Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “INFLAMMATORY BOWEL DISEASE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources

Rofecoxib and early relapse of inflammatory bowel disease: an open-label trial.

BACKGROUND: The safety and efficacy of selective cyclo-oxygenase-2 inhibitors in inflammatory bowel disease are under investigation. AIM: To assess, in a prospective, open-label trial, the efficacy and safety of rofecoxib (12.5 mg/day) in inflammatory bowel disease patients and controls. METHODS: The inflammatory bowel disease group included 45 inactive patients (25 Crohn's disease; 20 ulcerative colitis) with associated arthralgia. The control group included 30 dyspeptic patients. The efficacy and safety of rofecoxib were assessed in inflammatory bowel disease patients and controls before and after treatment (range, 3 days to 3 months). RESULTS: In inflammatory bowel disease, nine of the 45 patients (20%) required rofecoxib withdrawal due to gastrointestinal symptoms inducing clinical relapse, which subsided on drug discontinuation. The percentage of patients requiring rofecoxib discontinuation was comparable in patients with Crohn's disease and ulcerative colitis (20% vs. 20%), but was higher in inflammatory bowel disease patients than in controls (20% vs. 3%; P < 0.001). In inflammatory bowel disease, arthralgia relief was reported by 32 patients (71%): complete relief by eight patients (18%) and partial relief by 24 (53%). Thirteen patients (29%) reported no benefit. A comparable percentage of inflammatory bowel disease patients and controls reported arthralgia relief (71% vs. 70%). CONCLUSIONS: Rofecoxib appears to control arthralgia in almost two-thirds of inflammatory bowel disease patients. Side-effects requiring drug discontinuation are observed, however, in almost one-quarter of patients.

Adult↗

Does monitoring prevent cancer in inflammatory bowel disease?

Surveillance colonoscopy for patients who have inflammatory bowel disease with colonic involvement has gained widespread acceptance. From an evidence-based perspective, however, the foundation for this practice remains weak. There are no randomized controlled trials, prospective cohort studies, or case-control studies that definitively prove a benefit for surveillance colonoscopy (i.e., reduction in colorectal cancer-related mortality). Nevertheless, circumstantial evidence indirectly suggests a benefit. This article reviews risk factors for colorectal cancer in inflammatory bowel disease and the evidence supporting the practice of colonoscopic surveillance. The benefits of frequent physician visits and compliance with medication regimens with regard to reduction in colorectal cancer risk are also reviewed.

Colonoscopy↗

Bilateral adrenal hemorrhage as a complication of intravenous ACTH infusion in two patients with inflammatory bowel disease.

We report two patients with inflammatory bowel disease in whom intravenous corticotropin therapy was complicated by bilateral adrenal hemorrhage. In one, the initial presentation was acute and unilateral, simulating colonic perforation and/or abscess. The diagnosis was made only at exploratory laparotomy. In the second patient, the presentation was subacute; multiple episodes of adrenal hemorrhage occurred subsequent to the course of corticotropin, and ultimately, hypoadrenalinism developed. Pertinent clinical and computed tomographic findings are reviewed.

Adrenal Gland Diseases↗

Management of inflammatory bowel disease: 30 years of observation.

Management of inflammatory bowel disease has become more precise and effective in the last 30 years, ensuring long, productive lives for most patients. Data such as family history, duration of disease, the onset of complications, and type of therapy are presented from 450 patients with inflammatory bowel disease treated during a 10-year period ending in 1984. The incidence of general complications over three decades is compared. Perianal disease and intestinal obstructions dominate complications of Crohn's disease. The most common nongastrointestinal complication for patients with either disease is monarticular large joint arthritis. Approximately 75% of patients with Crohn's disease will eventually undergo surgery. In the first decade of data collection, 50% of patients with ulcerative colitis had surgery; in the second decade, 26%; and in the third decade, 39%. The changing percentages correspond initially to advances in medical therapy and then to advances in surgical therapy.

Adolescent↗

Thrombosis in inflammatory bowel diseases: role of inherited thrombophilia.

BACKGROUND: Inflammatory bowel diseases (IBD) are characterized by an increased risk for venous and arterial thrombosis. Although the pathogenetic mechanisms of this predisposition are unclear, a possible role of inherited risk factors for thrombosis in determining this predisposition has been suggested. AIM: To evaluate the role of factor V Leiden (G1691A) and G20210A prothrombin gene mutations in determining the occurrence of thrombosis in IBD patients. PATIENTS AND METHODS: Forty-seven IBD patients (30 ulcerative colitis and 17 Crohn's disease) with a positive history for thrombosis (9 at arterial sites and 38 at venous sites) were enrolled in the study. For each patient, two non-IBD subjects matched for sex and age, type, and site of thrombosis were used as controls. Peripheral blood DNA specimens were amplified by PCR using appropriate primers and analyzed by restriction analysis on agarose gel electrophoresis. Statistical analysis was performed by means of Fisher's exact test. RESULTS: The total number of subjects with one or both mutations was significantly lower in IBD patients with thrombosis than in control subjects (12.8%vs 29.8%, respectively; p= 0.035, OR = 0.34, 95% CI 0.13-0.90). The total frequency of the mutated alleles was also significantly lower in IBD than in controls (7.4%vs 16.5%, respectively; p= 0.041, OR = 0.40, 95% CI 0.17-0.96). Prothrombotic mutations were particularly unfrequent in IBD patients with active disease at the time of thrombosis compared with patients with quiescent disease (8.0%vs 36.4%, respectively; p= 0.057, OR = 0.15, 95% CI 0.02-1.01). CONCLUSIONS: The major inherited risk factors for thrombosis are significantly less frequent in thrombotic IBD patients than in thrombotic non-IBD subjects, suggesting that acquired risk factors play the most relevant role in determining thromboembolic events observed in IBD patients, particularly during active phases of the disease.

Adult↗

A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes.

Cohort Studies↗

Inducible nitric oxide synthase-dependent DNA damage in mouse model of inflammatory bowel disease.

Increased cancer risk occurs in inflammatory bowel disease (IBD) undergoing long-term chronic inflammation. To evaluate whether inducible nitric oxide synthase (iNOS)-dependent DNA damage plays a role in the carcinogenic process triggered by IBD, we prepared a mouse model of IBD induced by transfer of CD45RBhighCD4+ T cells lacking regulatory T cells to female severe combined immunodeficiency (SCID) mice. CD45RBhighCD4+ T cells were isolated from mouse spleen after staining with fluorescein isothiocyanate (FITC)-conjugated anti-CD45RB monoclonal antibody, followed by anti-FITC-conjugated microbeads. This IBD mouse model showed that the bodyweight increased with aging to a lesser extent than non-treated controls, and that the intestine was shortened. Pathological findings of this mouse model, which showed severe inflammation in colon tissues, were similar to IBD patients. Double immunofluorescence technique revealed that both 8-nitroguanine and 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) were formed mainly in epithelial cells of the IBD mouse model. 8-Nitroguanine was formed in most of 8-oxodG-immunoreactive nuclei of epithelial cells. iNOS, proliferating cell nuclear antigen and p53 protein were also expressed in the colon epithelium. These results indicate that nitrative DNA damage, as well as oxidative DNA damage, is induced in colon epithelial cells of the IBD mouse model followed by proliferation of these cells, which may contribute to colon carcinogenesis.

Aging↗

Increased frequency of bronchial hyperresponsiveness in patients with inflammatory bowel disease.

Although bronchopulmonary manifestations are rare in inflammatory bowel disease (IBD), subclinical abnormalities have been described in up to 50% of cases. The pathophysiology of these abnormalities remains unknown. However, a latent inflammation of the bronchial mucosa secondary to the inflammation of the intestinal mucosa has been suggested. This subclinical inflammation may lead to increased bronchial responsiveness. We studied the bronchial responsiveness in 38 inflammatory bowel disease (IBD) patients, using the methacholine test. Bronchial hyperresponsiveness was defined by a PC20M < 16 mg/ml. Twenty-four healthy controls were also studied. There was no significant difference in baseline FEV1 between IBD patients and controls. However, there was a significantly greater fall in FEV1 in the IBD patients at the concentrations of methacholine tested. The frequency of bronchial hyperresponsiveness was significantly higher in the IBD population (45%) than in controls (17%; P < 0.03). Atopy, defined by skin test, was more common in IBD patients (42%) than in controls (21%). Even when only nonatopic subjects were considered, the frequency of bronchial hyperresponsiveness was significantly higher in IBD patients (41%) than in controls (5%; P < 0.02). Thus, subclinical bronchial hyperresponsiveness is common in IBD, and may be considered a further extraintestinal manifestation.

Adolescent↗

PDE4 inhibition: a novel approach for the treatment of inflammatory bowel disease.

Inflammation is a hallmark of inflammatory bowel disease (IBD), and elevation of cAMP levels can inhibit the pro-inflammatory and tissue-destructive properties of leukocytes. Phosphodiesterase 4 (PDE4) is the predominant enzyme that metabolizes cAMP in inflammatory cells, and the anti-inflammatory and immunomodulatory potential of PDE4 inhibitors in human leukocytes, endothelium and epithelium is well documented. Although PDE4 inhibitors have been investigated as treatments for several inflammatory diseases, this has focused mainly on asthma and chronic obstructive disease (COPD). Historically, their clinical utility has been limited by nausea and emesis. However, the PDE4 inhibitors cilomilast and roflumilast have recently shown efficacy in asthma and COPD, with a reduced propensity to cause nausea and emesis. In this review, we summarize for the first time the evidence that PDE4 inhibitors might have therapeutic benefit in IBD, and discuss mechanisms of action beyond the inhibition of inflammatory cells.

3',5'-Cyclic-AMP Phosphodiesterases↗

Immunological studies in inflammatory bowel disease.

Three aspects of immunological function were studied in patients with Crohn's disease and ulcerative colitis (inflammatory bowel disease): atopic status and serum IgE levels; serum concentration of C-reactive protein; and C3 activation. The incidence of atopy, assessed by prick testing with common allergens, did not differ in patients with inflammatory bowel disease from healthy controls. 12 of 39 patients with Crohn's disease and 5 of 20 with ulcerative colitis, among whom were some non-atopic subjects, had elevated serum levels of IgE. Serum levels of C-reactive protein in patients were significantly greater than normal, even in those in whom the disease was clinically quiescent. Symptomatic patients with Crohn's disease had significantly higher levels than similar patients with ulcerative colitis and in Crohn's disease the levels correlated well with an overall assessment of severity and disease activity. Although conversion of C3 was detected in fresh serum samples from inflammatory bowel disease patients and not controls, only minimal traces were present in just 7 of 89 samples of EDTA--plasma from 47 patients; this finding did not correlate with disease activity. However, there were low titres of immunoconglutinin in the sera of some patients, but not in controls, suggesting that complement activation may be occurring in vivo.

C-Reactive Protein↗

The interrelationship between sex, susceptibility factors, and outcome in ankylosing spondylitis and its associated disorders including inflammatory bowel disease, psoriasis, and iritis.

OBJECTIVE: To examine the evidence that families, where the mother has disease, carry more heritable factors and investigate the effect of maternal/paternal inheritance on phenotypic expression of disease in terms of (a) severity and outcome and (b) additional co-disorders. The children of women with ankylosing spondylitis (AS) develop the disease more often than the children of men. This suggests that either women with disease carry more susceptibility factors than men or that the uterine environment/breast feeding may play a role in AS. METHODS: The number of second degree relatives (i.e., grandparent, aunt/uncle) was calculated for those index patients with a mother with disease as opposed to a father. Outcome measures were compared and prevalence of secondary disorders (i.e., psoriasis, iritis, inflammatory bowel disease) was examined in patients with an AS mother as opposed to an AS father. RESULTS: The affected offspring of maternal cases had more second degree relatives with disease [20% vs 9%, respectively, p = 0.012, odds ratio (OR): 2.3, 95% confidence interval (CI): 1.2, 4.5] than did children of affected men. The affected children of a mother with AS were comparable in terms of disease activity, function, and radiology to children of a father with disease. Inflammatory bowel disease was more prevalent among children of AS mothers than AS fathers (15% vs 5%, respectively, p = 0.009, OR: 2.9, 95% CI: 1.3, 6.3). Psoriasis was less prevalent among sons of AS mothers than among sons of AS fathers (9% vs 22%, respectively, p = 0.03, OR: 0.4, 95% CI: 0.2, 0.9). CONCLUSION: The inherited susceptibility load is strongly linked to the sex of the parent with AS. Women with disease carry higher heritability (which is associated with inflammatory bowel disease) than do men. There is a male sex impact on susceptibility to psoriasis (when AS is present). However, there is no evidence that the susceptibility load has an effect on outcome or severity of disease (as measured by disease activity, function, and radiology), or that outcome is influenced by transmission of maternal as opposed to paternal factors.

Adult↗

Impact of chronic conditions on quality of life in patients with inflammatory bowel disease.

BACKGROUND: Although studies suggest that inflammatory bowel disease (IBD) has a significant impact on an individual's health-related quality of life, the added weight of other health conditions and comorbidities has not been investigated. The purpose of this study was to expand on prior research by taking into account the impact of other chronic health conditions on the health-related quality of life of individuals with IBD, and to develop a model to help clinicians understand the relative impact of various predictors of their patients' physical and mental health-related quality of life. METHODS: 615 patients from the gastroenterology outpatient practice of a large, urban university hospital received a self-administered survey including questions about their health conditions, the severity of their bowel symptoms, and their health-related quality of life (measured using the SF-36 instrument). RESULTS: 314 completed surveys were returned, resulting in a response rate of 51.1%. Two regression analyses were conducted to identify the role of patient demographic variables and other chronic conditions on the 2 primary outcomes of interest: the SF-36 Physical Component and Mental Component Summary scores. Statistically significant predictors of physical quality of life included IBD disease severity, arthritis, heart disease, age, anemia, back/shoulder pain, and hypertension; statistically significant predictors of mental health-related quality of life were IBD disease severity, depression/anxiety, age, and headaches. CONCLUSIONS: IBD disease severity is the most important predictor of both physical and mental health-related quality of life in patients with this condition despite the presence of other chronic conditions.

Adult↗

Prevention and treatment of osteoporosis in patients with inflammatory bowel disease.

Osteopenia or osteoporosis is common in patients with inflammatory bowel disease. The use of corticosteroids contributes to the decline in bone loss; however, osteoporosis may develop in patients with inflammatory bowel disease independent of corticosteroid use. Risk factors for the development of low bone mass in patients with inflammatory bowel disease include the general risk factors for osteoporosis as well as additional factors such as the presence of chronic inflammation, use of corticosteroids and other pharmaceuticals, and nutritional deficiencies as the result of small bowel disease or small bowel resections. Despite the high prevalence, few patients are entered into prophylactic regimens to prevent corticosteroid-induced bone loss. The American College of Rheumatology has recently published recommendations for the prevention and treatment of corticosteroid-induced osteoporosis. In this article, we highlight the special risks for osteoporosis in patients with IBD and adapt the recommendations for prevention and treatment of osteoporosis to this clinical setting.

Anti-Inflammatory Agents↗

Growth of prepubertal children with inflammatory bowel disease.

BACKGROUND: Growth retardation has been reported in children with chronic inflammatory bowel disease, especially in those with Crohn's disease. Most of these studies concern adolescent patients. METHODS: The growth of 47 prepubertal children (20 boys and 27 girls, mean age at diagnosis 7 years) with inflammatory bowel disease was studied at Tampere University Hospital, Department of Paediatrics. The mean height and height velocity standard deviation scores were calculated at diagnosis and, after that, yearly. The cumulative doses of oral and rectal prednisone per year were calculated. The severity of the disease was scored. The statistical analysis was carried out using the analysis of variance for repeated measurements. RESULTS: During the year preceding the diagnosis, children with inflammatory bowel disease had grown more slowly than their healthy peers. At diagnosis, they were slightly shorter as a group than are healthy children. During treatment and follow-up the mean height velocity of children with inflammatory bowel disease increased (change in the mean height velocity standard deviation scores from -0.84 to +1.08), normalizing the mean heights of these children compared with those of their healthy peers (change in the mean height standard deviation scores from -0.32 to +0.05). In the analysis of covariance, the poorest growth was seen in children with Crohn's disease, scored as severe, and the best growth in children with mild ulcerative colitis. No difference was seen in groups with or without prednisone treatment. CONCLUSIONS: Growth retardation is an important sign of chronic inflammatory bowel disease in prepubertal as well as adolescent children. During treatment, increasing growth velocity brings these children as a group to normal heights for age and sex.

Child↗

Pathological mimics of chronic inflammatory bowel disease.

When all of the macroscopic and microscopic features of Crohn's disease and ulcerative colitis are present, the correct diagnosis is usually made without difficulty. When some of the changes are absent, the accuracy of diagnosis is reduced. This review has outlined those diseases which feature some of these pathological changes and may masquerade as idiopathic chronic inflammatory bowel disease. Some of the pathological mimics are iatrogenic while other common diseases, such as bacterial infection, ischaemia, and diverticulosis may produce confusing histological appearances. The picture is complicated by the fact that many of these pathological imitators may themselves cause or predispose to chronic inflammatory bowel disease, or may complicate chronic inflammatory bowel disease. For example, drugs and infectious agents are recognisable causes of relapse in ulcerative colitis; Crohn's disease may cause diverticulitis in patients with diverticulosis; and lymphoma may complicate ulcerative colitis. It behooves all practising histopathologists to recognise these mimics of ulcerative colitis and Crohn's disease to ensure appropriate management for patients with inflammatory pathology of the intestines.

Anti-Inflammatory Agents, Non-Steroidal↗

Disability and need for rehabilitation among patients with inflammatory bowel disease.

Physicians who manage patients with inflammatory bowel disease (IBD) as well as the patients themselves need to know about the prospects of disability and the demand for rehabilitation associated with this chronic disease. The present study uses German social security statistics to characterize IBD patients undergoing a rehabilitation or having a disability and their employment status before and after rehabilitation. Each year, about 9 and 3% of all German employees with IBD underwent a rehabilitation or were granted a disability pension, respectively. In comparison with other diseases, IBD patients tended to be young, female and employed in white-collar occupations. Although they had significantly longer sick leaves, 87% were still employed before entering rehabilitation. The majority, i.e. 72%, improved under rehabilitation. Compared with other diseases, however, rehabilitation of patients with IBD was less successful, i.e. less patients improved, and more patients remained unchanged or even worsened during rehabilitation. After rehabilitation, continuation of the last employment was recommended in 82% of the cases, in 94% after additional medical or vocational measures. Overall, failed rehabilitation led to a similar rate of disability in IBD as in other diseases. Within the IBD population, however, female sex and white-collar occupations were associated with an increased risk, while male sex and blue-collar occupations were associated with a reduced risk for disability. These data reflect the underlying epidemiology of IBD as well as its natural history. Despite its severity and chronicity, the overwhelming majority of patients with IBD manage to stay in the work force and succeed in overcoming the obstacles posed by their disease.

Age Factors↗

Role of eicosanoids as mediators of inflammation in inflammatory bowel disease.

An unknown initiating event in inflammatory bowel disease (IBD) activates the immune system, which is followed by infiltration of the intestinal mucosa with inflammatory cells and the production of soluble mediators of inflammation. These mediators of inflammation include the metabolites of arachidonic acid. The results of research on arachidonic acid metabolites are reviewed, and it is concluded that the major arachidonic metabolites in human IBD mucosa are the lipoxygenase products leukotriene B4 (LTB4) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid. These metabolites are found in much higher concentrations in mucosa from patients with IBD than from healthy controls. Significantly more chemotactic activity is found in IBD mucosa than in healthy mucosa, and most of this activity is attributable to LTB4. Enhanced synthesis of LTB4 could account for much of the inflammatory response in IBD. Inhibition of the lipoxygenase pathway could be the mechanism that accounts for the therapeutic efficacy of mesalazine.

Arachidonic Acids↗

Bile composition in inflammatory bowel disease: ileal disease and colectomy, but not colitis, induce lithogenic bile.

BACKGROUND: Inflammatory bowel disease is a risk factor for gall-bladder stones, but there is controversy about the composition of these stones and whether such patients develop lithogenic bile. METHODS: In 54 gallstone-free inflammatory bowel disease patients and 13 non-inflammatory bowel disease patients with cholesterol-rich gallstones, we measured the biliary cholesterol saturation indices, nucleation times and bilirubin concentrations, and determined the bile acid composition and molecular species of phosphatidylcholine, in gall-bladder bile. RESULTS: Patients with Crohn's colitis or ulcerative colitis had less saturated bile (mean cholesterol saturation index, 0.9) and longer nucleation times (median, 21 days) than those with ileal Crohn's disease (1.5; 14 days) or those who had undergone colectomy (1.6; 5 days). In patients with ileal Crohn's disease, the mean biliary bilirubin concentration was two- to three-fold higher than that in the other groups, and was associated with a decrease in the percentage of biliary deoxycholate and an increase in the percentage of ursodeoxycholate, compared with disease controls, but phosphatidylcholine species were similar. CONCLUSIONS: Patients with small bowel Crohn's disease, or who have undergone colonic resection, have supersaturated bile and an increased risk of cholesterol gallstone formation. In patients with ileal disease, the presence of high biliary bilirubin concentrations and low percentage of deoxycholic acid may also favour the formation of mixed, pigment-rich, gallstones.

Adult↗