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PubMed2006

No evidence for an involvement of the p38 and JNK mitogen-activated protein in inflammatory bowel diseases.

Involvement of mitogen-activated protein (MAPK) in inflammatory bowel disease (IBD) remains enigmatic. We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. P38 and JNK were quantified in colonic mucosa of 28 IBD patients and 19 controls and in 77 TNBS or control mice treated or not with SB203580. Colitis severity was assessed by survival, macroscopic and microscopic scoring, and molecular markers. Expression and activity of p38 and JNK were similar in IBD patients and controls and not modified by inflammation. In mice, p38 and JNK expression or activity did not increase following the induction of colitis. SB203580 decreased the p38 activity but displayed no clinical nor biological therapeutic effect. In conclusion, these results minimize the role of p38 and JNK in inflammatory colitis and the interest of p38 as a therapeutic target in IBD.

Adult↗
PubMed2006

The complexity and challenges of genetic counseling and testing for inflammatory bowel disease.

Inflammatory bowel disease (IBD) is an umbrella term referring to two chronic idiopathic intestinal diseases: ulcerative colitis (UC) and Crohn's disease (CD). Both UC and CD are characterized by immune activation that leads to symptoms, but the location, severity and behavior of the inflammation varies among individuals and in characteristic ways between UC and CD. A majority of patients with IBD are diagnosed in young adulthood, but the response to therapy is variable and difficult to predict, with some patients demonstrating a prompt and effective remission while others have continuous symptoms that do not respond to existing medical options. Surgery remains a frequent and necessary occurrence among patients with IBD, but in UC it is considered curative, while in CD only temporizing. Clinical observations, epidemiological studies, and molecular genetics have provided strong evidence that both genetic and environmental factors are important determinants for disease susceptibility. In recent years, a number of genes have been identified that associate with CD and UC, although the clinical utility of these discoveries in patients or in susceptible family members has not been determined. Nonetheless, it is hoped that these fundamental advances in our understanding of IBD will lead to better therapies for patients and prevention strategies for those who are susceptible. Effective incorporation of clinical genetic testing for IBD into practice will require appropriate education and counseling.

Crohn Disease↗
PubMed2003

Recent advances in the diagnosis and classification of inflammatory bowel disease.

The availability of an increasing number of inflammatory bowel disease (IBD)-specific serologic antibodies, the discovery of disease-susceptibility genes, the introduction of pharmacogenetic markers, and the recent application of wireless capsule enteroscopy to the evaluation of patients with IBD are providing new types of information that must be integrated with more traditional IBD paradigms. The challenge facing researchers and clinicians is to determine how to incorporate these potentially clinically relevant insights into our understanding of disease pathogenesis and to define the spectrum of potential applications to the management of patients with IBD. The ultimate diagnostic and predictive value of these tests will likely be optimized when they are applied in combination, rather than individually. As the clinical relevance of this expanding diagnostic armamentarium is defined, it is hoped that these tests will enable clinicians not only to diagnose IBD accurately but also to determine disease patterns prospectively, suggest prognoses, and allow for individualization of therapeutic regimens.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2004

Relevance of serologic studies in inflammatory bowel disease.

The serologic panel for inflammatory bowel disease (IBD) is rapidly expanding. Antineutrophil cytoplasmic antibodies (ANCA) and anti-Saccharomyces cerevisiae mannan antibodies (ASCA) have remained the most widely studied markers, but immune reactivity against a new group of bacterial antigens such as I2, OmpC (outer membrane porin C), and flagellin, has been described in Crohn's disease. Several clinical avenues have been explored, such as the usefulness of serologic markers as screening tools for IBD and in accelerating a diagnosis in patients with indeterminate colitis. Another area of interest is disease stratification. Emerging data suggest there is a diversity of qualitative and quantitative responses to environmental antigens that differs among groups of IBD patients and may be associated with different clinical behaviors. As a result, it may be possible to tailor therapy on the basis of serologic responses. Prospective studies are needed before translating this concept into clinical practice. Clustering of IBD patients into more homogeneous subgroups based on antibody responses may help to unravel the pathophysiology of subsets of IBD.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2003

Inflammatory Bowel Disease After Age 60.

New-onset idiopathic inflammatory bowel disease (IBD) is not uncommon among the elderly, although more common are colonic infection, ischemia, or neoplasia, all of which may mimic IBD. Although the clinical presentation of IBD in the elderly often resembles that of younger subjects, atypical manifestations are common and may lead to difficulty in diagnosis. Much progress has been made in both medical and surgical therapy for IBD, but such therapy poses additional challenges in the elderly, who are more likely to experience adverse effects of medications or complications of surgery. The elderly generally have a favorable outcome to both medical and surgical therapy for IBD. Although concern about possible untoward effects of therapy is warranted, treatment should not be withheld because of fear of complications.

Journal Article↗
PubMed2006

Genetic advances in inflammatory bowel disease.

The translation of basic science advances to tangible benefits in clinical practice remains a fundamental goal of biomedical research. Genetic approaches provide a unique opportunity to enhance bench-to-bedside translational efforts, with inflammatory bowel disease (IBD) being a model genetic disorder in several respects. The association of the NOD2 (CARD15) mutations to Crohn's disease (CD) represents, in complex human disorders, one of the clearest cases of a definitive disease association. The NOD2 gene is located in the IBD1 genetic linkage region on chromosome 16 and functions as an intracellular pattern recognition receptor for components of bacterial peptidoglycan. CD-associated variants within NOD2 have a decreased capacity to appropriately signal with peptidoglycan and provide an important example of gene-environment interactions. Genetic variation in other innate immune receptors, notably Toll-like receptor (TLR)4, has been defined and may also play a role in CD pathogenesis. Replicated CD association in the IBD5 region on chromosome 5q has been reported, and candidate functional polymorphisms within the organic cation transporters OCTN1 (SLC22A4) and OCTN2 (SLC22A5) have been described. Confirmatory studies demonstrating altered OCTN activity and expression in primary human cells stratified on the IBD5 risk haplotype would provide important confirmatory support for disease contribution. A comprehensive understanding of IBD will involve integrating information from animal models, functional human polymorphisms, and expression studies from human IBD tissues. Genes and pathways implicated as contributing to IBD pathogenesis through multiple lines of evidence should be more intensively examined, including the tumor necrosis factor-alpha, MDR1, and peroxisome proliferator-activated receptor (PPAR)gamma pathways. To attain full advantage of new genetic information, novel methods of classifying patients that go beyond phenotypic classifications presently utilized will be required. Genetic data will need to be integrated with novel biomarker development in IBD, including functional, expression (mRNA or protein), or biochemical indicators of physiologic/disease processes and responses to therapies.

Journal Article↗
PubMed1992

New therapeutic agents in the treatment of inflammatory bowel disease.

Despite intense investigation, the etiology of inflammatory bowel disease (IBD) remains unknown. Recent studies with new therapeutic agents provide insight into the pathogenesis of IBD through analysis of the clinical response to pharmacologic agents whose mechanism of action is understood. Until new agents are established, IBD will be treated with conventional drugs directed toward modifying the inflammatory responses responsible for gastrointestinal mucosal damage. Sulfasalazine, mesalamine (5-aminosalicylic acid), and corticosteroids will continue to be the mainstay of therapy for the foreseeable future. Antibiotics such as metronidazole and immunosuppressants such as 6-mercaptopurine and methotrexate are useful in Crohn's disease and ulcerative colitis in selected cases. Many new exciting agents are being investigated and show encouraging results in the treatment of IBD. This article reviews the agents used in IBD with an emphasis on new therapeutic agents.

Adjuvants, Immunologic↗
PubMed1986

Altered patterns of secretion of monomeric IgA and IgA subclass 1 by intestinal mononuclear cells in inflammatory bowel disease.

Intestinal mononuclear cells (MNC) from patients with inflammatory bowel disease (IBD) demonstrated altered patterns of spontaneous secretion of immunoglobulin A (IgA). Control intestinal MNC had markedly high spontaneous secretion of IgA compared to IBD intestinal MNC. Control intestinal MNC secreted predominantly dimeric IgA (only 31% monomeric IgA), whereas IBD intestinal MNC secreted increased amounts (43%-53%) of monomeric IgA. Control intestinal MNC secreted 61% IgA subclass 1 (IgA1), whereas IBD intestinal MNC secreted 71%-74% IgA1. Intestinal MNC from involved portions of resected specimens secreted more of both monomeric IgA and IgA1 than MNC from uninvolved areas of the same bowel. Therefore, intestinal MNC from involved IBD intestinal specimens secrete less total IgA but high percentages of monomeric IgA and IgA1 compared to control intestinal MNC. This could be caused by increased homing of monomeric IgA- and IgA1-producing cells into involved intestine, or the in situ proliferation of monomeric IgA and IgA1 precursor cells resulting from immunoregulatory alterations. These observations may represent the normal mucosal IgA immune response to infectious agents or inducing factors of either a primary or a secondary nature.

Cell Movement↗
PubMed1993

Treatment of anemia in inflammatory bowel disease with recombinant human erythropoietin: results in three patients.

Inflammatory bowel disease (IBD) is often associated with anemia. Of 85 patients with IBD, 28 were anemic and had an inadequately low plasma erythropoietin (EPO) concentration. Three patients with a long-standing history of IBD and refractory chronic anemia (hemoglobin values < 10 g/dL, plasma EPO concentrations below 100 mU/mL) were treated with recombinant human EPO, which was administered subcutaneously three times per week at a dose of 200-300 U/kg of body weight. Bone marrow biopsy specimens taken before therapy showed slightly decreased erythropoiesis with a shift of erythroid precursors toward more immature stages. EPO treatment resulted in a marked increase in hemoglobin values in all 3 patients. Bone marrow biopsies after EPO therapy showed quantitatively and qualitatively normal erythropoiesis in all of them. Correction of anemia was followed by improved well-being, and all patients were able to cope much better with their IBD. In all three patients, there was an increase in body weight and their Karnofsky index improved. After a complete workup and exclusion of any other cause for anemia, erythropoietin treatment, although expensive, should be considered in patients with IBD and refractory anemia.

Anemia, Refractory↗
PubMed1995

Lack of association between smoking and inflammatory bowel disease in Jewish patients in Israel.

BACKGROUND/AIMS: An excess of smokers in patients with Crohn's disease (CD) and a paucity of smokers in patients with ulcerative colitis (UC) were reported in many studies. The aim of this study was to examine the association between smoking and inflammatory bowel disease (IBD) in Israel. METHODS: Two independent studies were performed. Patients with recent IBD in comparison with matched population and outpatient controls and patients with chronic UC and CD were studied. Altogether, 475 subjects were investigated. RESULTS: In both studies, the presence of current smokers was lower in CD (9% and 18%) than in UC (24% and 26%). The proportions of nonsmokers in both studies were similar (UC, 61% and 65%; CD, 67% and 70%) and comparable to those found in their two control groups (57% and 61%; 63% and 68%, respectively) and to the general population of Israel. All differences in smoking habits between patient groups and their controls were not statistically significant, except for the paucity of current smokers in the small group of patients with newly diagnosed CD (P < 0.05). A matched analysis produced similar results. CONCLUSIONS: The expected associations between smoking and IBD could not be confirmed. Two hypotheses are considered: (1) the association between smoking and IBD may not be universal, and (2) our findings may be related to the higher genetic predisposition to IBD in Jewish people.

Adult↗
PubMed1996

Relationship between the use of unconventional therapies and disease-related concerns: a study of patients with inflammatory bowel disease.

We studied the use of unconventional therapies of a well-defined population of 105 patients with inflammatory bowel disease (IBD; 72 with Crohn's disease and 33 with ulcerative colitis) who were attending a university out-patient clinic. The following items were used to compare those patients who used unconventional therapies with those who did not. We compared disease-related data, sociodemographic variables, patients' disease-related concerns, and their perceived level of information about IBD. Concerns were measured with the Rating Form of IBD Patient Concerns (RFIPC), inflammatory disease activity was assessed by physicians with the Crohn's disease activity index (CDAI) and the clinical activity index (CAI). Of the 97 (92.4%) patients who answered all questions, 33 (34%) reported using unconventional therapies in addition to conventional therapy. In their level of information about IBD and in their clinical and sociodemographic data, they were not different from the IBD patients who were not using alternative treatments. In their duration of disease, there was a significant difference (p < 0.0002). The longer the disease duration, the more often patients used unconventional therapies. The most important differences between users and nonusers were the following: patients who used unconventional therapies were more concerned about having surgery (p < 0.001), being treated as different (p < 0.04), and feeling out of control (p < 0.05). We conclude that there is a relationship between the use of unconventional therapies and some disease-related concerns, which should be considered in clinical practice. This may help these patients avoid using unproven and expensive alternative therapies.

Adult↗
PubMed1996

Hemostatic abnormalities in inflammatory bowel disease.

Patients affected by inflammatory bowel disease (IBD) frequently suffer from thromboembolic events. Aims of this study were to investigate hemostatic system and the presence of antiphospholipid antibodies (aPL) in IBD patients. Forty-one patients affected by Crohn's disease (CD) and 19 by ulcerative colitis (UC) were studied, compared to 40 healthy control subjects. Platelet count (PLT), PT, aPTT, fibrinogen (Fib), prothrombin fragment F1+2, antithrombin (AT), protein C (PC), protein S (PS), factor XIII (FXIII), plasminogen (PLG), plasminogen activator inhibitor (PA1), spontaneous platelet aggregation in platelet-rich plasma (PRP-SPA) and in whole blood (WB-SPA), and antiphospholipid antibodies (aPL) were evaluated. PLT, Fib, F1+2 and WB-SPA were significantly increased in IBD patients (p at least <0.05) both in active and inactive phases; aPL positivity was more frequent (p<0.05) and FXIII was significantly decreased (p<0.05) in comparison to control subjects. The thrombophilic state of IBD patients is not related to the degree of activity of the disease or to previous thrombotic events; aPL express the immunological alterations connected with IBD and are not the main cause of thrombotic events.

Adolescent↗
PubMed1984

T-cell abnormalities in inflammatory bowel disease are mediated by interleukin 2.

Inflammatory bowel disease (IBD) may be an immunologically mediated disorder in which T cells are unable to respond appropriately to cell surface-associated antigens. To test this possibility, 37 patients with IBD, 24 with Crohn's disease and 13 with ulcerative colitis who were not being treated with immunosuppressive therapy were studied. The ability of T cells to proliferate in response to autologous or allogeneic cells, i.e., the autologous or allogeneic mixed-lymphocyte reaction (MLR) was tested. The autologous MLR was depressed using patient cells compared to control cells, regardless of disease type or activity (1564 +/- 223 cpm versus 3300 +/- 381 cpm, P less than 0.05) while the allogeneic MLR was depressed in patients with active disease only (29,833 +/- 2871 cpm versus 46,799 +/- 3340 cpm, P less than 0.01). The ability of T cells to recognize and lyse allogeneic cells, allogeneic cell-mediated lympholysis (CML), was also low in patients with active disease (24 +/- 4% versus 37 +/- 3%, P less than 0.05). Since T-cell proliferation and cytotoxicity depend upon adequate production of and response to a T-cell growth factor, interleukin 2 (IL-2), IL-2 production and responsiveness in IBD were studied. IL-2 production by patient T cells in response to phytohemagglutinin was only 39% of control values, P less than 0.05. The response to IL-2 was measured by the increase in T-cell proliferation in the autologous MLR in medium alone or medium supplemented with IL-2. Control T-cell proliferation rose from 3300 +/- 381 cpm to 10,761 +/- 428 cpm with exogenous IL-2 (P less than 0.001). Patient T-cell proliferation rose from 1564 +/- 223 cpm to 6817 +/- 771 cpm with IL-2 (P less than 0.001) but did not reach the level of the IL-2-supplemented control autologous MLR (P less than 0.05). In addition, the percentage of activated patient T cells having Tac antigen (IL-2 receptor) was depressed (P less than 0.05). These findings did not vary with disease type or activity. It is concluded from these data that peripheral blood T lymphocytes from patients with IBD have a diminished response to cell surface antigens which is associated with a decrease in IL-2 production and receptor generation. These defects may be responsible for the depressed T-cell proliferation and cytotoxicity that accompany IBD.

Adolescent↗
PubMed1990

Immunosuppression and histopathological changes in the bursa of Fabricius associated with infectious bursal disease vaccination in chicken.

The effect of the infectious bursal disease (IBD) live virus vaccine on the immune response of chicken was evaluated by the assessment of antibody response following vaccination as well as resistance to challenge with virulent virus. Birds were vaccinated at various ages and later challenged with a heterologous vaccine (NDV) or wild-type IBD virus. The BF was examined for histological changes at regular intervals. Antibody levels to NDV were monitored. Significantly higher mortality rates were observed in birds vaccinated with IBD vaccine than unvaccinated birds (P less than 0.01) following challenge, BF from vaccinated birds showed marked lymphocyte depletion and cellular infiltration with mononuclear cells. Intraocular NDV (NDV-i/o) vaccine given at day old largely prevented the immunodepressive effect of IBD vaccination on NDV vaccine. Groups that received IBD vaccine on day 14 but no NDV i/o suffered higher mortality (41.2%) and showed lower antibody response than those vaccinated on day 1 (0%) or controls which did not receive IBDV (11.8%).

Animals↗
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↗
PubMed2006

Advances and perspectives in the genetics of inflammatory bowel diseases.

Several clinical and biological phenotypes define complex diseases such as inflammatory bowel disease (IBD). There is a critical role of the caspase recruitment domain protein 15/nucleotide-binding oligomerization protein 2-dependent (CARD15-NOD2) sensing of bacterial cell wall components in health and disease. The current etiologic model for IBD emphasizes an interaction between susceptibility and modifier genes along with environmental factors. Together, these lead to disease progression. However, further work should clarify the pathophysiological mechanisms leading to IBD and how innate immune signaling confers susceptibility to intestinal inflammation. This is a prerequisite for rational clinical management of IBD. Genetic, functional, serologic testing and development of therapeutics in IBD are discussed.

Crohn Disease↗
PubMed2006

Duodenal EUS to identify thickening of the extrahepatic biliary tree wall in primary sclerosing cholangitis.

BACKGROUND: Diagnosing primary sclerosing cholangitis (PSC) is problematic and requires meeting a burden of proof through clinical, biochemical, radiologic, and histological features. Endoscopic ultrasound yields detailed images of the extrahepatic biliary tree, but its value in contributing to the diagnosis of this condition is unknown. OBJECTIVES: To determine the potential for transduodenal EUS to detect common bile duct wall thickening in PSC. DESIGN: A prospective, controlled study with retrospective, blinded data analysis. SETTING: Single tertiary referral center for inflammatory bowel disease and EUS. PATIENTS: Four groups of patients were assessed with radial endosonography: PSC (n = 9); inflammatory bowel disease (IBD) with abnormal liver blood tests (n = 21); choledocholithiasis (n = 15); and normal controls (n = 50). Measurements were made of the common bile duct diameter and wall thickness. INTERVENTIONS: Transduodenal radial EUS of the biliary tree. MAIN OUTCOME MEASUREMENTS: Common bile duct diameter and wall thickness. RESULTS: The mean diameter (SD) of the common bile duct for the PSC, IBD, choledocholithiasis, and normal control groups measured 8.9 mm (2.8), 5.4 mm (1.7), 7.2 mm (2.2), and 5.0 mm (1.9), respectively (PSC and choledocholithiasis groups compared to the IBD group, P < .05 for a single test of hypothesis, but correction for the multiple testing of data removed this significance; normal control group P < .005). Mean ductal wall thickness (SD) was 2.5 mm (0.8) for the PSC group, 0.7 mm (0.4) for the IBD group, 0.8 mm (0.4) for the choledocholithiasis group, and 0.8 mm (0.4) for the normal control group, respectively (PSC group compared to the other 3 groups, P < .005). LIMITATIONS: Assessment of intrahepatic PSC is problematic. CONCLUSION: Thickening (>1.5 mm) of the common bile duct wall is seen in patients with PSC but not in those with apparently uncomplicated IBD or choledocholithiasis. The results of this study suggest that standard endosonography contributes to the imaging and potentially to the diagnosis of PSC.

Adult↗
PubMed2004

Treatment of inflammatory bowel disease with antibiotics.

Although antibiotics are clearly recognized as having a role in treating the infectious complications of inflammatory bowel diseases (IBD), their impact in the primary treatment of IBD has long been an area of speculation. Over the past decade there is increasing evidence that luminal gut bacteria play a role in the pathogenesis of IBD, particularly Crohn's disease. Compelling evidence that normal commensal bacteria induce chronic intestinal inflammation in susceptible rodents provides an excellent rationale for treatment of human IBD with antibiotics. This article summarizes published studies of antibiotics in IBD patients and reviews available data for the use of antibiotic therapy in Crohn's disease and ulcerative colitis.

Anti-Bacterial Agents↗