B signaling in intestinal epithelial cells by blocking I,B kinase and ameliorates acute murine colitis

INFLAMMATORY BOWEL DISEASES, Issue 12 2006
Jae Hee Cheon MD
Abstract Background/Aims: The plant sterol guggulsterone has been shown to have anti-inflammatory properties. It remains unknown, however, whether guggulsterone is effective for the treatment of inflammatory bowel disease (IBD). Therefore, we investigated anti-inflammatory effects of guggulsterone on intestinal epithelial cells (IEC) and on experimental murine colitis models and elucidated its molecular mechanisms. Methods: Human Caco-2 cells and rat non-transformed IEC-18 cells were stimulated with interleukin (IL)-1, or lipopolysaccharide (LPS) with or without guggulsterone. The effects of guggulsterone on nuclear factor (NF)-,B signaling in IEC were examined by intercellular adhesion molecule (ICAM)-1 real-time reverse-transcription polymerase chain reaction, NF-,B transcriptional activity assay, Western blotting for I,B phosphorylation/degradation, electrophoretic mobility shift assay, and in vitro I,B kinase (IKK) assay. For in vivo study, dextran sulfate sodium (DSS)-treated mice were fed with or without guggulsterone. Colitis was quantified by disease activity index and evaluation of macroscopic and microscopic findings. Phosphorylation of I,B and IKK in colon mucosa was assessed by Western blotting and immunohistochemistry. Results: Guggulsterone significantly inhibited LPS- or IL-1,-induced ICAM-1 gene expression, NF-,B transcriptional activity, I,B phosphorylation/degradation, and NF-,B DNA binding activity in IEC. Moreover, guggulsterone strongly blocked IKK activity. Administration of guggulsterone significantly reduced the severity of DSS-induced murine colitis as assessed by clinical disease activity score, colon length, and histology. Furthermore, tissue upregulation of I,B and IKK phosphorylation induced by DSS was attenuated in guggulsterone-treated mice. Conclusion: Guggulsterone blocks NF-,B signaling pathway by targeting IKK complex in IEC and attenuates DSS-induced acute murine colitis, which suggests that guggulsterone could be an attractive therapeutic option in the treatment of IBD. [source]

Medical management of left-sided ulcerative colitis and ulcerative proctitis: Critical evaluation of therapeutic trials

INFLAMMATORY BOWEL DISEASES, Issue 10 2006
Miguel Regueiro MD
Abstract Background: The goal of this work was to critically evaluate the published studies on the treatment of ulcerative proctitis (UP) and left-sided ulcerative colitis (L-UC). The results of this review provided the content for the accompanying treatment guidelines, Clinical Guidelines for the Medical Management of Left-sided Ulcerative Colitis and Ulcerative Proctitis: Summary Statement. Methods: All English language articles published between 1995 and September 2005 were identified through a comprehensive literature search using OVID and PubMed. The quality of the data supporting or rejecting the use of specific therapies was categorized by a data quality grading scale. An "A+" grade was assigned to treatment supported by multiple high-quality randomized controlled trials with consistent results, whereas a "D" grade was given to therapy supported only by expert opinion. The therapeutic efficacy of a treatment was defined by its success in treating UP and L-UC compared with placebo. A medication was ranked as "excellent" if it was specifically studied for UP and L-UC and had consistently positive results compared with placebo or another agent. Quality and efficacy scores were agreed on by author consensus. Results: For the acute treatment of UP or L-UC, the rectally administered corticosteroids and mesalazine (5-ASA), either alone or in combination with oral 5-ASAs, are the most effective therapy: evidence quality, A+; efficacy, excellent. Only rectally administered 5-ASA received an A+/excellent rating for maintenance of remission. Infliximab received an A+ grade for induction and maintenance of remission but only a "good" rating because the studies were performed in all UC, not specifically UP or L-UC. Conclusions: This critical evaluation of treatment provides a "report card" on medications available for the management of patients with UP and L-UC. The guidelines should provide a useful reference and supplement for physicians treating UC patients. [source]

Role of NK1.1+ and AsGm-1+ cells in oral immunoregulation of experimental colitis

INFLAMMATORY BOWEL DISEASES, Issue 2 2003
Shivti Trop
Abstract NK1.1 and AsGm-1 expressing cells play a role in immunomodulation. Our purpose was to determine the role of NK1.1+ and AsGm-1+ expressing cells in the inflammatory/tolerance paradigm in experimental colitis. Oral tolerance towards colitis-extracted proteins had previously been shown to alleviate experimental colitis. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzenesulfonic acid (TNBS). Oral tolerance was induced via five oral doses of proteins extracted from TNBS-colitis colonic wall. Clinical, macroscopic, and microscopic scores were used for colitis assessment. To evaluate the putative role of AsGm-1 in tolerance induction, depletion of AsGm-1 expressing cells was performed. To evaluate the mechanism of tolerance induction, liver-associated NKT lymphocytes were harvested 14 days following tolerance induction, and cultured with concanavalin A (con A) and colitis-extracted proteins. T cell subsets were measured by flow cytometry. Cytokine expression was measured by intracellular staining and enzyme-linked immunosorbent assay (ELISA). Orally tolerized mice exhibited significant alleviation of the clinical, macroscopic, and microscopic parameters of colitis, with increased CD4+IL4+/CD4+IFN,+ lymphocyte ratio, increased IL-4, and decreased IFN, and IL-12 serum levels. In contrast, orally fed mice that were AsGm-1 depleted showed evidence of severe colitis. These mice exhibited significant decreased CD4+IL4+/CD4+IFN,+ ratios, and an increase in IFN, and IL-12, with decreased IL-4 levels. NKT cells harvested from tolerized mice secreted high levels of antiinflammatory cytokines. In contrast, in nontolerized mice, NKT cells mainly secreted proinflammatory cytokines. In a tolerized environment, both NK1.1 and AsGm-1 expressing cells are essential for disease alleviation. In contrast, in a nontolerized environment, AsGm-1 expressing cells support an antiinflammatory immune paradigm, while NKT lymphocytes support a proinflammatory shift. [source]

Dysphagia and Unexpected Myasthenia Gravis Associated with Primary Biliary Cirrhosis, Ulcerative Colitis and Vitiligo

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2004
Peter McCann MRCP
No abstract is available for this article. [source]

A comparative study of the preventative effects exerted by three probiotics, Bifidobacterium lactis, Lactobacillus casei and Lactobacillus acidophilus, in the TNBS model of rat colitis

JOURNAL OF APPLIED MICROBIOLOGY, Issue 4 2007
L. Peran
Abstract Aims:, The intestinal anti-inflammatory effects of three probiotics with immunomodulatory properties, Lactobacillus casei, Lactobacillus acidophilus and Bifidobacterium lactis, were evaluated and compared in the trinitrobenzenesulphonic acid (TNBS) model of rat colitis. Methods and Results:, Colitis was induced in rats by intracolonic administration of 10 mg of TNBS dissolved in 0·25 ml of 50% ethanol. Each probiotic was administered orally (5 × 108 CFU suspended in 0·5 ml of skimmed milk) for 3 weeks, starting 2 weeks before the administration of TNBS. Colonic damage was evaluated histologically and biochemically 1 week after TNBS instillation. The results obtained revealed that all probiotics assayed showed intestinal anti-inflammatory effects, macroscopically evidenced by a significant reduction in the colonic weight/length ratio. Only B. lactis showed a lower incidence of diarrhoea in comparison with untreated rats. Biochemically, all probiotics restored colonic glutathione levels, depleted as a consequence of the oxidative stress of the inflammatory process. Bifidobacterium lactis treatment reduced colonic tumour necrosis factor (TNF)-, production, and inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) expression; L. acidophilus administration reduced colonic leukotriene B4 production and iNOS expression and L. casei intake was associated with a decrease in colonic COX-2 expression. Conclusion:, The three probiotics assayed have shown intestinal anti-inflammatory activity in the TNBS model of rat colitis, although each probiotic shows its own anti-inflammatory profile. Significance and Impact of the Study:, These probiotics could be considered as potential adjuvants in the treatment of inflammatory bowel disease, although more studies are required in order to demonstrate their efficacy in humans. [source]

The effect of sildenafil, a phosphodiesterase-5 inhibitor, on acetic acid-induced colonic inflammation in the rat

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 6 2009
Sevgin Ozlem Iseri
Abstract Background and Aim:, Sildenafil, a selective and potent inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase (PDE)5, has a relaxant effect on the smooth muscle cells of the arterioles supplying the human corpus cavernosum acting via nitric oxide (NO)-dependent mechanism. This study aimed to investigate the possible protective effect of sildenafil citrate on the extent of tissue integrity, oxidant-antioxidant status and neutrophil infiltration to the inflamed organ in a rat model of acetic acid-induced colitis. Methods:, Colitis was induced by intrarectal administration of 1 mL of 5% acetic acid to Sprague-Dawley rats (200,250 g; n = 7,8/group). Control rats received an equal volume of saline intrarectally. In treatment groups, the rats were treated with either sildenafil citrate (5 mg/kg/day; subcutaneously) or saline for 3 days. After decapitation, distal colon was weighed and scored macroscopically and microscopically. Tissue samples were used for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity, and oxidant production. Trunk blood was collected for the assessment of serum tumor necrosis factor (TNF)-, and interleukin (IL)-1, levels. Results:, In the colitis group, the colonic tissue was characterized by lesions, increased lipid peroxidation with a concomitant reduction in GSH content, increased MPO activity and oxidant production. Serum TNF-, and IL-1, levels were higher in the colitis group compared to control values. Sildenafil reversed these inflammatory parameters nearly back to control values. Conclusions:, Sildenafil citrate administration to rats with acetic acid-induced colitis seems to be beneficial via prevention of lipid peroxidation, oxidant generation, cytokine production and neutrophil accumulation. [source]

Aseptic Subcutaneous Abscess Associated With Ulcerative Colitis

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 10 2003
Fukunori Kinjo
No abstract is available for this article. [source]

Systematic review: steroid withdrawal in anti-TNF-treated patients with inflammatory bowel disease

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 3 2010
E. Bultman
Aliment Pharmacol Ther 2010; 32: 313,323 Summary Background, The increasing awareness of increased risk for opportunistic infections when combining several immunosuppressant drugs led to new treatment goals for inflammatory bowel disease including limited use of steroids. Aim, To conduct a systematic review to establish figures for steroid withdrawal in anti-TNF treated inflammatory bowel disease-patients. Methods, Medline was searched using the search-terms Ulcerative Colitis (UC) [Mesh], Crohn Disease (CD) [Mesh], IBD [Mesh], crohn, colitis, IBD and steroid sparing, all combined with infliximab and adalimumab. We selected English-language publications that addressed the effect of anti-TNF on steroid withdrawal. Studies had to assess patients with luminal CD or UC. Numbers of patients who were able to withdraw steroids were calculated. Results, Six studies could be included; five reporting on infliximab and one on adalimumab. Studies were heterogeneously designed. Overall, in the adult population, up to 38% of the patients were able to withdraw corticosteroids during infliximab therapy. In the paediatric population, up to 75% of the patients were able to withdraw corticosteroids during infliximab therapy. Conclusions, Although a consensus on the definition of steroid-sparing is lacking, approximately two-thirds of the inflammatory bowel disease-patients are unable to withdraw corticosteroid treatment during anti-TNF therapy. [source]

Effect of oral iron supplementation on oxidative stress and colonic inflammation in rats with induced colitis

ALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 12 2001
J. Carrier
Background: Iron supplementation may increase disease activity in ulcerative colitis, possibly through the production of reactive oxygen species from the Fenton reaction. Aim: To assess the effects of two doses of oral iron on intestinal inflammation and oxidative stress in experimental colitis. Methods: Colitis was induced in rats by giving 5% dextran sulphate sodium in drinking water for 7 days. First, using a 2 × 2 factorial design, rats with or without dextran sulphate sodium received the regular diet or a diet containing iron 3%/kg diet. Second, rats with dextran sulphate sodium-induced colitis were supplemented with iron 0.3%/kg diet and compared with rats on dextran sulphate sodium and regular diet. The body weight change, histological scores, colon length, rectal bleeding, plasma and colonic lipid peroxides, colonic glutathione peroxidase and plasma vitamin E and C were measured. Faecal analysis for haem and total, free and ethylenediaminetetra-acetic acid-chelatable iron was also performed. Results: Iron 3% and iron 0.3% increased the activity of dextran sulphate sodium-induced colitis, as demonstrated by higher histological scores, heavier rectal bleeding and further shortening of the colon. This was associated with increased lipid peroxidation and decreased antioxidant vitamins. Faecal iron available to the Fenton reaction was increased in a dose-dependent manner. Conclusions: Iron supplementation taken orally enhanced the activity of dextran sulphate sodium-induced colitis and is associated with an increase in oxidative stress. [source]

Brain Endothelial Adhesion Molecule Expression in Experimental Colitis

MICROCIRCULATION, Issue 2 2001
MIQUEL SANS
ABSTRACT Objectives: 1) To determine if endothelial expression of adhesion molecules involved in leukocyte recruitment is increased in the brain and other organs in four different models of experimental colitis, and 2) to investigate whether leukocyte infiltration occurs in the brain of colitic animals. Methods: Endothelial vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) expression was quantified, using the dual radiolabeled antibody technique in rats with trinitrobenzenesulfonic acid (TNBS)-induced colitis, in mice with dextran sulfate sodium (DSS)-induced colitis, in SCID mice reconstituted with CD45RBhigh T-cells, and in IL-10,/, mice. Leukocyte infiltration in the brain of TNBS-induced colitic rats was assessed by myeloperoxidase activity and immunohistochemical staining with anti-CD45 monoclonal antibody. Results: Marked upregulation of brain endothelial VCAM-1 (2- to 5.5-fold) was consistently found in colitic animals in the four models studied. Brain VCAM-1 strongly correlated with colon VCAM-1 and colon weight. By contrast, upregulation of brain ICAM-1 in colitic animals was only observed in the CD45RBhigh transfer (3-fold) and the TNBS-induced (1.5-fold models). Heart and muscle VCAM-1 and ICAM-1 were not upregulated in colitic animals in the majority of models studied. There was no leukocyte infiltration into the brain of TNBS-induced colitic rats. Conclusions: Our study demonstrates a marked and specific upregulation of endothelial VCAM-1 in the brain of colitic animals. This activation of cerebral endothelial cells was not associated with an infiltration of leukocytes into brain tissue. [source]

Idiopathic colitis following cardiac transplantation: Three pediatric cases

PEDIATRIC TRANSPLANTATION, Issue 6 2003
Ghassan Wahbeh
Abstract:, Colitis can cause significant morbidity in pediatric solid organ transplant recipients. In many cases, despite intensive evaluation, a specific infectious, inflammatory, or immunologic etiology is not identified, and idiopathic colitis may be the ultimate diagnosis. We defined idiopathic colitis as the presence of gastrointestinal symptoms (vomiting, diarrhea, abdominal pain) with inflammatory changes seen on intestinal biopsy in the absence of identifiable bowel disease. We describe three cases of idiopathic colitis following cardiac transplantation. In each case, the post-transplant course was complicated by persistent abdominal pain, diarrhea, and in two cases, vomiting. All three patients' post-transplant courses were marked by multiple graft rejection episodes, and all received intensified immune therapy in addition to usual maintenance immunosuppression. Differential diagnosis of the patients' gastrointestinal symptoms included drug side effect, indolent opportunistic infections, inflammatory bowel disease, post-transplant lymphoproliferative disease, and microvascular ischemic colitis. Continued symptoms led these patients to extensive evaluation including imaging studies, endoscopy and tissue biopsy, and stool, blood and tissue cultures for viral, bacterial and parasitic pathogens. Definitive differentiation presented significant diagnostic challenge, and once identifiable etiologies were excluded, the diagnosis of idiopathic colitis was assigned. We conclude that idiopathic colitis following pediatric cardiac transplantation can be a cause of significant morbidity. Endoscopic evaluation of patients who present with gastrointestinal symptoms after transplant is warranted to identify the presence of idiopathic colitis once common causes are ruled out. Further study is needed to identify its incidence, etiology, therapeutic options and prognosis. [source]

Bridging Mucosal Vessels Associated with Rhythmically Oscillating Blood Flow in Murine Colitis

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 1 2008
Aslihan Turhan
Abstract Oscillatory blood flow in the microcirculation is generally considered to be the result of cardiopulmonary influences or active vasomotion. In this report, we describe rhythmically oscillating blood flow in the bridging vessels of the mouse colon that appeared to be independent of known biological control mechanisms. Corrosion casting and scanning electron microscopy of the mouse colon demonstrated highly branched bridging vessels that connected the submucosal vessels with the mucosal plexus. Because of similar morphometric characteristics (19 ± 11 ,m vs. 28 ± 16 ,m), bridging arterioles and venules were distinguished by tracking fluorescent nanoparticles through the microcirculation using intravital fluorescence videomicroscopy. In control mice, the blood flow through the bridging vessels was typically continuous and unidirectional. In contrast, two models of chemically induced inflammation (trinitrobenzenesulfonic acid and dextran sodium sulfate) were associated with a twofold reduction in flow velocity and the prominence of rhythmically oscillating blood flow. The blood oscillation was characterized by tracking the bidirectional displacement of fluorescent nanoparticles. Space,time plots and particle tracking of the oscillating segments demonstrated an oscillation frequency between 0.2 and 5.1 cycles per second. Discrete Fourier transforms demonstrated a power spectrum composed of several base frequencies. These observations suggest that inflammation-inducible changes in blood flow patterns in the murine colon resulted in both reduced blood flow velocity and rhythmic oscillations within the bridging vessels of the mouse colon. Anat Rec, 291:74,82, 2007. © 2007 Wiley-Liss, Inc. [source]

Population-Specific Susceptibility to Crohn's Disease and Ulcerative Colitis; Dominant and Recessive Relative Risks in the Japanese Population

ANNALS OF HUMAN GENETICS, Issue 2 2010
Shigeki Nakagome
Summary Crohn's disease (CD), a type of chronic inflammatory bowel disease (IBD), is commonly found in European and East Asian countries. The calculated heritability of CD appears to be higher than that of ulcerative colitis (UC), another type of IBD. Recent genome-wide association studies (GWAS) have identified more than thirty CD-associated genes/regions in the European population. In the East Asian population, however, a clear association between CD and an associated gene has only been detected with TNFSF15. In order to determine if CD susceptibility differs geographically, nine SNPs from seven of the European CD-associated genomic regions were selected for analysis. The genotype frequencies for these SNPs were compared among the 380 collected Japanese samples, which consisted of 212 IBD cases and 168 controls. We detected a significant association of both CD and UC with only the TNFSF15 gene. Analysis by the modified genotype relative risk test (mGRR) indicated that the risk allele of TNFSF15 is dominant for CD, but is recessive for UC. These results suggest that CD and UC susceptibility differs between the Japanese and European populations. Furthermore, it is also likely that CD and UC share a causative factor which exhibits a different dominant/recessive relative risk in the Japanese population. [source]

HLA,B27 misfolding and the unfolded protein response augment interleukin-23 production and are associated with Th17 activation in transgenic rats

ARTHRITIS & RHEUMATISM, Issue 9 2009
Monica L. DeLay
Objective To determine whether HLA,B27 misfolding and the unfolded protein response (UPR) result in cytokine dysregulation and whether this is associated with Th1 and/or Th17 activation in HLA,B27/human ,2 -microglobulin (Hu,2m),transgenic rats, an animal model of spondylarthritis. Methods Cytokine expression in lipopolysaccharide (LPS),stimulated macrophages was analyzed in the presence and absence of a UPR induced by chemical agents or by HLA,B27 up-regulation. Cytokine expression in colon tissue and in cells purified from the lamina propria was determined by real-time reverse transcription,polymerase chain reaction analysis, and differences in Th1 and Th17 CD4+ T cell populations were quantified after intracellular cytokine staining. Results Interleukin-23 (IL-23) was found to be synergistically up-regulated by LPS in macrophages undergoing a UPR induced by pharmacologic agents or by HLA,B27 misfolding. IL-23 was also increased in the colon tissue from B27/Hu,2m-transgenic rats concurrently with the development of intestinal inflammation, and IL-17, a downstream target of IL-23, exhibited robust up-regulation in a similar temporal pattern. IL-23 and IL-17 transcripts were localized to CD11+ antigen-presenting cells and CD4+ T cells, respectively, from the colonic lamina propria. Colitis was associated with a 6-fold expansion of CD4+ IL-17,expressing T cells. Conclusion The IL-23/IL-17 axis is strongly activated in the colon of B27/Hu,2m-transgenic rats with spondylarthritis-like disease. HLA,B27 misfolding and UPR activation in macrophages can result in enhanced induction of the pro-Th17 cytokine IL-23. These results suggest a possible link between HLA,B27 misfolding and immune dysregulation in this animal model, with implications for human disease. [source]

Effect of Different Doses of Thalidomide in Experimentally Induced Inflammatory Bowel Disease in Rats

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2008
Om Prakash
Adult Wistar rats of either sex were used (n = 36). Colitis was induced by a single intra-colonic application of 20 mg 2,4,6-trinitrobenzene sulfonic acid (TNBS) dissolved in 35% ethanol into the descending colon. Rats were divided into six groups (n = 6). Animals were treated with vehicle (ethanol), TNBS dissolved in 35% ethanol, thalidomide (with different doses of 50, 100 and 150 mg/kg body weight), and sulfasalazine (360 mg/kg body weight) for 14 days. After completion of 14 days of treatment, animals were killed and the following parameters were assessed: morphological score, histological score and biochemical parameters (myeloperoxidase, malondialdehyde and tumour necrosis factor-,). Results showed thalidomide with different doses provided protection against TNBS-induced colonic damage. There was significant protection with thalidomide 150 mg/kg body weight compared to controls (P < 0.001). All the biochemical parameters were highly reduced in the entire thalidomide-treated group compared to controls particularly with thalidomide 150 mg/kg body weight (P < 0.001). Treatment with thalidomide restored malondialdehyde as well as reduction of myeloperoxidase and tumour necrosis factor-, towards normal levels. Morphological and histological score were significantly reduced in all the treated groups with significant effect found with 150 mg/kg (P < 0.001). Our results indicate efficacy of thalidomide in TNBS induce experimental colitis model in rats but present findings requires further investigation to establish the real safety and efficacy in human beings. [source]

Treatment of Distal Colitis with Local Anaesthetic Agents

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 4 2002
Stellan Björck
The original observation was an adrenergic hyperinnervation of the inflamed mucosa (hyperinnervation hypothesis). In order to silence local nervous reflexes, the mucosa was treated topically with 2% lidocaine gel. The clinical results are promising and no side effects have been observed. The relapse rate is relatively high and related to the duration of treatment. In studies of experimental colitis a potential antagonism between harmful adrenergic nerves (vasoconstrictor substances and proinflammatory cytokines) and mucosa-protective visceral afferents (antiinflammatory cytokines) in the pathogenesis of colitis is intriguing. Other studies have emphasized the importance of neutrophils for causing damage to the colon epithelium (neutrophil hypothesis) and local anaesthetics have potent effects on several steps of the inflammatory response in addition to the nervous blockade. [source]

Colitis: it is not just for the colon anymore

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2003
David R Linden
British Journal of Pharmacology (2003) 139, 185,186. doi:10.1038/sj.bjp.0705250 [source]

The Management of Acute Severe Colitis: ACPGBI Position Statement

COLORECTAL DISEASE, Issue 2008
S. R. Brown
First page of article [source]