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At least 37 records · Page 2Linked to original sources
PubMed1999

Development of a quality-of-life index for pediatric inflammatory bowel disease: dealing with differences related to age and IBD type.

BACKGROUND: A child- and adolescent-generated IBD quality-of-life index was designed to be descriptive (to be used to assess the overall impact of IBD on individual patients), and evaluative (to be used as an outcome measure in clinical trials). METHODS: Item-generation and item-reduction interviews with 82 patients with IBD aged 8 to 17 years (61 with Crohn's disease, 21 with ulcerative colitis; 36 girls, 45 boys) generated a list of ways in which their lives were affected by IBD. These issues were incorporated into an item-reduction questionnaire, which was administered to 117 patients (87 Crohn's disease, 30 ulcerative colitis). Patients indicated on a visual analog scale how important an item was to them and how often it bothered them. Mean and median importance-plus-frequency scores for each issue were calculated for the entire group and among patients in subgroups according to age and IBD type. RESULTS: Ulcerative colitis and Crohn's disease affect the lives of children and adolescents differently. Bowel symptoms are more troubling and disabling to patients with ulcerative colitis, whereas systemic symptoms and body image concerns are greater for patients with Crohn's disease. The impact of Crohn's disease on ability to function in school and leisure activities is greater. Worries about future health problems and about the effects of IBD on the family are shared. Crohn's disease and ulcerative colitis trigger emotional responses of unfairness and frustration, but anger and embarrassment are more prevalent in ulcerative colitis. Disparities between age groups are fewer and less marked than those between types of IBD. CONCLUSION: In selection of items to be retained in a pediatric IBD quality-of-life measure, the variation in concerns with disease type must be considered. A single index to assess IBD-related quality of life must include items of major importance to one subgroup of patients, even if not important to all. Alternately, a core of common concerns could be supplemented by disease-specific modules, thereby increasing the content validity of the tool for all patients.

Adolescent↗
PubMed2001

Pediatric "PSC-IBD": a descriptive report of associated inflammatory bowel disease among pediatric patients with psc.

BACKGROUND: Inflammatory bowel disease (IBD) in adults with primary sclerosing cholangitis (PSC) is characterized by pancolonic involvement, a high frequency of rectal sparing, and an increased risk of pouchitis and colorectal neoplasia. The clinical features of IBD in pediatric patients with PSC have not been well described. The aim of this study was to characterize the frequency, clinical features, and natural history of IBD in pediatric patients diagnosed with PSC. METHODS: A retrospective chart review was performed for all patients 18 years of age or younger diagnosed with PSC seen at the Mayo Clinic between 1975 and 1999. Endoscopic and histologic features and surgical and postsurgical outcomes were recorded. RESULTS: Fifty-two children with PSC were identified. Forty-three patients (84%) were also diagnosed with IBD. In 36 of 43 cases, there was a sufficient diagnostic evaluation to allow a detailed review. Thirty-two of 36 patients (89%) had ulcerative colitis and 4 of 36 patients (11%) had Crohn's disease. In 4 of 36 patients (11%), IBD was asymptomatic. Although the most frequent endoscopic presentation of IBD was universal colitis, endoscopic rectal sparing was frequently noted (27% of colonoscopic studies). Of the four patients diagnosed with Crohn disease, in none did perianal, fistulizing, or stricturing disease develop. Proctocolectomy was performed in six patients (17%); three operations were performed for dysplasia. Pouchitis complicated four of the five ileal pouch-anal anastomoses procedures. CONCLUSIONS: Among pediatric patients (1) PSC without IBD is uncommon; (2) asymptomatic IBD may be associated with PSC; (3) because the time to dysplasia may be accelerated, once the diagnosis of IBD is made in the setting of PSC, heightened endoscopic surveillance may be indicated; (4) pouchitis occurs frequently in these patients.

Adolescent↗
PubMed2001

An investigation of the association of the prothrombin G20210A gene mutation and inflammatory bowel disease: Factor II and IBD.

BACKGROUND: A thrombotic etiology for inflammatory bowel disease (IBD) has been proposed as a result of its association with thromboembolic complications, smoking, the oral contraceptive pill, and the response of ulcerative colitis (UC) patients to heparin. We have previously demonstrated an increased prevalence of the Factor V Leiden mutation in UC and wished to investigate the frequency of the recently discovered prothrombin G20210A gene mutation in IBD. The aim of the study was to investigate the hypothesis that the prothrombic state associated with the prothrombin G20210A gene mutation is involved in the etiology of IBD. PATIENTS AND METHODS: A prospective cohort study of patients attending the Bristol Royal Infirmary and Gloucestershire Royal Hospital's IBD clinics was performed. Thirty-nine patients with IBD (24 with Crohn's disease and 15 with UC) and 100 historical controls were screened for the presence of the prothrombin gene mutation using a heteroduplex-based polymerase chain reaction technique. None of the patients with IBD had a personal history of thromboembolism, while three of them had a family history. RESULTS: No IBD patients had the prothrombin gene mutation compared with four (4%) controls (allelic frequency 2%). CONCLUSION: There does not appear to be an association of the prothrombin gene mutation with IBD and therefore it is unlikely to be involved in the etiology of IBD.

Cohort Studies↗
PubMed2005

PSC-IBD: a unique form of inflammatory bowel disease associated with primary sclerosing cholangitis.

BACKGROUND: Inflammatory bowel disease associated with primary sclerosing cholangitis (PSC-IBD) may have a high prevalence of rectal sparing, backwash ileitis, and colorectal neoplasia. AIMS: To describe the clinical features and outcomes of PSC-IBD and compare these to a group of chronic ulcerative colitis (CUC) patients. METHODS: The medical records of all patients with PSC-IBD evaluated at the Mayo Clinic Rochester between 1987 and 1992 were abstracted for information on endoscopic and histological features, colorectal neoplasia, surgery, and other clinical outcomes. Patients referred for colorectal neoplasia and those who did not undergo colonoscopy with biopsies were excluded. A control group of CUC patients matched for sex, duration of IBD at first clinic visit, and calendar year of first clinic visit was identified, and similar information was abstracted. RESULTS: Seventy one PSC-IBD patients and 142 CUC patients without PSC were identified. Rectal sparing and backwash ileitis were more common in the PSC-IBD group (52% and 51%, respectively) than in controls (6% and 7%, respectively). Overall, colorectal neoplasia developed in 18 cases and 15 controls, including 11 cancers (seven cases and four controls). An increased risk of colorectal neoplasia or death was not detected in a matched analysis. Although the cumulative incidence of colorectal neoplasia was higher in cases (33%) than in controls (13%) at five years, this was of borderline statistical significance (p=0.054, unmatched log rank test). Overall survival from first clinic visit was significantly worse among cases (79% v 97%) at five years (p<0.001, unmatched log rank test). CONCLUSION: PSC-IBD is frequently characterised by rectal sparing and backwash ileitis. Colorectal neoplasia develops in a substantial fraction and overall survival is worse. PSC-IBD may represent a distinct IBD phenotype.

Adolescent↗
PubMed2005

Brain effects of chronic IBD in areas abnormal in autism and treatment by single neuropeptides secretin and oxytocin.

Recent research points to the connection between behavioral and gut disorders. Early adverse events are associated with inflammatory bowel disease (IBD). In animal models, maternal deprivation and social isolation predispose to gastric erosion and brain pathology. This study examined (1) brain effects of chronic gastrointestinal inflammation in a rat model of acquired IBD and (2) whether such changes are resolved by individual secretin (S) or oxytocin (OT) peptide treatment. Neurological manifestations of IBD were mapped by c-fos gene expression in male Sprague-Dawley rats (n = 10) with trinitrobenzene sulfonic acid (TNBS)-induced IBD vs controls (n = 11). IBD was characterized by moderate/severe infiltration of inflammatory cells 10 d after TNBS infusion. Age-matched pairs were processed for immunocytochemical detection of Fos, expressed when neurons are stimulated. S or OT (100 mg/250 mL saline) or equivolume saline was administered iv by Alzet pump for 20 d after disease onset. Degree of resolution of colitis-induced brain activation was assessed by c-fos expression, and mean numbers of Fos-immunoreactive nuclei for each group were compared using Independent Samples T-test. Chronic IBD activated periventricular gray, hypothalamic/visceral thalamic stress axes and cortical domains, and septal/preoptic/amygdala, brain areas abnormal in autism. Single peptide treatment with S or OT did not alter the effects of inflammation on the brain. Brain areas concomitantly activated by visceral inflammation are those often abnormal in autism, suggesting that IBD could be a model for testing treatments of autism. Other single and combined peptide treatments of IBD should be tested. The clinical implications for treating autism, IBD, and concomitant sickness behaviors with peptide therapy, with or without maternal nurturing as a natural equivalent, are presented.

Amygdala↗
PubMedDate not supplied

[Assessment of disease severity and outcome of dietary, antibiotic, and immunosuppressive interventions by use of the canine IBD activity index in 21 dogs with chronic inflammatory bowel disease].

Recently, the canine IBD activity index (CIBDAI) was developed for evaluation of the severity of illness, therapeutic strategies, and efficacy of therapy. The aim of the present study was to assess the severity of illness and the therapeutic strategy in dogs with IBD by the use of CIBDAI, serum albumin concentration, and histologic score (HPEG). Furthermore the use of CIBDAI and the efficacy of therapy in a prospective study during a 3 month treatment period were evaluated. Twentyone dogs with inflammatory bowel disease (lymphocytic-plasmacytic enteritis and enterocolitis) were examined in this study. In 11 dogs with IBD the severity of illness was assessed as low, according to CIBDAI and HPEG (CIBDAI score 4 or between 5 and 10 with HPEG score between 1 and 1.5). Six dogs were treated with hypoallergenic diet (Group D), five dogs were treated with hypoallergenic diet and metronidazole (15.6-22,3 mg/kg/day) (Group M). In 10 dogs with IBD the severity of illness was assessed as high (CIBDAI <10, or CIBDAI between 5 and 10 with HPEG score between 2 and 3 or hypoalbuminemia (< or = 2.5 g/dl)). This group (Group I) was treated with immunosuppressive therapy. Treatment consisted of prednisolone (n=10; 0.9-2 mg/kg/day), azathioprine (n=5; 0.9-2.3 mg/kg/day), sulfasalazine (n=4; 18.2-25 mg/kg/day) and hypoallergenic diet (n=10). Efficacy of therapy was evaluated prospectively 3 times in a 12 weeks treatment period. Remission (CIBDAI score < 4) indicated good therapeutic response, chronic or recurrent disease (CIBDAI score persistent or recurrent > or =4) indicated poor therapeutic response. Age, CIBDAI score and HPEG score were significantly different in IBD dogs with low severity of illness (age: median 60 months; CIBDAI score: median 5; HPEG score: median (1) and IBD dogs with high severity of illness (age: median 90 months; CIBDAI score: median 9.5; HPEG score: median 2.25) (p = 0.0101 and p = 0.0099, respectively). The presence of hypoalbuminemia was not significantly different between these two groups (p = 0.3108). There was no significant correlation between CIBDAI score and serum albumin concentration (r = 0.0394; p = 0.0802) or between CIBDAI score and HPEG score (r = 0.2587; p = 0.2574). In the treatment groups, HPEG score was only significantly different between D-group and group I (p < 0.01). The CIBDAI score decreased significantly in group I after 4 weeks of treatment (median 4th week: 3; p < 0.05), and in the D-group after 8 weeks of treatment (median 8" week 1; p < 0.05). No significant decrease of CIBDAI score was seen in the M-group (median 12th week: 1.75; p > 0.05). All dogs in group D, four of five dogs in group M, and six from ten dogs in group I went into remission. Poor therapeutic response (1 dog in group M and 5 dogs in group I; one dog died) was seen in 6 dogs, where as 15 dogs showed good therapeutic response. There was no significant association between efficacy of therapy and age (p = 0.8455), CIBDAI score (p = 0.3293), or serum albumin concentraton (p = 0.8455). Poor therapeutic response was weekly associated with HPEG score > or =2 (p = 0.0635). Using CIBDAI in dogs with IBD as a single parameter to assess the severity of illness and the therapeutic response, misinterpretations are possible. The assessment of the severity of illness by the combination of CIBAI, HPEG, and serum albumin concentration is leading to adaequate therapeutic results. Dogs with low grade IBD benefit from hypoallergenic diet, whereas dogs with high grade IBD benefit from immunosuppressive therapy. The effect of antibiotic treatment is questionable.

Animals↗
PubMed2003

[Inflammatory bowel diseases (IBD) -- critical discussion of etiology, pathogenesis, diagnostics, and therapy].

AIMS: Crohn's disease and ulcerative colitis are the most frequent inflammatory bowel diseases (IBD) with a prevalence of approximately one out of 500. Cytokine research opened new and potent treatment options and thus stimulated clinical and basic research.However, the IBD still remain a challenge for patients and physicians,demanding close cooperation between gastroenterologists,radiologists and surgeons. The basic understanding of IBD,which is necessary for efficient diagnostic and therapeutic concepts is reviewed. METHODS: Based upon recent publications and our clinical experience we discuss aspects of etiology,pathogenesis,diagnostics,and therapy of Crohn's disease and ulcerative colitis. RESULTS: A genetically influenced, exaggerated and sustained immune response against the own gut flora seems to be one of the most important factors in the pathogenesis of IBD. Not less important are environmental influences. For instance, cigarette smoking had been judged to have some negative influence on the natural course of Crohn's disease.Now,however, recent studies show that smoking is even a significant independent risk factor in the pathogenesis of IBD. Since IBD and especially Crohn's disease can effect the whole body, detailed analysis of inflammatory organ involvement is necessary before therapy. For instance, the MRI enteroclysis technique adds a necessary diagnostic tool for the exploration of those parts of the small bowel that cannot been reached by routine endoscopy like the upper ileum and the lower jejunum. In terms of therapy, a change of paradigms can be observed: patients will no longer be treated only when symptoms arise, but will early be integrated into a therapeutic concept, which is determined by site and extent of the disease and adapted to the abilities and needs of the patient.Furthermore,immunosuppressive agents like azathioprine and 6-mercaptopurine will establish as central concept in the medical treatment of IBD. DISCUSSION: IBD-therapy should rather be adapted to the patient's individual inflammatory pattern than be oriented to schematic treatment rules. New endoscopic and radiologic techniques provide the necessary diagnostic tools.

Adrenal Cortex Hormones↗
PubMed1999

Investigation of the expression of IL-1beta converting enzyme and apoptosis in normal and inflammatory bowel disease (IBD) mucosal macrophages.

Activated mucosal macrophages are derived from circulating monocytes and appear to play a major role in the pathogenesis of IBD. We have recently shown that IBD, but not normal, mucosal macrophages express the active form of IL-1beta converting enzyme (ICE) and are therefore capable of releasing mature IL-1beta. ICE expression by other mucosal cell types is unknown. Active ICE expression has also been implicated in apoptosis. The aim of this study was to investigate ICE expression (using an antibody that recognizes both active and precursor forms) in normal and IBD mucosa and to determine whether ICE-expressing macrophages are undergoing apoptosis. Normal and active IBD mucosal cells, in tissue sections and after isolation, were studied by immunohistochemistry and flow cytometry. In the mucosa, macrophages were the predominant ICE-expressing cell type. In contrast to normal, most IBD mucosal macrophages expressed ICE. Of IBD colonic macrophages 11.8 +/- 3.2%, and of normal colonic macrophages 6.6 +/- 0.6% expressed Apo2.7, a marker for apoptotic cells. Similar data were obtained when annexin V was used to identify cells undergoing apoptosis. DNA fluorescence flow cytometric analysis of normal and IBD lamina propria cells showed the presence of only small hypodiploid DNA peaks. We conclude that in the human intestinal mucosa, macrophages are the predominant ICE-expressing cell type. Expression of the active form of ICE and macrophage apoptosis are not interdependent. One mechanism of loss of resident macrophages from normal mucosa and of recruited macrophages from IBD mucosa is by apoptosis.

Apoptosis↗
PubMed2003

IBD and genetics: new developments.

BACKGROUND: Inflammatory bowel disease (IBD) is a complex disorder with an aetiology that is only partly understood. Apart from environmental factors, inheritance contributes to IBD. REVIEW: Family studies show an increased risk among family members of a patient with IBD, particularly among first-degree relatives. In twin studies, concordance for disease type and localization is observed. In genetically isolated groups there is a higher prevalence of IBD. For instance. Ashkenazi Jews carry the highest risk. Further evidence comes from animal species that spontaneously develop IBD. Unlike Mendelian inheritance, in complex genetic diseases like IBD, genes are expected to be low penetrant and therefore less prone to selection, which results in higher expected gene frequencies. NOD2/CARD15, the first gene associated with IBD, is a polymorphic gene involved in the innate immune system. The gene has over 60 variations. Three of these play a role in 27% of patients with CD, with a predilection for patients with ileal disease. CONCLUSION: Genetics plays an important role in unravelling the pathogenesis of IBD leading to possible new therapeutic approaches.

Carrier Proteins↗
PubMed2002

Generational differences in the age at diagnosis with Ibd: genetic anticipation, bias, or temporal effects.

OBJECTIVE: Previous cross-sectional research has demonstrated generational differences in age at diagnosis (AAD) in inflammatory bowel disease (IBD). This observation has at times been ascribed to genetic anticipation, but could also be due to biases related to case ascertainment or follow-up or to temporal changes in IBD epidemiology. We aimed to explore this issue using a population-based database. METHODS: In 1995 we used the comprehensive administrative databases in the province of Manitoba, Canada to establish a population-based IBD Research Registry that includes clinical and demographic information for persons. We contacted those subjects within our Research Registry who reported having any family members with IBD and their family members for verification of diagnosis and AAD. Differences in AAD between familial pairs were calculated. In addition, to assess whether duration of follow-up accounted for generational differences in AAD, we computed the mean AAD for subjects with and without family histories of IBD based on age at the time of interview (i.e., < 45 and > or = 45 yr of age). RESULTS: Of the 2445 persons with IBD in the Research Registry, 548 reported positive family histories, and 315 of these (58%) were reached by telephone. There were 169 Crohn's disease and 146 ulcerative colitis subjects with positive family histories. The mean AADs for the parents, aunts/uncles, and grandparents were significantly greater than the mean AADs for the children, nieces/nephews, and grandchildren, respectively. There was a doubling of the mean AAD when comparing the grandparent/grandchild cases with the parent/child or aunt/uncle-niece/nephew cases. No statistically significant difference in anticipation was observed, whether or not the older generation was male or female or had Crohn's disease or ulcerative colitis. The AAD was substantially greater for those interviewed at > or = 45 yr of age for subjects with and without family histories. However, there was no substantial difference in mean AAD between familial and nonfamilial subjects. CONCLUSION: The present study has demonstrated that there is a tendency for children to be younger than their parents at the time of diagnosis of familial IBD, and that this difference in mean AAD is almost doubled for grandparent/grandchild pairs. However, we conclude that these differences are most likely due to a bias based on length of follow-up or recent multigenerational temporal changes in the risk of IBD, or both.

Adult↗
PubMed2006

Apoptosis as a therapeutic tool in IBD?

Defective apoptosis of mucosal cell populations seems to be a relevant pathogenetic mechanism in inflammatory bowel disease (IBD). It has been suggested that the induction of apoptosis in various effector cells may be a relevant therapeutic mechanism in IBD. Indeed, it was shown that different drugs used for treatment of IBD have the capacity to induce apoptosis in T cells or monocytes in vitro and in vivo. However, it remains unclear whether these observations are related to clinical efficacy of these agents. TNF-alpha is one of the most relevant proinflammatory mediators in IBD and anti-TNF treatment has been shown to be of particular benefit for patients with IBD. It could subsequently be shown that various anti-TNF-alpha agents, such as infliximab and adalimumab, can induce apoptosis in activated monocytes and lymphocytes in vitro and in vivo. This mechanism requires reverse signaling via transmembranous TNF, thereby eliciting a signal transduction cascade that results in programmed cell death. Although other mechanisms might also contribute to the clinical effect of anti-TNF-alpha, current data suggest that apoptosis is a relevant mechanism that is associated with clinical efficacy of anti-TNF agents. Induction of apoptosis in activated monocytes or T cells may be regarded as therapeutic tool not only for anti-TNF agents, but also for other drugs used in IBD. Future strategies should focus on identification of mechanisms that prevent apoptosis in the mucosa of patients with IBD and in targeting apoptotic pathways as a therapeutic strategy in IBD.

Apoptosis↗
PubMed2003

Chemokine expression in IBD. Mucosal chemokine expression is unselectively increased in both ulcerative colitis and Crohn's disease.

Mucosal changes in inflammatory bowel disease (IBD) are characterized by ulcerative lesions accompanied by prominent cellular infiltrates in the bowel wall. Chemokines are chemotactic cytokines that are able to promote leukocyte migration to areas of inflammation and are also able to initiate cell activation events. They have recently been implicated in the pathophysiology of many disease states. The aim of this study was to detail the degree and distribution of specific chemokines, interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, -2, and -3, and macrophage inflammatory protein (MIP)-1alpha and -1beta, in IBD mucosa. Thirty-nine patients were included, ten controls, 20 ulcerative colitis (UC), and nine Crohn's disease (CD), with a range of disease activity. Colonic mucosal biopsies were collected from UC, CD, and control patients and embedded in glycol methacrylate. Two-micrometre-thick sections were cut and stained using immunohistochemistry for chemokine protein expression. Sections were analysed using a light microscope. Expression of all types of chemokine protein was detected in colonic mucosa from both control and IBD patients. Patterns of staining between IBD patients and controls differed significantly, but CD and UC patients demonstrated similar patterns of staining. Individual chemokine expression was found to be significantly up-regulated in IBD when patients were compared with the non-diseased group in all areas of the mucosal sections. Up-regulated chemokine expression correlated with increasing activity of the disease. It is concluded that human colonic chemokine expression is non-selectively up-regulated in IBD. The results supported the hypothesis that the degree of local inflammation and tissue damage in UC and CD is dependent on local expression of specific chemokines within IBD tissues.

Chemokine CCL2↗
PubMed1993

Seroprevalence of infectious bursal disease (IBD) in parts of Tamil Nadu, India.

Sera samples of 400 apparently healthy broiler poultry from 23 commercial farms and 120 sera samples from commercial layer poultry [with specific lesions of infectious bursal disease (IBD) in the internal organs] were screened for the presence of IBD serotypes I, II and the variant strain by the agar gel immuno diffusion (AGID) test, employing standard antigens. Likewise the bursae, spleen and kidney specimen from 96 layer poultry with lesions suggestive of IBD were screened for the presence of IBD antigens employing standard antisera by the AGID test. The study revealed that antibodies to all three strains of IBD virus existed in 73.75% of sera from 400 broilers, while only serotype II antigen was detectable in tissues of the 96 layer birds that exhibited characteristic lesions of IBD. It was concluded that the serotype I vaccine did not protect the layer poultry against serotype II infection and the totally unvaccinated broiler poultry had suffered subclinical infection from all the three serotypes of IBD virus.

Animals↗
PubMed1998

Colonic explant production of IL-1and its receptor antagonist is imbalanced in inflammatory bowel disease (IBD).

IBD is associated with an increased activation of intestinal immune cells, which causes overproduction of proinflammatory cytokines such as IL-1beta. IL-1beta is implicated in mediating the sustained inflammatory response. IL-1 receptor antagonist (IL-1Ra), the naturally occurring inhibitor of IL-1, has been shown to have beneficial effects in experimental models of colitis. In this study we investigated the hypothesis that an imbalance between IL-1 and IL-1Ra exists in IBD by measuring their secretion by explant cultures of colonic biopsies. Freshly homogenized biopsies from involved tissue in IBD patients exhibited significantly lower IL-1Ra/IL-1beta ratios than control and uninvolved IBD mucosal tissue. Using explant cultures, in vitro production of IL-1beta and IL-1Ra increased progressively during the 4-18-h culture periods. IL-1beta secretion was higher in supernatants from involved Crohn's disease (CD) and ulcerative colitis tissue compared with control tissue, and IL-1beta levels increased with severity of inflammation. IL-1Ra secretion was not elevated in involved IBD samples, but significantly higher levels were released when moderate to severely involved tissue samples were compared with noninflammatory controls. Similar to freshly homogenized tissue, explant studies showed that the IL-1Ra/IL-1beta ratios were significantly decreased in involved IBD tissue, but not in uninvolved CD or inflammatory control specimens. These data support the hypothesis of an imbalance between IL-1beta and IL-1Ra in IBD.

Adolescent↗
PubMed2006

Elevated serum anti-I2 and anti-OmpW antibody levels in children with IBD.

BACKGROUND: Bacteria are implicated as important factors in the pathogenesis of inflammatory bowel disease (IBD). The aim of this study was to seek evidence of possible bacterial targets of the immune response related to IBD in children. METHODS: Seventy-eight children referred to the Department of Paediatrics at Tampere University Hospital on suspicion of IBD were included in the study. Upper and lower gastrointestinal endoscopies with biopsies were performed on all children. Sera from 75 children were tested for antibodies to the Pseudomonas fluorescens-associated sequence I2, a Bacteroides caccae TonB-linked outer membrane protein, OmpW, anti-Saccharomyces cerevisiae, and perinuclear anti-neutrophil cytoplasmic antibodies. RESULTS: The IBD diagnosis was confirmed in 35 children (18 with Crohn's disease [CD], 12 with ulcerative colitis [UC], and 5 with indeterminate colitis [IC]); 43 children were found to have no inflammation in the gut. Forty-three percent (15 of 35) of those with IBD evinced positive seroreactivity to I2 and 46% (16 of 35) to OmpW. In CD, seroreactivity to I2 and OmpW was 50% (9 of 18) and 61% (11 of 18), respectively. Serum anti-I2 and anti-OmpW immunoglobulin A levels were significantly elevated in children with CD in comparison with the non-IBD group (P = 0.007 and P = 0.001, respectively). A combination of OmpW, I2, and anti-S cerevisiae tests identified 94% of CD patients, and a combination of OmpW, I2, and perinuclear anti-neutrophil cytoplasmic antibodies detected 83% of UC cases. CONCLUSIONS: Among children with IBD, strong serological responses to microbial antigens can be found, suggesting that P fluorescens and B caccae antigens have a potential role in the microbiology and immunology of the disease. Furthermore, serologic reactivity to the set of antigens studied here seems to be applicable in the initial differential diagnosis of children with CD and UC.

Adolescent↗
PubMed2007

Azathioprine and mesalazine-induced effects on the mucosal flora in patients with IBD colitis.

BACKGROUND: The impact of azathioprine and 5-aminosalicylic acid (5-ASA) on the innate immunity and mucosal flora is unknown. The study investigated the influence of IBD treatment on the concentrations and spatial organization of mucosal bacteria using fluorescence in situ hybridization with 16s r-RNA targeting probes. METHODS: We prospectively investigated colonoscopic biopsies from five groups of 20 subjects each: patients with ulcerative or indeterminate colitis treated with azathioprine (group 1), azathioprine and 5-ASA (group 2), 5-ASA (group 3), untreated IBD (group 4), and healthy controls. RESULTS: The elevated numbers of leukocytes in mucus of IBD patients were reduced nearly to norm in patients treated with azathioprine alone. In contrast, 5-ASA therapy had no influence on mucus leukocyte migration and was associated with the lowest concentrations of mucosal bacteria of all IBD groups. The suppressed migration of leukocytes in azathioprine-treated patients was accompanied by a 28-fold higher concentration of mucosal bacteria when compared with the 5-ASA group or a 1000-fold increase when compared with healthy controls. The percent of the epithelial surface covered with adherent bacteria (P < 0.001) and the amenability of mucosal bacteria (P = 0.01) were also significantly increased in the azathioprine-treated group compared with all other IBD groups. The patients receiving both 5-ASA and azathioprine did not differ statistically from untreated IBD patients either in mucus leukocyte migration or in bacterial concentrations. CONCLUSIONS: Azathioprine and 5-ASA induce opposite effects on the mucus barrier. Concomitant therapy of 5-ASA and azathioprine mutually neutralizes the effects of both on the mucosal flora and the barrier function.

Adult↗
PubMed1986

Association of inflammatory bowel disease (IBD) with indolent soft-tissue sarcomas: report of two cases and review of literature.

Two patients with inflammatory bowel disease (IBD) and indolent forms of soft-tissue sarcomas (extraosseous osteogenic sarcoma and desmoid tumor) are presented. The literature is reviewed regarding these tumors, which have not previously been recognized in association with IBD. Despite the well-established relationship between IBD and neoplasms of epithelial and lymphoreticular origin, there have been limited data in this context pertaining to mesenchymal tumors. Two preceding reports have described the coexistence of IBD with another form of soft tissue sarcoma (Kaposi's sarcoma). Given that this relationship has now been observed in four cases, the possibility that soft-tissue sarcoma and IBD do not coexist fortuitously must be considered. This suggestion is raised in light of the rare incidence of these disorders, the limited understanding of factors governing their expression, and the known association of IBD with other forms of neoplasia.

Adult↗
PubMed2006

A comprehensive mouse IBD database for the efficient localization of quantitative trait loci.

Traditional fine-mapping approaches in mouse genetics that go from a linkage region to a candidate gene are very costly and time consuming. Shared ancestry regions, along with the combination of genetics and genomics approaches, provide a powerful tool to shorten the time and effort required to identify a causative gene. In this article we present a novel methodology that predicts IBD (identical by descent) regions between pairs of inbred strains using single nucleotide polymorphism (SNP) maps. We have validated this approach by comparing the IBD regions, estimated using different algorithms, to the results derived using the sequence information in the strains present in the Celera Mouse Database. We showed that based on the current publicly available SNP genotypes, large IBD regions (>1 Mb) can be identified successfully. By assembling a list of 21,514 SNPs in 61 common inbred strains, we inferred IBD regions between all pairs of strains and confirmed, for the first time, that existing quantitative trait genes (QTG) and susceptibility genes all lie outside of IBD regions. We also illustrated how knowledge of IBD structures can be applied to strain selection for future crosses. We have made our results available for data mining and download through a public website ( http://www.mouseibd.florida.scripps.edu ).

Algorithms↗