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PubMed2005

Inflammatory bowel disease associated with Yersinia enterocolitica O:3 infection.

BACKGROUND: Certain microorganisms may be associated with the development of inflammatory bowel disease (IBD). These pathogens may possess such properties as immunological capability or tissue invasiveness. An association between Yersinia enterocolitica infection and ulcerative colitis (UC) was suggested 30 years ago, and a connection with Crohn's disease (CD) may also exist. The aim of this study was to further elucidate the association between Y. enterocolitica O:3 infection and IBD. METHODS: During the period 1990-1997, antibody response against Y. enterocolitica was estimated in 1588 patients by tube agglutination. Forty-one patients with Y. enterocolitica infection (titer = 320) constituted the study group; 1041 patients without antibody response constituted the control group. The study was completed in 2003, after 6-13 years. RESULTS: At diagnosis of Y. enterocolitica infection, UC of acute onset was demonstrated in three males; another suffered from CD. At follow-up, two additional patients had developed UC and two CD. In the control group, 32 patients were diagnosed as having UC and 10 CD. This difference in IBD prevalence is significant (8/41>42/1041, p=0.00035), as were the differences in prevalence of UC and CD separately (p=0.006; viz. p<0.015). CONCLUSION: The present study supports the concept of the Y. enterocolitica infection as a trigger of chronic IBD.

Journal Article↗
PubMedDate not supplied

Social learning, affective state and passive coping in irritable bowel syndrome and inflammatory bowel disease.

The association between the use of passive coping strategies to deal with pain and reported levels of anxiety, depression, and parental reinforcement of illness behavior was examined in individuals with Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD). Individuals with IBS and IBD recruited primarily from outpatient clinics completed questionnaire measures of pain-coping (the Vanderbilt Pain Management Inventory, VPMI) as well as measures of anxiety and depression, parental reinforcement of illness behavior and physical symptoms. Factor analysis of the passive coping sub-scale of the VPMI indicated that it was comprised of two components corresponding to emotional and behavioral facets of passive coping. Higher levels of behavioral passive coping were associated with higher levels of parental reinforcement of illness behavior and higher levels of depression, but only amongst individuals with IBS. In contrast emotional passive coping was associated in both groups with higher levels of anxiety and depression (but not illness-related social learning). Different factors predict the use of emotional and behavioral passive coping strategies in IBS and IBD. It is suggested that illness-related social learning occurring during childhood influences the development of habitual illness behaviors and that, because of the more benign nature of symptoms in IBS, individuals with IBS may be more likely than individuals with IBD to revert to such habitual behaviors to cope with symptoms. The degree to which the emotional component of passive coping, associated with psychological distress in both groups, can be considered in terms of 'coping strategies', rather than markers of illness-related distress, is discussed.

Adaptation, Psychological↗
PubMed2004

General principles of medical therapy of inflammatory bowel disease.

Ulcerative colitis and Crohn's disease are chronic gastrointestinal diseases that affect patients in the prime of their lives. Because inflammatory bowel disease (IBD) patients generally live a normal lifespan, chronic medical therapy for IBD must be tolerable, simple to adhere to, and have as few side effects as possible. This article discusses the impact of IBD on quality of life and stresses the importance of appropriate and individualized medical therapy. To help clinicians determine the efficacy of particular IBD medications, this article offers a brief, practical interpretation of clinical, endoscopic, and quality-of-life end points used in clinical trials. Finally, it provides a summary of the current accepted medical therapies for ulcerative colitis adn Crohn's disease and recommendations for using these medications in clinical practice.

Adrenal Cortex Hormones↗
PubMed2004

Treatment of inflammatory bowel disease with azathioprine and 6-mercaptopurine.

6-Mercaptopurine and azathioprine have become important therapeutic options for patients with inflammatory bowel disease (IBD). Although accumulating data in the literature have supported the use of these immunomodulators in the management of IBD, marked variation exists in the pattern of clinical practice regarding azathioprine or 6-mercaptopurine therapy in patients with IBD. This article provides a critical review of the data on the clinical efficacy and toxicities of 6-mercaptopurine and azathioprine in the management of IBD. Emerging literature on the potential application of pharmacogenetic testing and metabolite monitoring are also discussed.

Azathioprine↗
PubMed2006

Chemoprevention: risk reduction with medical therapy of inflammatory bowel disease.

The ideal chemopreventative agent, in addition to being efficacious in the prevention of cancer, must be easily administered, affordable, safe, and well tolerated, with minimal side effects. In the past decade, a growing body of literature has emerged on the prevention of CRC in patients with long-standing CD and UC. The data are not definitive and consist almost exclusively of retrospective case-control and cohort studies rather than the more rigorous prospective RCTs. 5-ASA compounds have been most thoroughly studied, and most of the existing data support the use of 5-ASA in the prevention of CRC. Although the precise dose and duration are unclear, studies suggest that chronic systemic administration of 5-ASA at a dose of at least 1.2 g/d is most likely to be effective. A beneficial effect of folate, albeit not statistically significant, has been consistently shown in every study performed for this purpose. Folate supplementation, which is safe and affordable, should also be recommended for all patients with IBD, especially those taking sulfasalazine. UDCA has been shown to exert a protective effect in most studies on patients with UC and concomitant PSC. Because this patient population is at particularly high risk for CRC, it is advisable to consider UDCA in all patients with colitis complicated by PSC. For patients without PSC, sufficient data do not exist to recommend it for the purpose of cancer prevention. Five of the six corticosteroid studies have found a beneficial effect of systemic steroids, although most did not reach statistical significance. Regardless, given the frequent and serious adverse effects associated with chronic steroid use, systemic corticosteroids should not be prescribed for this indication. Budesonide, an oral corticosteroid with minimal systemic absorption, is a potential alternative, although it has not yet been studied as a chemopreventative agent. Similarly, until the long-term safety of chronic NSAID use can be demonstrated in patients with IBD, the role of NSAIDs in chemoprevention remains undefined. Although the data are conflicting, immune-modulating medications, such as AZA, do not seem to confer any reduction in the risk of dysplasia or CRC. The data on calcium supplementation and statin use are still too limited to endorse their use for the prevention of colitis-related CRC. Chemoprevention is an area that holds great promise in the reduction of morbidity and mortality associated with IBD. Further studies, including prospective trials when possible and cost-effectiveness analyses, need to be performed to develop an optimal strategy for the reduction of cancer risk in patients with IBD.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2006

Treatment of immune-mediated extraintestinal manifestations of inflammatory bowel disease with infliximab.

The introduction of infliximab into clinical practice is one of the most significant advances in the care of patients who have IBD. Infliximab has become an important part of the medical armamentarium to treat extraintestinal manifestations that often are refractory to other medications and are a significant cause of morbidity in these patients. Two other TNF inhibitors recently have demonstrated efficacy in CD: certolizumab pegol and adalimumab. The Food and Drug Administration has approved adalimumab for use in RA. One predicts that these agents also may have activity in the extraintestinal manifestation for IBD. To determine whether future biologics are effective in the EIM of IBD, one may need to look no further than the vast clinical trial experience in primary chronic inflammatory diseases of the joints and skin: RA and psoriasis. For example, the Food and DRug Administration recently has approved an anti-B-cell therapy, rituximab, and a T-cell costimulation modulator, abatacept, for use in RA. It certainly will be of interest to determine whether these biologic agents demonstrate efficacy in the intestinal and EIM of IBD.

Anti-Inflammatory Agents↗
PubMed2006

Biologics for inflammatory bowel disease: drug approval and monitoring in the United States.

Biologics are a primary focus for research and development of new treatments for IBD and other immune disorders. CDER, which is a branch of the FDA, oversees most of the biologics that are being used or tested for IBD, and it regulates nonbiologic medications for IBD. The approval process for most biologics for IBD is similar to the process for nonbiologics. FDA regulation of a new drug or biologic can be divided into three stages: the commercial IND, the NDA, and postmarketing (phase 4) studies. It is unclear if generic versions of biologics can be approved within the current legislation.

Biological Products↗
PubMed2006

Inflammatory bowel disease: current insights into pathogenesis and new therapeutic options; probiotics, prebiotics and synbiotics.

Inflammatory bowel disease (IBD) is a chronic relapsing disorder involving a dysregulated host-microbiota interaction. IBD patients have been shown to possess an increased risk for the development of colorectal cancer. Recently, focus has been placed on probiotic and prebiotic therapies, which aim to restore balance to the gastrointestinal microbiota, and reduce intestinal inflammation. Probiotics have been assessed extensively in animal models, with a number of clinical trials also demonstrating potential therapeutic benefits. However, it is widely accepted that more double-blind randomised placebo-controlled trials are required. Future research also needs to focus on determining which probiotics are the most efficacious in the IBD setting, and how the genetic and bacterial profiles of the patient will influence treatment responsiveness. Prebiotics have been studied less extensively, however, they may become an ideal treatment or co-treatment option due to their capacity to increase endogenous lactobacillus and bifidobacteria. Probiotics and prebiotics may offer a new therapeutic option for the treatment of IBD, however, a greater understanding of the mechanisms behind their action on the gastrointestinal microbiota is required in order to determine which probiotic, prebiotic or combinations thereof are the most beneficial.

Animals↗
PubMed2005

Development and validation of a novel IL-10 deficient cell transfer model for colitis.

A number of rodent models for inflammatory bowel disease (IBD) have been developed, but most cannot be used to develop and validate new therapies for IBD. From the models developed, the IL-10 deficient mouse model is the one that results in a disease similar to human IBD; however, in this model, colitis occurs with variable incidence taking 3-4 months to develop. These are serious problems with the model when evaluating a new therapy because of the large-scale experiments required and the difficulty in performing an accurate pharmacological analysis. In this study, the IL-10 deficient mouse model was modified by transferring whole spleen and mesenteric lymph node cells from IL-10 deficient mice to CB-17 SCID mice. In this IL-10 deficient cell transfer model, chronic intestinal inflammation developed in all recipients within 2-3 weeks, which was far earlier than in donor IL-10 deficient mice. The pathological phenotypes were similar to those of IL-10 deficient mice and CD45RBhi T cell-transfer models. In addition, we assessed several agents for inflammatory bowel disease to validate the general utility of this cell transfer model. It is worth noting that TNFR-Ig or prednisolone, which is effective for treatment of patients with severe-fulminant Crohn's disease, markedly attenuated pathological clinical indices in this colitis model, whereas the immunosuppressive agents, azathioprine, tacrolimus, and cyclosporine A produced no significant effect. These results suggest that the IL-10 deficient cell transfer model is a good experimental model to use for developing new and effective therapies for active IBD.

Adrenal Cortex Hormones↗
PubMed2006

Reconstitution of Scid mice with CD4+CD25- T cells leads to rapid colitis: an improved model for pharmacologic testing.

Improved experimental colitis models are needed for evaluation of treatment strategies for IBD. Most current models either lack resemblance to IBD, are complicated to establish, or the colitis occurs slowly and inconsistently. Our aim was to characterize the course of colitis in C.B-17 Scid mice reconstituted with syngeneic CD25-depleted CD4+ cells, including the identification of useful biomarkers, and assessment of the similarities to IBD with focus on the relationship between colonic epithelial proliferation and inflammatory parameters. Groups of reconstituted and un-reconstituted mice were sacrificed weekly from week 1 to 4. Clinical signs of colitis occurred approximately 2 weeks after reconstitution. Disease onset and severity based on histopathology correlated well with the colonic weight:length ratio, fecal consistency score, presence of occult blood in feces, and fecal IL-1beta content. Loss in body weight was not apparent until colitis was well established and exhibited lower coefficient of correlation to the histologic score. Early colonic histopathology was dominated by epithelial hyperproliferation, loss of mucus and mild lymphoid infiltration. Epithelial hyperproliferation was paralleled by increased fecal soluble tumor necrosis factor receptor II content. Cytokines in colonic tissue homogenates exhibited a Th1-like profile. We conclude that adoptive transfer of CD4+CD25- T cells results in colitis resembling IBD with a rapid onset and limited variability between individuals. Purification of CD4+CD25- T cells is a simple procedure, and does not require flow-cytometric sorting. Fecal consistency score and colonic weight:length ratio are readily measurable and consistent disease parameters. This model is thus highly suitable for pharmacological testing of intervention strategies.

Adoptive Transfer↗
PubMed2005

Increased prevalence of primary sclerosing cholangitis among first-degree relatives.

BACKGROUND/AIMS: The aim of the present study was to investigate the familial occurrence of autoimmune diseases in a large group of patients with primary sclerosing cholangitis (PSC). METHODS: All patients with PSC treated at Huddinge University Hospital between 1984 and 1999 were included (n=145). For every patient with PSC and inflammatory bowel disease (IBD) (n=126) we randomly selected a control patient with IBD (n=126), matched for age, sex and type of IBD. A questionnaire comprising information about autoimmune diseases among first-degree relatives was answered by all patients and controls. RESULTS: We identified 22 index cases with PSC from 21 families with a first-degree relative with either chronic liver disease and/or IBD. Five patients with PSC had a first-degree relative with PSC (3.4%). The prevalence of PSC among first-degree relatives was 0.7% (5/717). In siblings the prevalence was 1.5% (4/269). The prevalence of first-degree relatives with autoimmune diseases outside the liver was similar in PSC patients and controls. CONCLUSIONS: First-degree relatives of patients with PSC have a PSC prevalence of 0.7%. This represents a nearly 100-fold increased risk of developing PSC compared with the general population, supporting the hypothesis that genetic factors are of importance for development of PSC.

Autoimmune Diseases↗
PubMed2006

Primary sclerosing cholangitis can present with acute liver failure: Report of two cases.

BACKGROUND/AIMS: The aim of the present study was to determine whether PSC can present with acute liver failure (ALF) and to determine its frequency. METHODS: Medical records from all patients with a well-defined PSC (n=246), treated at Karolinska University Hospital, Huddinge between 1984 and 2004 were scrutinized. Information on PSC and inflammatory bowel disease (IBD) characteristics including mode of presentation of PSC was evaluated. A group of patients with ALF of indeterminate cause at our hospital diagnosed (1993-2003) was identified as a reference group (n=46). RESULTS: Two patients with PSC presented with ALF (1%) and are described in detail. Both of them had an underlying IBD. Nobody in the reference group had IBD. CONCLUSIONS: In conclusion, PSC patients can present with ALF in approximately 1% of all patients. PSC should be considered as a differential diagnosis in patients with ALF of indeterminate cause, especially in patients with IBD.

Adult↗
PubMed2004

Hepatocyte growth factor treatment ameliorates diarrhea and bowel inflammation in a rat model of inflammatory bowel disease.

BACKGROUND/PURPOSE: Transfection of the HLA-B27 gene into normal Fischer rats induces phenotypic changes similar to inflammatory bowel disease (IBD). This study investigated the benefits of 2 doses of hepatocyte growth factor (HGF) on the manifestations of IBD in this rat model. METHODS: Fischer rats and HLA-B27 rats were divided into 4 groups: Fischer rats treated with saline, HLA-B27 rats treated with saline, HGF at 150 microg/kg/d, and HGF at 300 microg/kg/d. HGF or saline was infused for 14 days via an osmotic pump attached to a catheter in the internal jugular vein. After treatment, rats were evaluated for diarrhea and reduction in gross and microscopic bowel inflammation. Statistics were determined using analysis of variance (ANOVA). A P value < or =.05 was considered significant. RESULTS: Administration of HGF at 150 microg/kg/d decreased diarrhea by 40%, gross inflammation by 41%, and microscopic inflammation by 72% (P < or =.05). At 300 microg/kg/d HGF decreased diarrhea by 46%, gross inflammation by 45%, and microscopic inflammation by 54% (P < or =.05). CONCLUSIONS: HGF administration reduces the clinical manifestations of IBD in this rat model. Similar effects were seen at both doses of HGF administration, implying that there is a plateau above which further increases in HGF levels provides no added benefit. HGF administration may be clinically useful in the management of IBD.

Animals↗
PubMed2004

Glucagonlike peptide-2 analogue: a possible new approach in the management of inflammatory bowel disease.

BACKGROUND/PURPOSE: Glucagonlike peptide-2alpha (GLP-2alpha) has been shown to be a growth factor for the small intestine. This study investigated the benefits of intravenous and intraluminal administration of GLP-2alpha using a rat model of inflammatory bowel disease (IBD). METHODS: Normal Fisher rats and HLA-B27 (IBD) rats were treated for 14 days as follows: Fisher, intravenous saline (n = 6); HLA-B27, intravenous saline (n = 6); HLA-B27, intravenous GLP-2alpha (50 microg/kg/d; n = 5); Fisher, intraluminal saline (n = 5); HLA-B27, intraluminal saline (n = 5); or intraluminal GLP-2alpha (50 microg/kg/d; n = 5). Rats were evaluated for frequency of diarrhea, and the bowel was analyzed for gross and microscopic lesions. Statistical evaluations were determined using analysis of variance (ANOVA). A P value of.05 was significant. RESULTS: Intravenous GLP-2alpha decreased diarrhea and the number of bowel lesions (P <.05). Microscopic inflammation was reduced by 24% but was not statistically significant. Intraluminal GLP-2alpha decreased the number of small intestine lesions (P <.05) and the microscopic inflammation (P <.05) but did not significantly reduce diarrhea or the overall number of bowel lesions. CONCLUSIONS: GLP-2alpha ameliorates the signs of IBD in HLA-B27 rats. Intravenous GLP-2alpha reduces diarrhea more effectively than intraluminal administration, and both routes are equally effective in ameliorating inflammation. GLP-2alpha potentially provides a new modality for the treatment of IBD.

Analysis of Variance↗
PubMed2006

Vitamin D and its role in immunology: multiple sclerosis, and inflammatory bowel disease.

Autoimmune diseases like multiple sclerosis (MS) and inflammatory bowel disease (IBD) occur because of an inappropriate immune-mediated attack against self-tissue. Analyses of genetically identical twins shows that besides genetics there are important environmental factors that contribute to MS and IBD development. Vitamin D availability due to sunshine exposure or diet may play a role in the development of MS and IBD. Compelling data in mice show that vitamin D and signaling through the vitamin D receptor dictate the outcome of experimental MS and IBD. Furthermore, the evidence points to the direct and indirect regulation of T cell development and function by vitamin D. In the absence of vitamin D and signals delivered through the vitamin D receptor, auto reactive T cells develop and in the presence of active vitamin D (1,25(OH)(2)D(3) ) and a functional vitamin D receptor the balance in the T cell response is restored and autoimmunity avoided.

Animals↗
PubMed2006

Inflammatory bowel disease--environmental modification and genetic determinants.

Inflammatory bowel disease (IBD) is a complex disease, controlled by multiple risk factors that evolve and interact together. In a genetically susceptible host, there are multiple processing steps controlled by the host and the environment, from environmental exposure to the clinical and biological expression of IBD-related phenotypes. This article discusses the recent genetic discoveries, along with the proposed environmental risk factors that have been implicated in IBD. Technical advances of the HapMap project and the promise of whole genome association scans have given hopes for clarifying gene-environmental interactions in IBD that ultimately lead to a clearer understanding of the pathogenesis.

Child↗
PubMed2003

Mononuclear leukocytes bind to specific hyaluronan structures on colon mucosal smooth muscle cells treated with polyinosinic acid:polycytidylic acid: inter-alpha-trypsin inhibitor is crucial to structure and function.

Inflammatory bowel disease (IBD) is a chronic disorder whose etiology is linked to triggering events, including viral infections, that lead to immunoregulatory dysfunction in genetically susceptible people. Characteristic pathological changes include increased mononuclear leukocyte influx into the intestinal mucosa as well as mucosal smooth muscle cell (M-SMC) hyperplasia. Virus infection or viral mimic [polyinosinic acid:polycytidylic acid (polyI:C)] treatment of human colon M-SMCs in vitro increases cell surface hyaluronan (HA), and nonactivated mononuclear leukocytes bind to virus-induced HA structures by interactions that involve the HA-binding receptor CD44. In this study, confocal microscopy reveals increased HA on poly I:C-treated M-SMC surfaces within 3 hours, arrayed in coat-like structures. By 17 hours, novel, lengthy cable structures are evident, and these are primarily responsible for mediating leukocyte adhesion. Immunohistochemical staining demonstrates components of the inter-alpha-trypsin inhibitor (IalphaI) complex in both coat-like and cable structures. M-SMCs co-treated with polyI:C and a polyclonal antibody to IalphaI display HA in coats but with diminished cables, and they bind significantly fewer leukocytes than M-SMCs treated with polyI:C alone. Western blot data suggest that heavy chains of IalphaI are specifically associated with cable structures. Staining of tissue sections from patients with IBD demonstrates the presence of HA in inflamed colon tissue, and shows that HA-associated IalphaI staining increases in the mucosa of inflamed IBD specimens compared to noninflamed sections from the same patient, establishing a probable link between the observations in vitro and the progression of the inflammatory process in IBD.

Alpha-Globulins↗
PubMed1998

In situ expression of interleukin-10 in noninflamed human gut and in inflammatory bowel disease.

A dysregulated secretion of contra-inflammatory cytokines such as interleukin-10 (IL-10) could play a role in the pathogenesis of inflammatory bowel disease (IBD). We have investigated the expression of IL-10 in gut tissues from patients with Crohn's disease (CD), ulcerative colitis (UC) and controls by mRNA in situ hybridization and immunohistochemistry. Intestinal epithelial cells were found to express IL-10 mRNA and IL-10 protein in all of the tissues investigated without any major differences in the expression patterns. However, compared with noninflamed gut, significantly increased numbers of mononuclear cells (MNCs) producing IL-10 were present in inflamed gut, both in CD and UC. This cytokine was expressed most prominently by inflammatory infiltrates enriched in macrophages, although T cells seem to contribute to its production as well. Elevated IL-10 expression in IBD was mainly detected in the submucosa, whereas IL-10 production by lamina propria cells remained comparably low. In contrast, the expression of IL-1beta mRNA was preferentially increased in the lamina propria. Our data argue against a general deficiency in IL-10 production in IBD. The results suggest rather that the local production of IL-10 by mucosal MNCs in IBD is insufficient to down-regulate pro-inflammatory cytokines such as IL-1beta in the lamina propria compartment.

Adult↗