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At least 145 records · Page 8Linked to original sources
PubMed1997

A randomized, double-blind study of the effect of olestra on disease activity in patients with quiescent inflammatory bowel disease. Olestra in IBD Study Group.

PURPOSE: To determine the effects of olestra, a zero-calorie fat substitute that is neither digested nor absorbed, on the well-being and disease state of persons with chronic inflammatory bowel disease (IBD) in remission. PATIENTS AND METHODS: Eighty-nine patients with mild to moderate ulcerative colitis (n = 43) or Crohn's disease (n = 46) in remission, with a history of disease of 2 years or longer, were enrolled in this prospective study from nine private practices, three university-based medical centers, and one Veterans Administration medical center in the United States. Forty-four patients were randomly assigned to receive olestra and 45 to receive triglycerides in chips or cookies daily for 4 weeks. At Week 4, patients were classified as in remission, worsened, or relapsed according to an investigator's global assessment based on sigmoidoscopy (for ulcerative colitis) or the Crohn's disease activity index, laboratory findings, and clinical course. RESULTS: At Week 4, the olestra and triglyceride groups did not differ significantly with respect to the percentages of patients who relapsed (P = 0.494; difference = 2.4%; upper 95% CL = 8.8%) or with respect to the percentages of patients who experienced any worsening of their symptoms (P = 0.630; difference = 0.2%; upper 95% CL = 13.3%). Of evaluable patients, 90% (37 of 41) given olestra remained in remission with no worsening, compared with 90% (38 of 42) given triglycerides. Gastrointestinal symptoms were comparable between the treatment groups, and there were no treatment-related laboratory abnormalities. Six patients were excluded from analysis for reasons unrelated to treatment. CONCLUSION: Olestra did not affect the activity of quiescent mild to moderate IBD.

Abdominal Pain↗
PubMed2002

Quantitative analysis for human glucocorticoid receptor alpha/beta mRNA in IBD.

We have previously reported that in peripheral blood mononuclear cells (PBMC), the augmented expression of the beta isoform of the human glucocorticoid receptor (hGRbeta), as a putative dominant negative regulator of glucocorticoid action, is associated with glucocorticoid (GC) unresponsiveness of UC patients. In this study, we quantified the levels and serial changes of hGR transcripts in PBMC of IBD patients by a real-time fluorescence monitoring of PCR. As results, relative hGRbeta mRNA expression was significantly higher in the active stage of UC than in inactive periods of UC or CD patients. Longitudinal analysis revealed that hGRbeta mRNA expression in UC was increased after the relapse of inflammation, suggesting that the overproduction of cytokines during inflammation may be responsible. In in vitro culture experiments of human lymphoid cell (CEM) and human PBMC, IL-7, and IL-18 increased hGRbeta mRNA expression in these cells but GC itself did not. Through these analyses, it is indicated that the inflammatory cytokines altered the splicing condition of the primary transcript of hGR gene in IBD patients.

Adult↗
PubMed2005

Azathioprine induced nodular regenerative hyperplasia in IBD patients.

Purine analogues are major drugs in the treatment of inflammatory bowel diseases (IBD). We present four cases of nodular regenerative hyperplasia of the liver (NRH) developed in patients with IBD treated with azathioprine. All patients had either abnormal liver tests and/or low platelet count. Although biochemical and hematological abnormalities regressed after azathioprine withdrawal, the long term evolution of the hepatic lesions (and the risk to develop further complications including portal hypertension) remains to be determined. Male gender seems to be a major risk factor by providing a predisposing pharmacogenetic profile of purine analogue metabolism. Clinicians should be aware of this serious complication which may occur with any of the purine analogues (azathioprine, 6-mercaptopurine, and 6-thioguanine).

Adult↗
PubMed2003

Transitioning the paediatric IBD patient to adult care.

Transitioning an adolescent patient to an internist/gastroenterologist's care requires an understanding of the specific issues and challenges involved in the diagnosis and management of paediatric inflammatory bowel disease (IBD). Even though diagnostic criteria, as well as methods are the same in children and adults, younger patients may experience more insidious presentations. A high level of suspicion is necessary for an early and accurate diagnosis. Management of IBD in the paediatric population begins with the assessment of disease extent and activity as well as the identification of potentially serious complications (such as malnutrition, growth/sexual retardation and osteoporosis), which are often present at the time of diagnosis. Treatment includes not only medical, nutritional or surgical therapy but also a multidisciplinary or holistic approach taking into consideration the psychological as well as social impact of the disease on the patient and family.

Adolescent↗
PubMed1998

Catalase and alpha-enolase: two novel granulocyte autoantigens in inflammatory bowel disease (IBD).

In IBD, the target antigens of anti-neutrophil cytoplasmic autoantibodies (ANCA) have not been fully identified, which limits the analysis of the diagnostic significance as well as of the possible pathophysiological role of these antibodies. In this study, we identify the target antigens of ANCA in large groups of patients with ulcerative colitis (UC) and Crohn's disease (CD). Apart from antibodies against lactoferrin and bactericidal/permeability-increasing protein (BPI), which have been reported before, antibodies against two novel granulocyte antigens were identified: antibodies against a 57/56-kD doublet were found in 38% of samples from UC patients and in 26% of samples from CD patients, whereas antibodies against a 47-kD protein were found in 10% of samples from UC patients and in 18% of samples from CD patients. Partial purification and amino acid sequence analysis identified the 57-kD protein as catalase and the 47-kD protein as alpha-enolase. This study is the first to report catalase and alpha-enolase as granulocyte antigens for autoantibodies in IBD.

Antibodies, Antineutrophil Cytoplasmic↗
PubMed2004

[Immunosuppressive therapy for inflammatory bowel disease: consensus by the Austrian working group on IBD].

Azathioprine (AZA) or 6-mercaptopurine (6-MP) are the immunosuppressive drugs of choice in the treatment of inflammatory bowel disorders (IBD). Optimal dosage for AZA is around 2.5 mg/kg body weight and induction of remission by these drugs may take 6 - 7 months. Intramuscularly applied Methotrexate (MTX) is the second choice, while its efficacy starts earlier than that of AZA; studies assessing oral low-dose MTX treatment are lacking. Cyclosporin is the standard treatment in case of steroid-refractory severe ulcerative colitis. This drug may also be used in patients with severe extraintestinal manifestations of IBD. Regarding other immunosuppressive drugs such as mycophenolic acid or 6-thioguanine respective controlled clinical study data are not available. The risk of malignancy using immunosuppressive drugs such as AZA is low and furthermore, especially AZA and 6-MP can be used rather safely during pregnancy.

Administration, Oral↗
PubMed2003

A method for the detection of eosinophilic granulocytes in colonoscopic biopsies from IBD patients.

Eosinophilic granulocytes were found to be autofluorescent when Giemsa-stained sections were stimulated with indirect light fluorescence (ILF). The frequency of autofluorescent eosinophils was assessed in areas with diffuse and focal inflammation in 76 consecutive colonoscopic biopsies from patients with inflammatory bowel disease (IBD), Crohn's disease (CD = 32), ulcerative colitis (UC = 30), and collagenous colitis (CC = 7). All IBD cases had moderate to severe pancolitis. In areas with diffuse inflammation, severe eosinophilia was recorded in 39.6% or in 38 of 96 high power fields investigated in patients affected by CD, and in 3.3% or in 3 of 90 high power fields examined in patients with UC. In areas with focal inflammation, the mean percentage of eosinophils in CD was 57% (range 44-70%), and 9% in UC (range 6-26%). No focal inflammation was present in CC. In the submucosa of some CD patients, a large number of autofluorescent eosinophils and many autofluorescent cell-free granules were seen. It was inferred that these autofluorescent granules had been released from eosinophils, and that the eosinophilic granulocytes from which these granules had originated were no longer discernible. Focal eosinophilic mucosal infiltration in CD is more common than epithelioid cell granulomas, and emerges as an important parameter in the histologic differential diagnosis between colonic CD and UC.

Adolescent↗
PubMed1999

Day-old vaccination with live-in-oil vaccines: Newcastle disease (ND) and infectious bursal disease (IBD) in chicks and ND in turkey poults.

One-day-old broiler chicks were vaccinated with live Newcastle disease (ND) vaccine incorporated in oil alone or in killed-in-oil ND vaccine. Incorporation of live vaccine in oil emulsions was carried out just prior to vaccination. Live-in-oil ND vaccine containing 106.0 median embryo lethal doses (ELD50/dose induced the same protection following challenge and the same level of antibody at 42 days post-vaccination as did commercial killed-in-oil ND vaccine containing about 250 times as much antigen (108.4 ELD50/dose). Incorporation of live ND vaccine in killed-in-oil vaccine contributed markedly to protection rates and antibody levels, as compared to those obtained following vaccination with killed-in-oil vaccine only. One-day-old turkey poults also showed the advantage of incorporation of live ND vaccine in killed-in-oil vaccine when challenged 3 months post-vaccination. One-day-old broiler chicks, vaccinated with live ND and infectious bursal disease vaccine (IBD) incorporated in killed-in-oil combined ND + IBD vaccine, showed better protection against challenge with IBDV and higher antibody levels to NDV as compared to vaccination with killed-in-oil vaccine alone.

Journal Article↗
PubMed2003

IBD International Genetics Consortium: international cooperation making sense of complex disease.

The Inflammatory Bowel Disease International Genetic Consortium was formed in Oxford in 1997. Since then it has grown to include twelve groups from around the world that are each actively involved in identifying the genes that are involved in susceptibility to IBD. The approach of the IBDIGC is to attempt to overcome one of the major issues in complex disease analysis-that of obtaining sufficient power to analyze successfully the inheritance of IBD-by collaboratively studying large numbers of well documented families with multiple affected individuals. This strategy has been marked by considerable success with the publication of a paper authored by the IBDIGC substantiating the localization of IBD1 to chromosome 16. This publication served to encourage researchers and eventually resulted in the identification by several groups simultaneously of risk alleles in the NOD2 gene that cosegregate with disease. The IBDIGC provides a model for studies in complex disease genetics, showing that research groups both large and small can participate equally in complex disease gene identification through the formation of large international consortia.

Congresses as Topic↗
PubMed2005

A comparative study of goblet cell and pancreatic exocine autoantibodies combined with ASCA and pANCA in Chinese and Caucasian patients with IBD.

BACKGROUND: The incidence of Crohn's disease (CD) and ulcerative colitis (UC) is increasing, but differentiating between them is often extremely difficult. Pancreatic (PAB) and goblet cell autoantibodies (GAB) are specific for CD and UC, respectively, but with low sensitivity. In combination with anti-Saccharomyces cerevisiae (ASCA) and anti-neutrophil cytoplasmic antibodies (pANCA) testing, these antibodies may improve differentiation between the diseases. This study determined the sensitivity, specificity, and positive and negative predictive values (PPV and NPV) of PAB and GAB +/- ASCA and pANCA testing in Chinese and Caucasian IBD populations. RESULTS: Patients were recruited from Caucasian and Chinese populations (CD, n = 100; UC, n = 99; controls, n = 100). PAB was highly specific for CD, and detection was greater in patients less than 35 years old and in Chinese compared with Caucasian patients with CD (CD, 46% versus 22%, P = 0.018; UC, 2% versus 6%; controls, 0% versus 2%). GAB detection was poor in all groups (<2%). PAB showed a PPV of 93% to differentiate all patients with CD from patients with UC, but only 62% for those with isolated colonic disease. The PPV of PAB increased to 100%, specificity was 100%, and sensitivity was 21% for isolated colonic disease when combined with pANCA and ASCA. PAB expression was not associated with stricturing or perforating CD. CONCLUSIONS: This study identified that GAB was not useful in our patients with IBD. PAB expression was highly specific for CD and more sensitive in Chinese than Caucasian patients with CD. The combination of PAB, pANCA, and ASCA testing improved the differentiation between UC and CD, particularly in isolated colonic disease, compared with pANCA and ASCA testing alone.

Adolescent↗
PubMed2006

Galectin-3 modulates T cell activity and is reduced in the inflamed intestinal epithelium in IBD.

BACKGROUND: Galectins are involved at different stages in inflammation. Galectin-3, although mostly described as proinflammatory, can also act as an immunomodulator by inducing apoptosis in T cells. The present study aims to determine galectin-3 expression in the normal and inflamed intestinal mucosa and to define its role in T cell activity. MATERIALS AND METHODS: Galectin-3 was detected by quantitative polymerase chain reaction with total RNA from endoscopic biopsies and by immunohistochemistry. Biopsies and peripheral blood mononuclear cells (PBMC) were stimulated in vitro and were used to assess the functional consequences of inhibition or exogenous addition of galectin-3. RESULTS: Galectin-3 is expressed at comparable levels in controls and inflammatory bowel disease (IBD) patients in remission. In the normal mucosa, galectin-3 protein was mainly observed in differentiated enterocytes, preferentially at the basolateral side. However, galectin-3 was significantly downregulated in inflamed biopsies from IBD patients. Ex vivo stimulation of uninflamed biopsies with tumor necrosis factor led to similar galectin-3 messenger RNA downregulation as in vivo. When peripheral blood mononuclear cells (PBMC) were analyzed, galectin-3 was mainly produced by monocytes. Upon mitogen stimulation, we observed increased proliferation and decreased activation-induced cell death of peripheral blood T cells in the presence of galectin-3-specific small interfering RNA. In contrast, exogenous addition of recombinant galectin-3 led to reduced proliferation of mitogen-stimulated peripheral blood T cells. CONCLUSIONS: Our results suggest that downregulation of epithelial galectin-3 in the inflamed mucosa reflects a normal immunological consequence, whereas under noninflammatory conditions, its constitutive expression may help to prevent inappropriate immune responses against commensal bacteria or food compounds. Therefore, galectin-3 may prove valuable for manipulating disease activity.

Adult↗
PubMed1995

Perspectives of identity by descent (IBD) mapping in founder populations.

In a founder population patients with a genetic disease are likely to share predisposing genes from a common ancestor. We show that, depending on the distance of the relationship, patients are expected to share extended segments of DNA around the disease gene. Because of the size of the shared segment, a genomic search with DNA markers for such shared segments, identity by descent (IBD) mapping, can efficiently find the map position of genes, particularly due to genetic drift leading to reduction of heterogeneity and the large number of meioses that is implicitly observed. The statistical power of this method and the approximate cost are given as a function of the density of the map of tested markers and the number of generations since a common ancestor. Initial marker spacings between 5 and 15 centiMorgans are shown to be optimal. IBD mapping is applicable to many genetic diseases, because it does not presuppose a specific genetic model.

Alleles↗
PubMed1995

Circulating antiinflammatory cytokine IL-10 in patients with inflammatory bowel disease (IBD).

IBD is characterized by increased serum concentrations of different cytokines. IL-10 inhibits the production of proinflammatory cytokines such as IL-1, tumour necrosis factor-alpha (TNF-a), interferon-gamma (IFN-gamma) and IL-6 through inhibitory action on Th1 cells and macrophages, and it is thought to be a suppressor type cytokine. In the present study we determined serum concentrations of IL-10 in patients with ulcerative colitis (UC) and Crohn's disease (CD). We measured human IL-10 by our own newly established ELISA system using PharMingen antibodies. Serum antibodies were assessed in 44 patients with UC, 40 patients with CD, and in 30 healthy controls. Human IL-10 serum levels were significantly increased in patients with active UC (144 +/- 34 pg/ml (mean +/- s.e.m.), P < 0.001) and in active CD (132 +/- 32 pg/ml, P < 0.001) compared with healthy controls (44 +/- 9.5 pg/ml). Only patients with active CD and active UC presented with significantly increased IL-10 serum levels, while patients with inactive disease did not show any significant increase. There was no statistically significant difference between IL-10 serum levels in patients with CD or UC. Compared with clinical disease activity indices there was a significant correlation between IL-10 serum concentration and CDAI in patients with CD (r = 0.45, P < 0.01) and CAI in UC patients (r = 0.39, P < 0.05). Comparing IL-10 serum levels with serum concentrations of other proinflammatory cytokines there was a significant correlation to serum levels of sIL-2R (r = 0.417, P < 0.05) and IL-6 (r = 0.387, P < 0.05) in patients with CD. Serum cytokine levels in patients with UC did not show any significant correlation to IL-10 serum concentration. IL-10 is elevated in serum of patients with active CD and UC, suggesting that IL-10 acts as a naturally occurring damper in the acute inflammatory process of IBD.

Acute Disease↗
PubMed1978

The affected sib pair IBD distribution for HLA-linked disease susceptibility genes.

The distribution of identity by descent (IBD) scores for sib pairs affected with a disease determined by a disease susceptibility (DS) locus tightly linked to the HLA complex is derived. It is shown that the sib pair IBD distribution differs from its a priori distribution and, moreover, is completely specified by three observable population parameters--the additive and dominance variances and the prevalence of the disease in the population. An application of the model is illustrated using data on juvenile diabetes mellitus.

Chromosome Mapping↗
PubMed1978

The generalized sib pair IBD distribution: its use in the detection of linkage.

General expression for the distribution of identity by descent (IBD) scores at a marker locus have been derived given neither, one or both sibs affected with a disorder determined by a linked trait locus with arbitrary gene frequency and penetrance vector. It is shown that the distirbution of IBD scores depends only on the additive and dominance variances and the population prevalence of the disorder. A one-sided test is suggested as an appropriate means of statistically testing the hypothesis that the recombination fraction is significantly less than 1/2. This sib pair approach is designed primarily to detect the presence of a critical disease susceptibility locus but when the assumptions of the incompletely penetrant single locus model are correct the methodology proposed here results in consistent estimates of the recombination fraction. The affected sib pair methodology seems especially suited to traits determined by single loci with non-Mendelian transmission.

Alleles↗
PubMed2006

On studying the connection between stress and IBD.

A number of investigators over the years have attempted to determine if a relationship exists between flares of inflammatory bowel disease (IBD) and stress. There are many complexities to addressing this issue, including determining the appropriate tools to measure stress, determining the appropriate measures of quantifying a disease flare and also determining the point at which the timing of the stress could be seen to be reasonably related to the onset of the flare. While advances have been made in understanding physiological responses to acute stress, it is unclear whether it is acute, chronic, or recurrent stress that might most impact on a chronic inflammatory disease. In the case of IBD, the disease itself poses a stress to the individual further clouding the issue.

Humans↗
PubMed2006

Role of interleukin 6 in a murine model of Crohn's ileitis: are cytokine/anticytokine strategies the future for IBD therapies?

Although the precise causes of inflammatory bowel disease (IBD) have yet to be discovered, important therapeutic advances have resulted from the manipulation of cytokine function(s) using anticytokine/cytokine therapies, such as targeting of tumor necrosis factor. We discuss the future of this area of investigation in the context of preclinical experimentation using animal models of IBD. In particular, we pinpoint the roles played by interleukin 6 and its intracellular signalling pathways in the SAMP1/Yit murine model of Crohn's-like ileitis.

Animals↗
PubMed1995

Incidence of inflammatory bowel disease in southeastern Norway: evaluation of methods after 1 year of registration. Southeastern Norway IBD Study Group of Gastroenterologists.

To assess the feasibility of a prospective incidence study of inflammatory bowel disease (IBD), the registration methods and incidence figures during 1990 were evaluated. The study was a collaboration between 14 hospitals in an area of close to one million inhabitants. Common diagnostic criteria for ulcerative colitis (UC), Crohn's disease (CD) and indeterminate colitis (IND) were established prior to the start of the study. There was an overall incidence rate for IBD of 19.3 per 10(5) inhabitants, with 10.6 for UC, 5.1 for CD and 3.6 for IND. The age-specific incidence rates showed a peak between 25 and 34 years for UC and between 15 and 25 for CD. There was a male predominance for UC and a female preponderance for CD. These results are comparable with the previous registrations in western and northern areas of Norway.

Adolescent↗