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PubMed2005

The fight for 'health-related normality': a qualitative study of the experiences of individuals living with established inflammatory bowel disease (ibd).

This article reports on the experiences of individuals living with IBD and identifies a range of coping strategies used by them. Qualitative data from 15 individual interviews and three focus groups were analysed using a grounded theory approach. The main focus is on the emergent core concept of 'health-related normality'. A theoretical framework is proposed to explain how individuals with IBD assess their health-related normality, their fight to maintain it and their need to retain the appearance of normality to others. It is concluded that individuals maintain their health-related normality along certain time and context sensitive continuums rather than fitting into a distinct typology.

Adaptation, Psychological↗
PubMed2004

Lumbar spine bone mineral density at diagnosis and during follow-up in children with IBD.

Lumbar spine body mineral density (BMD) was measured in 123 children (65 male, 58 female) suffering from inflammatory bowel disease (IBD) (82 Crohn's disease, 41 ulcerative colitis) and in 46 children (25 male, 21 female) without any history of bone disease. Results in normal children showed that densitometer-derived reference values overestimated spine BMD, particularly for young children, such that the reported mean Z-scores for normal 10-yr-old children were -0.83 for males and -0.72 for females. For children with Crohn's disease, the lumbar spine BMD was further reduced (Z-score = -1.44 for males, Z-score = -1.37 for females). For children with ulcerative colitis, the lumbar spine BMD was similar to that of normal children (Z-score = -0.93 for males, Z-score = -0.56 for females). There was no statistically significant reduction in average spine BMD Z-scores during follow-up periods ranging from 1.7 to 8.7 yr. When growth patterns were examined in individual children, six patients (three Crohn's disease, three ulcerative colitis) were identified as losing spine BMD with respect to their baseline value and their expected pattern of BMD increase associated with normal growth. The children suffering from IBD who, most likely, will not maintain expected growth-related increases in spine BMD are those who are male, relatively young at diagnosis, and unlikely to be taking immunosuppressants.

Absorptiometry, Photon↗
PubMed2005

On tolerability and safety of a maintenance treatment with 6-thioguanine in azathioprine or 6-mercaptopurine intolerant IBD patients.

AIM: To determine the tolerability and safety profile of a low-dose maintenance therapy with 6-TG in azathioprine (AZA) or 6-mercaptopurine (6-MP) intolerant inflammatory bowel disease (IBD) patients over a treatment period of at least 1 year. METHODS: Database analysis. RESULTS: Twenty out of ninety-five (21%) patients discontinued 6-TG (mean dose 24.6 mg; mean 6-TGN level 540 pmol/8 x 10(8) RBC) within 1 year. Reasons for discontinuation were GI complaints (31%), malaise (15%) and hepatotoxicity (15%). Hematological events occurred in three patients, one discontinued treatment. In the 6-TG-tolerant group, 9% (7/75) could be classified as hepatotoxicity. An abdominal ultrasound was performed in 54% of patients, one patient had splenomegaly. CONCLUSION: The majority of AZA or 6-MP-intolerant IBD patients (79%) is able to tolerate maintenance treatment with 6-TG (dosages between 0.3 and 0.4 mg/kg per d). 6-TG may still be considered as an escape maintenance immunosuppressant in this difficult to treat group of patients, taking into account potential toxicity and efficacy of other alternatives. The recently reported hepatotoxicity is worrisome and 6-TG should therefore be administered only in prospective trials.

Adult↗
PubMed2006

Effect of IBD sera on expression of inducible and endothelial nitric oxide synthase in human umbilical vein endothelial cells.

AIM: To study the expression of endothelial and inducible nitric oxide synthases (eNOS and iNOS) and their role in inflammatory bowel disease (IBD). METHODS: We examined the effect of sera obtained from patients with active Crohn's disease (CD) and ulcerative colitis (UC) on the function and viability of human umbilical vein endothelial cells (HUVEC). HUVECs were cultured for 0-48 h in the presence of a medium containing pooled serum of healthy controls, or serum from patients with active CD or UC. Expression of eNOS and iNOS was visualized by immunofluorescence, and quantified by the densitometry of Western blots. Proliferation activity was assessed by computerized image analyses of Ki-67 immunoreactive cells, and also tested in the presence of the NOS inhibitor, 10(-4) mol/L L-NAME. Apoptosis and necrosis was examined by the annexin-V-biotin method and by propidium iodide staining, respectively. RESULTS: In HUVEC immediately after exposure to UC, serum eNOS was markedly induced, reaching a peak at 12 h. In contrast, a decrease in eNOS was observed after incubation with CD sera and the eNOS level was minimal at 20 h compared to control (18%+/-16% vs 23%+/-15% P<0.01). UC or CD serum caused a significant increase in iNOS compared to control (UC: 300%+/-21%; CD: 275%+/-27% vs 108%+/-14%, P<0.01). Apoptosis/necrosis characteristics did not differ significantly in either experiment. Increased proliferation activity was detected in the presence of CD serum or after treatment with L-NAME. Cultures showed tube-like formations after 24 h treatment with CD serum. CONCLUSION: IBD sera evoked changes in the ratio of eNOS/iNOS, whereas did not influence the viability of HUVEC. These involved down-regulation of eNOS and up-regulation of iNOS simultaneously, leading to increased proliferation activity and possibly a reduced anti-inflammatory protection of endothelial cells.

Adolescent↗
PubMedDate not supplied

[Antibodies anti granulocytic antigens in IBD: from microscopic morphology to antigenic specificity].

OBJECTIVE: ANCA (p-ANCA and x-ANCA) have been documented to occur in many inflammatory disorders. The specific ANCA antigens and the clinical correlation of a positive ANCA test in these disorders are still for the most part obscure. The aim of the present study was to investigate the prevalence of and the target antigens for ANCA in patients with IBD. METHODS: 104 patients (67 age between 3-18 years, mean age 8+/-3 and 37 age between 25-70 years, mean age 48+/-15) clinically and hystopathologically diagnosed as: 67 ulcerative colitis, 16 Crohn' disease, 21 other colitis (7 indeterminate colitis) were enrolled in our study. ANCA were determined by ELISA and IIF methods. RESULTS: We observed a good performance in terms of sensibility and specificity of ANCA, and a good correlation between the two methods used; as regard ELISA determination the antigen frequently found in our cases was lactoferrin (60%). CONCLUSIONS: Is still unclear the role of these "minor antigens" in the diagnosis and pathogenesis of IBD, but is clear that only morphologic evaluation is no more sufficient.

Adolescent↗
PubMed1998

Immunopotentiating effects of Azadirachta indica (Neem) dry leaves powder in broilers, naturally infected with IBD virus.

Effects of feeding of powdered dry leaves of A. indica (AI) were investigated on humoral and cell mediated immune responses, in a flock of broilers which had survived an outbreak of infectious bursal disease (IBD). AI (2 g/kg) treatment significantly enhanced the antibody titres against new castle disease virus (NCDV) antigen and also potentiated the inflammatory reactions to 1. Chloro-2,4-di- nitro benzene (DNCB) inskin contact test. The results indicate that AI could be beneficial in immunosuppressed condition like IBD, in poultry.

Adjuvants, Immunologic↗
PubMed2000

IBD: immunologic research at The Mount Sinai Hospital.

An evolution in our understanding of the inflammatory bowel diseases (IBD), ulcerative colitis and Crohn's disease, correlates with increased knowledge of the function of the mucosal immune system. In the early 1960s and 1970s, IBD was considered to be an autoimmune disease in which there was a directed attack by humoral and cellular elements of the immune system against intestinal tissues. These studies did not withstand the test of time, and from the 1970s through the 1990s there was a growing appreciation that defects in cellular immunity, not auto-reactive in nature, played a larger role in disease pathogenesis. Research at Mount Sinai focused in on these cellular T cell defects and helped pave the way for the current model of disease pathogenesis.

Allergy and Immunology↗
PubMed2003

Significant role of genetics in IBD: the NOD2 gene.

Inflammatory bowel disease (IBD) clusters within families, suggesting a genetic component to disease pathogenesis. Studies have identified a gene on chromosome 16cen that confers susceptibility to Crohn's disease. The affected gene codes for the NOD2/CARD15 protein, which is involved in the immune system's response to bacterial infection. Multiple mutations have been identified, three of which have been shown to be independently associated with Crohn's disease-arg702trp, gly908arg, and leu1007fsinsC. Taken together, these three variants confer a 15%-20% attributable population risk among cases of familial Crohn's disease, with decreased contribution among the more common sporadic cases of the disease. The presence of an NOD2 risk allele has been shown to be associated with ilial disease as well as an earlier age of disease onset. Further studies are needed to clarify the relationship between IBD genotype and disease behavior.

Carrier Proteins↗
PubMed2003

Leukocytapheresis for treatment of IBD.

The recent development of effective and safe devices to remove leukocytes selectively from circulating blood has facilitated the application of leukocytapheresis for the treatment of inflammatory bowel disease (IBD). Successful results of preliminary trials of leukocytapheresis for IBD led to several nationwide multicenter clinical trials in Japan. As a result, five or six consecutive leukocytaphereses, which were undergone weekly, improved both symptoms and endoscopic findings in approximately 60%-80% of patients with ulcerative colitis (UC). In Japan, leukocytapheresis is now considered to be one of the standard treatments for UC patients with refractory disease to avoid surgery. Here, the current status of indications and mechanisms of action on UC are analyzed by reviewing the results of Japanese multicicenter trials, and the possible application for Crohn's disease is also discussed.

Adult↗
PubMed2003

The future of IBD treatment.

Throughout most of the past 50 years, treatment of Crohn's disease and ulcerative colitis has been dominated by the use of agents whose efficacy was defined on an empiric basis. Many of these, including most especially 5-amino salicylic acid (5-ASA)-based agents and corticosteroids, remain mainstays of current treatment even as research is catching up with clinical experience to define the mechanistic basis of their efficacy. Other agents, also of established utility in at least a subset of patients, were developed on the basis of general inferences about disease pathogenesis. These agents are exemplified by antibiotics (metronidazole) and immunosuppressive agents (azathioprine/6-mercaptopurine, methotrexate, and cyclosporine); attention was directed on the assumption of the general likely importance of microbial species and immunoactivation, respectively. However, the rapid progress, even if still incomplete in understanding of pathophysiological mechanisms that play a role in IBD, has transformed the development of new therapeutic agents, enabling the development of several agents now available or currently in advanced clinical development. It is notable that each of the major overall thrusts in development of new therapeutic strategies parallels, and may be reasonably viewed as the partial outgrowth of, dominant areas of progress in understanding of disease mechanisms relevant to IBD.

Colitis, Ulcerative↗
PubMedDate not supplied

Polyunsaturated fatty acids (n-3 PUFAs) and inflammatory bowel disease (IBD): pathogenesis and treatment.

There is considerable evidence to suggest that polyunsaturated fatty acids (PUFAs) alleviate a number of inflammatory diseases, mainly the fish derivatives, n-3 PUFAs. My aim is to briefly review the literature involving clinical interventions with these lipid compounds in the treatment of Ulcerative Colitis (UC) and Crohn's Disease (CD), Inflammatory Bowel Disease (IBD). Data available are conflicting and the reason for the discrepancies in the findings could reside in the different study designs. Often studies are limited by the choice of placebo and insufficient washout period and direct comparison of trials is hampered by the use of various formulations and dosages of n-3 PUFAs. The importance of the n-3 PUFAs formulation in lowering the incidence of side effects along with careful selection of patients and experimental design seems to be associated with benefits. It is possible these fatty acids act by reducing low-grade active inflammation rather than by preventing reinitiation of the inflammatory process from a truly quiescent state. Whether this treatment is applicable to all patients with IBD has not been fully elucidated. Nevertheless, taken together, all these studies suggest the effectiveness of these new therapeutic approaches, not only when the conventional treatment fails or it is not possible to treat chronically, but also, in some instances as first choice.

Clinical Trials as Topic↗
PubMed2005

Mapping autoimmune disease genes in humans: lessons from IBD and SLE.

The inflammatory bowel diseases (IBD) and systemic lupus erythematosus (SLE) are common autoimmune diseases that affect 2-3 million people in the USA alone. Crohn's disease (CD) and ulcerative colitis (UC), the inflammatory bowel diseases, are idiopathic, chronic inflammatory disorders of the gastrointestinal tract. SLE is a chronic, multi-system autoimmune disease that generally presents in women of childbearing age as fatigue, arthralgia and rash. Although the aetiology of these two diseases is not fully known, it is believed that genetic, hormonal and environmental influences contribute to susceptibility. Genomewide linkage scans in IBD have revealed significant loci that, upon comprehensive association mapping strategies, yield what are believed to be causal susceptibility alleles. Human linkage studies performed to date in SLE have not been as informative, although genetic mapping in mouse models of SLE as well as candidate gene approaches have provided important clues to the genetic susceptibility in humans. We will examine how some of the recent advances in our understanding of genetic variation in the human genome are greatly improving our ability to map autoimmune disease genes in humans.

Autoimmune Diseases↗
PubMed2006

[Current concepts in the genetics of hereditary and sporadic colorectal cancer and the role of genetics in clinical practice: sporadic and IBD-associated colorectal tumors, significance of genetic tests in diagnosis, prognosis and assessment of chemotherapy outcome].

There has been a major improvement in our understanding in the area of the genetics of CRC in the last decade. Reason for this is partly that CRC has a strong hereditary trait and premalignant lesions are frequent and easily accessible. In the 1990-ies the mutations responsible for the adenoma-carcinoma sequence were discovered on after the other. In the second part of the review the authors discuss the genetic background of sporadic and IBD associated colorectal cancers as well as the role of genetics in the diagnosis, prognosis and prediction of therapy. Chromosomal instability (85%) and microsatellite instability with or without change in DNA methylation (15%) are the main mechanisms involved in the pathogenesis of sporadic colorectal cancers. It became evident that no ultimate mutations exist. Most of neoplasms are genetically heterogeneous, independent pathways and simultaneous tumorigenesis may exist within the same organ, also in the colon. Gene expression profile, clinical phenotype and prognosis may also vary according to the location. Similar genetic mutations may be found in IBD associated colorectal cancers, however, the typical sequence and importance of mutations is different. In future, fecal DNA testing may be an important screening tool for colorectal cancer; however, its routine use is still limited by its low sensitivity. Similarly, genetic investigation may play an increasing role in the prediction of prognosis, therapy and complication of chemotherapy. A more distant goal may be the individualization of the therapy.

Adenomatous Polyposis Coli↗
PubMed1991

Immunology of inflammatory bowel disease: summary of the proceedings of the Subcommittee on Immunosuppressive Use in IBD.

As outlined, scanty data exist with regard to immunologic therapy in children with IBD despite the fact that the pediatric population affords a unique opportunity for clinical evaluation. Children are less affected by modifying conditions such as smoking, alcohol ingestion, and the long-term use of medications, and because of their specific needs for ponderal and linear growth, children might benefit most from immunological therapy that has been proven to be steroid sparing. Therefore, clinical trials to evaluate the efficacy of 6-MP and/or azathioprine in growing children with Crohn's disease would appear to provide a fruitful avenue for collaborative research. Efforts to organize a multicenter evaluation of these agents have been initiated. The studies are crucial in evaluating the efficacy and safety of immunosuppressive therapy in the pediatric population with IBD.

Aminosalicylic Acids↗
PubMed2005

Increased risk of breast cancer in first-degree relatives of Crohn's disease patients. An IG-IBD study.

BACKGROUND: Increased rates of colorectal cancer have been reported in patients with ulcerative colitis as well as with Crohn's colitis. This risk could be the result of shared genetic susceptibility and could be co-inherited rather than being just secondary to a long-standing, extensive mucosal inflammation. AIM: To assess the prevalence of all malignancies in first-degree relatives of Crohn's disease patients in order to establish whether any association exists. PATIENTS AND METHODS: A total of 632 outpatients with a diagnosis of Crohn's disease and 632 control subjects were recruited. Information concerning the presence of malignancies was collected in 3,292 first-degree relatives of Crohn's disease patients and in 3,303 first-degree relatives of controls. RESULTS: Two hundred and fourteen (6.5%) subjects were found to be affected by malignancy in the first-degree relatives of Crohn's disease patients and 180 (5.5%) in the first-degree relatives of controls. Forty-seven (7.4%) of Crohn's disease patients had a first-degree relative with IBD, but none of them had cancer. The frequency of extra-intestinal malignancies was higher in first-degree relatives of Crohn's disease patients than in those of controls (p=0.011). Frequency of breast cancer in female relatives of Crohn's disease patients, mainly in mothers, was two-fold higher than that in controls (0.91% versus 0.42%; odds ratio=2.16; 95% confidence interval=1.14-4.08; p=0.015). The presence of breast cancer showed no association with any specific phenotype of disease in Crohn's patients. CONCLUSIONS: These results did not corroborate the hypothesis about a common genetic susceptibility between Crohn's disease and colorectal cancer. An unexpected finding was the more frequent occurrence of extra-digestive malignancies. The prevalence of breast cancer in first-degree relatives of Crohn's disease patients, in particular the mothers, was more than double than in those of controls. This association, if confirmed, would suggest that there may exist common genetic and/or environmental factors for Crohn's disease and breast cancer.

Adult↗
PubMed2004

Tests for covariate-associated heterogeneity in IBD allele sharing of affected relatives.

Linkage studies that aim to map susceptibility genes for complex diseases commonly test for excess allele sharing among affected relatives. Conventional methods based on identical-by-descent IBD allele sharing do not allow for possible differences among families, such as arise in the case of locus heterogeneity, and thus have reduced ability to detect linkage in the presence of such heterogeneity. We investigated two approaches to test for heterogeneity in allele sharing, using a family-level covariate that may be associated with different disease mechanisms leading to differences in allele sharing. Likelihood ratio tests for heterogeneity were formulated based on an extension of the linear and exponential likelihood models developed by Kong and Cox. Alternatively, we examined the asymptotic and permutation distributions of T-tests for differences between mean allele-sharing linkage scores from two covariate-defined family subgroups, assuming exchangeability. The size and power of heterogeneity tests were evaluated for S(all) and S(pairs) allele-sharing scoring functions using data sets of families with affected sibling and cousin pairs, generated under a model of locus heterogeneity. In certain simulation scenarios, the likelihood ratio test statistics did not follow the expected asymptotic distributions. The type I error estimates for the T-statistics conformed to nominal 5 and 1% levels in all scenarios considered, and corresponding power was comparable to that of the likelihood ratio tests. Application of these tests for heterogeneity detected significant differences in allele sharing between subgroups of families with inflammatory bowel disease.

Algorithms↗
PubMed1996

Distribution of genome shared IBD by half-sibs: approximation by the Poisson clumping heuristic.

The distribution of the proportion of genome shared identical by descent (IBD) by c half-sibs is calculated for a general c. With data availability the consideration of the chromosome as a whole rather than discrete loci becomes of increasing practical importance. Assuming the genomic continuum model, which allows for recombination, the crossover process in a chromosome pedigree is viewed as a continuous-time Markov random walk on the vertices of a hypercube with time parameter map distance along the chromosome. The desired distribution corresponds to the distribution of sojourn times of the process in a small set of vertices. The sojourn times are well approximated via the Poisson clumping heuristic. It is shown explicitly that there is no "equivalent" number of independently segregating loci that will yield the same results as with the genomic continuum model. Results are given for the human genome.

Crossing Over, Genetic↗
PubMed2005

Application of a new IBD-based QTL mapping method to common wheat breeding population: analysis of kernel hardness and dough strength.

Mapping quantitative trait loci (QTL) in plants is usually conducted using a population derived from a cross between two inbred lines. The power of such QTL detection and the estimation of the effects highly depend on the choice of the two parental lines. Thus, the QTL found represent only a small part of the genetic architecture and can be of limited economical interest in marker-assisted selection. On the other hand, applied breeding programmes evaluate large numbers of progeny derived from multiple-related crosses for a wide range of agronomic traits. It is assumed that the development of statistical techniques to deal with pedigrees in existing plant populations would increase the relevance and cost effectiveness of QTL mapping in a breeding context. In this study, we applied a two-step IBD-based-variance component method to a real wheat breeding population, composed of 374 F6 lines derived from 80 different parents. Two bread wheat quality related traits were analysed by the method. Results obtained show very close agreement with major genes and QTL already known for those two traits. With this new QTL mapping strategy, inferences about QTL can be drawn across the breeding programme rather than being limited to the sample of progeny from a single cross and thus the use of the detected QTL in assisting breeding would be facilitated.

Breeding↗