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PubMed2000

Increased production of matrix metalloproteinase-3 and tissue inhibitor of metalloproteinase-1 by inflamed mucosa in inflammatory bowel disease.

Inflammatory bowel diseases (IBD) are characterized by a sustained inflammatory cascade that gives rise to the release of mediators capable of degrading and modifying bowel wall structure. Our aims were (i) to measure the production of matrix metalloproteinase-3 (MMP-3), and its tissue inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1), by inflamed and uninflamed colonic mucosa in IBD, and (ii) to correlate their production with that of proinflammatory cytokines and the anti-inflammatory cytokine, IL-10. Thirty-eight patients with IBD, including 25 with Crohn's disease and 13 with ulcerative colitis, were included. Ten controls were also studied. Biopsies were taken from inflamed and uninflamed regions and inflammation was graded both macroscopically and histologically. Organ cultures were performed for 18 h. Tumour necrosis factor-alpha (TNF-alpha), IL-6, IL-1beta, IL-10, MMP-3 and TIMP-1 concentrations were measured using specific immunoassays. The production of both MMP-3 and the TIMP-1 were either undetectable or below the sensitivity of our immunoassay in the vast majority of uninflamed samples either from controls or from those with Crohn's disease or ulcerative colitis. In inflamed mucosa, the production of these mediators increased significantly both in Crohn's disease (P < 0.01 and 0.001, respectively) and ulcerative colitis (P < 0.001 and 0.001, respectively). Mediator production in both cases was significantly correlated with the production of proinflammatory cytokines and IL-10, as well as with the degree of macroscopic and microscopic inflammation. Inflamed mucosa of both Crohn's disease and ulcerative colitis show increased production of both MMP-3 and its tissue inhibitor, which correlates very well with production of IL-1beta, IL-6, TNF-alpha and IL-10.

Adult↗

PubMed1998

[Cyclosporine in inflammatory bowel disease].

Inflammatory Bowel Disease (IBD), as Ulcerative Colitis (UC) as well as Crohn's Disease (CD), can appear as severe outbreak resistant to steroid treatment. These cases require surgery or immunosupressive therapy (mercaptopurine or azathioprine). Cyclosporine A (CYA) is a selective, reversible immunosupressor of the T helper lymphocites, used in the treatment of organ transplants and in certain autoimmune diseases. CYA is not a first line therapy for IBD. In spite of the positive results obtained in some uncontrolled studies, only one randomized trial has shown the superiority of CYA over the placebo in the treatment of UC and avoided colectomy in one third of the patients with the severe form of this disease. It can also contribute to the healing of resistault CD fistulaes. The potential toxicity of CYA and the few controlled clinical trials limit its use. However CYA needs to define its role in the treatment of IBD through II more controlled trials.

Cyclosporine↗

PubMed2006

Alterations in intestinal fatty acid metabolism in inflammatory bowel disease.

Inflammatory bowel disease (IBD) constitutes a severe intestinal disorder in developed countries with increasing incidence worldwide. Upcoming evidence indicates an important role of intestinal epithelial barrier function in the development of IBD. Fatty acids exert nutritional and protective effects on enterocytes, serve as activators of transcription and constitute precursors of inflammatory mediators. The aim of this study was to investigate differential regulation of genes involved in fatty acid uptake and endogenous fatty acid biosynthesis in IBD. Mucosal biopsy specimens from non-affected regions of the intestine were subjected to DNA microarray analysis. Gene array analysis revealed a variety of genes involved in fatty acid uptake and synthesis to be differentially expressed in ileum and colon of selected IBD patients. To verify these results, real-time RT-PCR was performed for selected regulated candidate genes in larger IBD sample numbers. In single biopsy analysis long chain acyl-CoA synthetase (ACSL) 1 and 4 were upregulated in IBD (P<0.05), while a significant decrease in fatty acid synthase expression was found in ileum and colon of ulcerative colitis patients (P<0.001). Expression of the transcription factor liver X receptor (LXR) which was previously shown to induce fatty acid synthase gene expression was not altered on mRNA level in IBD. However, in cell culture experiments using the human intestinal cell line LS174T induction of fatty acid synthase by the LXR ligand T0901317 was inhibited by TNFalpha. Moreover, these experiments indicated a decrease of LXR protein levels by TNFalpha treatment. These data suggest that the decrease of fatty acid synthase expression in ulcerative colitis patients could be at least partially due to a loss of LXR expression and function in the presence of pro-inflammatory cytokines. Observed alterations in expression of genes of fatty acid metabolism may contribute to the pathophysiology of ulcerative colitis.

Animals↗

PubMedDate not supplied

Lymphocyte homing in the pathogenesis of extra-intestinal manifestations of inflammatory bowel disease.

Inflammatory bowel disease is associated with extra-intestinal manifestations which occur either at the same time as flares of bowel inflammation (skin and eye disease) or run a course that is independent to inflammation in the bowel (liver and some joint syndromes). It has been suggested that the skin and eye complications occur as a consequence of the recruitment of activated effector cells released from the gut into the circulation to extra-intestinal site where they cause acute damage. However, this does not explain how patients can develop primary sclerosing cholangitis many years after having their colon removed for colitis. We propose that long-lived populations of memory lymphocytes arise as a consequence of bowel inflammation and that these cells express homing receptors that direct their subsequent migration not only to the gut but also to the liver. These long-lived cells may recirculate to the liver for many years and, in the absence of a local activating stimulus, will not cause damage. However, if they are subsequently activated in the liver this will lead to the development of inflammation and tissue damage which promotes the recruitment of more mucosal lymphocytes resulting in persistent inflammation and disease. The recent findings that MAdCAM-1 and CCL25, previously thought to be restricted to the gut, are up-regulated in the liver during inflammatory liver diseases that complicate IBD support the concept that common mechanisms control lymphocyte recruitment to the inflamed liver and gut.

Cell Movement↗

PubMed1989

Prothrombotic abnormalities in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is known to be associated with a thrombotic tendency, which is often attributed to thrombocytosis, elevated fibrinogen, or decreased antithrombin III. We prospectively studied eight patients with IBD, seven of whom had little or no disease activity, to determine if they had any laboratory abnormality known to be associated with an increased risk of thrombosis. Abnormalities in fibrinolysis were noted in five patients: four with high plasminogen activator inhibitor levels and one with poor release of tissue plasminogen activator following venous occlusion. Circulating immune complexes were present in the sera of five patients. Fibrinogen was mildly elevated in one patient, and two patients had mild thrombocytosis. Decreased levels of antithrombin III, protein C, or protein S were not observed. There appears to be a high incidence of abnormalities in fibrinolysis in inactive IBD, which may contribute to the high frequency of thrombosis seen in IBD. The presence of circulating immune complexes may contribute to vascular injury and thrombosis.

Adult↗

PubMed2005

Therapy insight: Vascular complications in patients with inflammatory bowel disease.

Inflammatory bowel disease (IBD) is associated with an increased risk of vascular complications. The most important of these complications are arterial and venous thromboembolism, which represent a significant cause of morbidity and mortality in IBD patients. Recent data suggest that thromboembolism is a disease-specific extraintestinal manifestation of IBD. The most common thrombotic manifestations in IBD are deep vein thrombosis of the leg and pulmonary emboli. It has been suggested that disease activity and the extent of colonic localization are correlated with the risk of developing thromboembolism. The occurrence of thrombosis in patients with IBD is partially attributed to the existing hypercoagulable state in IBD. Both coagulation and fibrinolysis are activated in patients with IBD; this is especially true for those with active disease. The most common risk factors for thrombophilia in IBD patients with venous thromboembolism are Leiden mutation in the gene encoding factor V, hyperhomocysteinemia, and antiphospholipid antibodies. The main genetic defects that have been established as risk factors for venous thrombosis are rather uncommon in IBD, but when present increase the risk of thromboembolism. Screening for coagulation defects seems justified only in IBD patients with a history of thrombosis or a family history of venous thromboembolic events. Antithrombotic treatment of IBD patients with venous thromboembolism is similar to that of thrombotic non-IBD patients.

Humans↗

PubMed1996

Increased oxidative stress and decreased antioxidant defenses in mucosa of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is characterized by chronic intestinal inflammation whose cellular components are capable of oxidative respiratory bursts that may result in tissue injury. Mucosal biopsies were analyzed for protein carbonyl content (POPs), DNA oxidation products [8-hydroxy-2'-deoxyguanosine (8-OHdG)], reactive oxygen intermediates (ROIs), trace metals (copper, zinc, and iron) and superoxide dismutase (Cu-Zn SOD). In Crohn's disease biopsies, there was an increase in ROIs, POPs, 8-OHdG, and iron, while decreased copper and Cu-Zn SOD activity were found in inflamed tissues compared to controls. For ulcerative colitis, there was an increase in ROIs, POPs, and iron in inflamed tissue compared to controls, while decreased zinc and copper were observed. An imbalance in the formation of reactive oxygen species and antioxidant micronutrients may be important in the pathogenesis and/or perpetuation of the tissue injury in IBD and may provide a rationale for therapeutic modulation with antioxidants.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1991

Evaluation of a psychological treatment for inflammatory bowel disease.

Inflammatory bowel disease (IBD) encompasses two related gastrointestinal-tract diseases, ulcerative colitis (UC) and Crohn's Disease (CD). This study, a randomized controlled trial, compared the effectiveness of a multi-component behavioral treatment package (n = 11), which included IBD education, progressive muscle relaxation, thermal biofeedback, and training in use of cognitive coping strategies, to the effectiveness of symptom-monitoring (n = 10) as a control condition; 8 controls subsequently completed treatment. At posttreatment, the treatment group showed mean reductions on 5 symptoms, while the symptom monitoring controls showed mean reductions on all 8 symptoms. On a measure of Total Symptomatic change, the controls showed more improvement than the treated group; the treated controls at posttreatment, showed increases on all 8 symptoms. However, treated subjects perceived themselves as coping better with IBD, as feeling less IBD-related stress, and as experiencing less depression and anxiety. It is hypothesized that inherent differences may have existed between CD and UC subjects which could have led to the differences seen in treatment responses.

Adaptation, Psychological↗

PubMed2005

New oral delivery systems for treatment of inflammatory bowel disease.

Inflammatory bowel disease (IBD) is often localized to specific sites in the gastrointestinal tract (GIT). As a result, this disease can be treated with oral site-specific (targeted) drug delivery systems. Targeted delivery systems for treatment of IBD are designed to increase local tissue concentrations of antiinflammatory drugs from lower doses compared with systemic administration. This review addresses the impact disease has or may have on oral targeted delivery for treatment of IBD as well as a number of delivery approaches currently used in marketed products or under investigation. Delivery systems reviewed rely on temporal control, changes in pH along the GIT, the action of local enzymes to trigger drug release, and changes in intraluminal pressure. Dissolution of enteric polymer coatings due to a change in local pH and reduction of azo-bonds to release an active agent are both used in commercially marketed products. Newer approaches showing promise in treating IBD are based on polysaccharides. These materials are most effective when used as compression coatings around core tablets, which contain the active agent. More complex polymeric prodrugs systems are also under investigation. If the dose of the drug is sufficiently low, this approach may also prove useful in improving treatment of IBD.

Administration, Oral↗

PubMed2004

[Immunotherapy of inflammatory bowel diseases].

Inflammatory bowel diseases (IBD), namely ulcerative colitis (UC) and Crohn's disease (CD) are chronic disorders which appear to be immunologically related. The basic therapeutic agents used in IBD treatment are 5-aminosalicilates and corticoids. In cases when this treatment is insufficient, immunosuppressive therapy is recommended. During an acute phase of the illness most useful is cyclosporine A and in the maintenance therapy, azathioprine and 6-mercaptopurine. Because of insufficiency of this classic therapy in many cases, the new, more useful and safe methods of IBD treatment are wanted. Permanent researches have been focused on immunological reactions. The most useful appear to be TNFalpha antagonists (oxpentifilline, infliximab, entanercept, onercept and thalidomide), anti alpha-4 integrin antibodies (natalizumab), IL-10, anti-CD4, IL-6, IL-12, IL-18, IFNgamma, IL-2R antibodies and others. The best clinical experiences are connected with CD treatment using infliximab (monoclonal, chimeric anti TNFalpha antibodies). Its position in IBD therapy appears to be established now, whereas the other methods are still experimental. Most of clinical and experimental data indicate that it is possible to cure severe IBD using agents which affect metabolism of the cytokine playing key role in pathogenesis of the illness. The modern immunotherapy will probably play important role in the future IBD treatment.

Humans↗

PubMed2004

[TNF-alpha inhibitors in inflammatory bowel disease].

Inflammatory bowel disease (IBD) is a chronic immunoinflammatory response to an stimulus that activates a chain of cellular mediators causing intestinal damage. One of the most well recognized proinflammatory mediators involved in the pathogenesis of IBD is tumor necrosis factor alpha (TNFalpha). The treatment of IBD has advanced in parallel to the improvement of the knowledge of its physiopathology, leading to the development of biological therapies. An example of this kind of treatment is the use of substances that antagonize TNFalpha, such as monoclonal antibodies infliximab, adalimumab, natalizumab, etanercept or onercept, with infliximab being the unique approved for use in IBD. Several studies have demonstrated that inhibition of TNFalpha is useful in the treatment of Crohn's disease (CD). In CD, infliximab induces the remission of relapses which are refractory to the conventional treatment, prevents more relapses and induces a closure of enterocutaneous and perianal fistula that do not respond to first line treatment. However, infliximab is not useful in ulcerative colitis. Infliximab treatment has some drawbacks, such as the development of anti-infliximab antibodies, which cause a loss of efficacy of the treatment and hypersensitivity reactions. Other reported adverse effects of infliximab are the development of autoimmunity, such as that related with antinuclear or anti-DNA antibodies, or the reactivation of infections such as tuberculosis. In fact, a screening for tuberculosis is necessary before administration of infliximab. To reduce the adverse effects due to infliximab immunogenicity, several trials with humanized or completely human agents, such as adalimumab or onercept, are under way. Until the precise stimulus that triggers IBD is identified, biological therapies have a great future and the selective antagonism of TNFalpha is already a reality.

Antibodies, Monoclonal↗

PubMed2006

Analysis of serum antibodies in patients suspected of having inflammatory bowel disease.

Inflammatory bowel disease (IBD) is the general term used for a heterogeneous group of intestinal disorders, including Crohn's disease (CD) and ulcerative colitis (UC). Serological markers such as anti-Saccharomyces cerevisiae antibodies (ASCA) and atypical perinuclear antineutrophilic cytoplasmic antibody (atypical pANCA) have proven useful in the diagnosis and differentiation of CD and UC. Immunoglobulin A (IgA) antibody directed against the outer membrane protein C (OmpC) of Escherichia coli is said by one group to have clinical utility in diagnosing IBD, specifically in ASCA-negative CD patients. Our objective in this study was to compare the results obtained from two separate laboratories offering similar IBD tests using sera from suspected IBD patients. One hundred ninety-seven sera received for IBD testing were included in the study. The agreement between the two laboratories was 93.4% for ASCA IgA, 90.9% for ASCA IgG, and 87.8% for atypical pANCA IgG. There were 25 sera with ASCA-negative/OmpC-positive results reported by one laboratory. Thirteen of these 25 (52.0%) ASCA-negative/OmpC-positive sera were also atypical pANCA positive (9 as determined by both laboratories, 3 by one, and 1 by the other). Atypical pANCA antibody is found primarily in IBD patients with UC and colon-limited CD (Crohn's colitis). We conclude that the ASCA and atypical pANCA assays showed good agreement between the two laboratories, but the data for ASCA-negative/OmpC-positive sera suggest that many (52.0%) of these patients were more likely to have had UC or Crohn's colitis based on the presence of an atypical pANCA.

Adult↗

PubMed2005

The education and employment status of patients with inflammatory bowel diseases.

Inflammatory bowel disease (IBD) has the propensity to affect patients who are in their late teens and early 20s, an age when most people decide on their educational and career directions. This review describes the effects that IBD has on the continuum of education and employment. Patients with Crohn's disease and ulcerative colitis attain a similar level of education as that of the general population. The quality of life of such patients in school, as measured by both patients' and teachers' perceptions, indicates that, despite the difficulties that students face in terms of missed school time and physical inconveniences, teachers are generally perceived by students to have favorable attitudes toward helping them. Even though earlier work in the area of employment has suggested that the occurrence of IBD is clustered among people in white-collar positions, recent data have suggested that certain environmental risks for IBD (i.e., sedentary or indoor jobs) may be associated with jobs classified as being white-collar, and therefore having a white-collar job may in itself not be a risk factor for the development of IBD. Patients with IBD have a higher rate of nonparticipation in the labor force, and the participation rate seems to maintain steady levels over time. A majority of patients with IBD continue in the same employment positions over a period of years. Patients with IBD, especially those who have undergone surgery, took more sick leave than their counterparts without IBD. A majority of patients with IBD favored the disclosure of their diagnosis to their employers and perceived little discrimination in the workplace. Furthermore, most employers were perceived by their employees with IBD as having fair attitudes toward the compensation provided for their employees with IBD.

Education↗

PubMed1995

Review article: the risks of malignancy from either immunosuppression or diagnostic radiation in inflammatory bowel disease.

Inflammatory bowel disease is associated with an increased risk of gastrointestinal malignancy. There has been concern that either diagnostic medical radiation and long-term drug therapy--particularly immunosuppression--might contribute to this increased cancer risk. For the major drug groups (5-aminosalicylates, steroids and immunosuppressants) data are scant but broadly reassuring. Only azathioprine (including 6-mercaptopurine) has been investigated at all carefully. Short- to medium-term therapy probably poses a very slightly increased risk of malignancy which is easily accepted given the current limitation of this agent to second-line use. Continuous therapy for more than two years is much less well documented, and caution should be maintained. A hypothetical model based on data from occupational radiation exposure has been constructed; this permits reasonable confidence that the medical use of ionising radiation contributes a negligibly increased risk of malignancy overall, and is particularly unlikely to add significantly to the incidence of gastrointestinal malignancy.

Azathioprine↗

PubMed2003

Relationship between the tumor necrosis factor alpha polymorphism and the serum C-reactive protein levels in inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic inflammatory disease of the gastrointestinal tract, including ulcerative colitis (UC) and Crohn's disease (CD). The aim of the study was to determine the prevalence of the tumor necrosis factor alpha (TNF-alpha) promoter polymorphisms at positions -238 and -308, and to measure the serum CRP levels in CD and UC patients and in a healthy population. The TNF-alpha gene polymorphisms were determined by the PCR-RFLP method. Samples of 74 CD and 50 UC patients and 138 healthy Hungarian volunteers were examined. The G-->A substitution at position -308 (designated the TNF2 allele) was significantly less frequent among IBD patients than in the control group (P=0.0009); 15% of the CD patients and 18% of the UC patients carried the mentioned allele, which was significantly less frequent compared with the healthy population (33%, P=0.0035 and P=0.036, respectively). No difference in the G-->A substitution at position -238 was observed. We found the median CRP levels to be significantly higher in the active phase of the disease than in the inactive phase among the -308A allele carriers (P=0.002), while this difference was not significant when the CRP levels in the active and inactive phases were compared among the -308GG homozygous patients (P=0.084). The decreased frequency of the TNF2 allele (known to be associated with elevated TNF-alpha production) in IBD may determine the severity of IBD through its interaction with plasma CRP levels, and may modify the pathogenesis of this chronic inflammatory disease.

Adult↗

PubMed2006

Increased circulating concentrations of growth-related oncogene (GRO)-alpha in patients with inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a chronic inflammatory state associated with increased risk of intestinal cancers. The aim of this study is to examine serum concentrations of growth-related oncogene (GRO)-alpha, a cytokine with inflammatory and growth-regulatory properties, in patients with IBD. We measured serum concentrations of GRO-alpha in 60 patients with ulcerative colitis, 42 patients with Crohn's disease, 16 patients with other colitides, 12 patients with colorectal cancer, and 40 normal subjects using an enzyme-linked immunosorbent assay. We then analyzed how the cytokine was related to clinical and laboratory variables. Serum GRO-alpha concentrations in patients with active IBD were significantly higher than those in patients with quiescent disease, which in turn were higher than those in normal controls. Concentrations in patients with active ulcerative colitis were higher than in patients with active Crohn's disease. Analysis of paired serum samples showed a decrease in GRO-alpha after initiation of therapy. Furthermore, serum GRO-alpha correlated well with laboratory markers of IBD activity. We conclude that GRO-alpha may have an important role in development of IBD, and might itself be used as a marker of activity. Manipulation of GRO-alpha function might prove therapeutically useful.

Adolescent↗

PubMed1987

Genitourinary complications of inflammatory bowel disease.

Inflammatory bowel disease affects the genitourinary tract not infrequently, either by way of direct extension of the gastrointestinal inflammatory process or through metabolic interrelationships between the two organ systems. The abnormalities that most frequently result include retroperitoneal abscess, ureteral obstruction, cystitis, enterovesical fistula, and urolithiasis. Some of these may be sufficiently symptomatic to draw attention to their presence, even, on occasion, overshadowing or preceding gastrointestinal disease symptoms. Other urinary lesions are clinically silent and require periodic uroradiologic evaluation for purposes of discovery.

Abscess↗

PubMed1999

Current management of pediatric inflammatory bowel disease.

Inflammatory bowel disease (IBD) is a relatively rare condition of childhood, although the wide range of presenting complaints, scope of complications, and choices of therapy for this condition make it particularly difficult to treat in children. Novel approaches to the management of Crohn's disease and ulcerative colitis have gained recent favor. This report summarizes the current medical and surgical management of IBD, recent advancements in clinical therapies, and particular aspects of IBD care for children.

Adjuvants, Immunologic↗