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Enterovesical fistula caused by inflammatory bowel diseases.

Enterovesical fistula caused by inflammatory bowel diseases is a rare disorder. Two male patients with recurrent cystitis had sigmoid colon diverticulitis causing enterovesical fistula. One female patient with Crohn's disease developed enterovesical fistula with abdominal and urinary symptoms. In each patient, a barium enema revealed causative bowel diseases. The precise diagnosis of enterovesical fistula was made either by cystography or cystoscopy. One-stage resection of the inflamed bowel with fistula and affected the bladder wall was proved to be an effective treatment for these three patients, while a long term follow up is specifically necessary in the patient with Crohn's disease.

Adult↗

Study of family history among patients with inflammatory bowel disease.

Of 838 patients with inflammatory bowel disease (IBD) treated at The Cleveland Clinic between 1955 and 1974, 37% had family histories positive for IBD. This high familial prevalence may reflect that the study was deliberately undertaken once the disease was established in the proband.

Adolescent↗

Potential of measurements of unsaturated vitamin B12-binding capacity in serial colonoscopic biopsy specimens for global and regional assessments of disease severity in inflammatory bowel disease.

We investigated whether measurements of unsaturated vitamin B12-binding capacity (UBBC), in homogenates of serial colonoscopic biopsy specimens, could be used as objective measures of disease severity in ulcerative colitis (UC) and Crohn's disease (CD). On a regional basis UBBC activity correlated with and showed good agreement with endoscopic and histologic activity scores (r = 0.8 and 0.6, respectively, for UC, and r = 0.7 and 0.7, respectively, for CD). For global assessment aggregate UBBC, endoscopic and histologic scores were compared with standard clinical activity scores. In UC, correlations with the van Hees index were r = 0.7, 0.8, and 0.7, respectively, and UBBC assays accurately reflected both regional and global disease activity. In CD, correlations with the CDAI were -0.1, 0.7, and 0.6, respectively. Thus, aggregate UBBC scores failed to reflect disease activity in CD, in which focal deep ulcers may produce high symptom scores but in which adjacent specimens may show no acute inflammation.

Biomarkers↗

[Role of lower digestive tract endoscopy and biopsy in inflammatory bowel diseases in adults].

The term inflammatory bowel diseases applies to two intestinal diseases (ulcerative colitis and Crohn's disease) localized to the colon. Clinical, morphological and histological data often point to one or the other of these diseases, but they are not always distinguishable, and intermediate forms classified under one name or the other are numerous. Lower digestive tract endoscopy and biopsies are determinant (1) for the diagnosis, as they provide a precise description of the lesions for each segment and evaluate their severity; (2) to monitor the course of the disease under treatment and detect precancerous lesions.

Biopsy↗

[Etiology of chronic inflammatory bowel diseases].

Furthermore the aetiopathogenesis of inflammatory bowel disease (IBD) is unknown. The familial accumulation makes a genetic disposition probable. Presumably, the development of Crohn's disease and ulcerative colitis is contingent upon several factors, including perhaps environmental factors in the broadest sense. A large number of microorganisms have been implicated, but there is still no convincing proof that any of them have an important role in the aetiopathogenesis of IBD. The observed immunological phenomena are as yet difficult to interpret.

Bacterial Infections↗

Chronic inflammatory bowel disease in Asian immigrants.

Chronic inflammatory bowel disease occurs sporadically among the immigrant Asian population in Britain, but information about the incidence and clinical features is lacking. We therefore report our experience of 13 patients seen in a gastrointestinal unit in Birmingham over the past 12 years.

Adolescent↗

Psychological distress and levels of disease activity in inflammatory bowel disease.

The aim of this study was to evaluate the association between anxiety and depression, and levels of disease activity (LDA) in IBD patients. One hundred and fifty IBD patients (91 males and 59 females) were assessed by means of the Hospital Anxiety and Depression scale, and divided into three LDA groups according to standard clinical criteria: LDA1 = absence, LDA2 = mild, LDA3 = moderate and severe. Using the analysis of variance and the Scheffé test, a significant difference was found in the anxiety score, but not in the depression score, between LDA1 and LDA3 (p < 0.005). The risk of developing anxiety and depression in relation to LDA was estimated by multiple logistic regression. A significant linear trend (p < 0.01) to develop anxiety was found in the highest LDA. Our study showed that anxiety was significantly associated with a higher disease activity and suggested that anxiety should be appropriately evaluated and treated with the exacerbated symptoms in IBD patients.

Adult↗

[New therapeutic possibilities in chronic inflammatory bowel diseases].

New therapeutic measures in inflammatory bowel diseases (IBD) are either based on actual data on disease pathogenesis or on new pharmaceutic preparations of known drugs. An overshooting immune response with T cell activation in the local gut associated immune system seems to be central in the etiopathogenesis of IBD. Modulation of the antigenic load in the gut lumen by parenteral or enteral nutrition or antibiotic treatment can alter disease activity. Immunosuppressive drugs are able to decrease the overshooting immune response. Azathioprin has its clear value in chronic active steroid dependent disease courses of Crohn's disease. According to recent studies, Methotrexate seems to be active as well, however, more studies are necessary. Several studies were not able to prove that Cyclosporine is of value in the treatment of Crohn's disease. Newer preparations of aminosalicylates have shown effectiveness in both active disease and prolongation of remission in Crohn's disease in high doses. Local release formulations of steroids with high first-pass-effect as Budesonide will have their indication in subgroups of IBD patients. However, systemic steroid application is still the gold standard in active disease.

Aminosalicylic Acids↗

The serum concentrations of zinc, copper and selenium in children with inflammatory bowel disease.

OBJECTIVE: To estimate the levels of trace elements in children with inflammatory bowel disease (IBD). DESIGN: Prospective cross sectional study. SETTING: Gastroentrology Unit, Great Ormond Street Children's Hospital, London, UK. SUBJECTS: Seventy four children with inflammatory bowel disease confirmed endoscopically and histologically (38 ulcerative colitis and 36 Crohn's disease) and 40 age matched controls had their serum zinc, copper and selenium assayed at presentation. MAIN OUTCOME MEASURE: Serum levels of zinc, copper and selenium in children with inflammatory bowel disease and age matched controls. RESULTS: Seventy four children with inflammatory bowel disease confirmed endoscopically and histologically (38 ulcerative colitis and 36 Crohn's disease) and 40 age matched controls had their serum zinc, copper and selenium assayed at presentation. The serum levels of selenium were significantly lower in cases of ulcerative colitis 0.63 +/- 0.25 mmol/L and Crohn's disease 0.69 +/- 0.25 mmol/L than in the controls 0.84 +/- 0.13 mmol/L (p < 0.01). The serum copper concentration was significantly higher in those with Crohn's disease 22.7 +/- 5.49 mmol/L than in those with ulcerative colitis 17.6 +/- 5.15 mmol/L and the controls 20.76 +/- 4.06 mmol/L (p < 0.01). Children with Crohn's disease had a lower serum zinc level 11.01 +/- 2.49 mmol/L compared to the control level of 13.6 +/- 1.63 mmol/L (p < 0.05), but the levels were not significantly different in the controls and ulcerative colitis (p > 0.10). Children with inflammatory bowel disease have abnormal levels of the trace elements which is more marked in those with Crohn's disease. CONCLUSION: Children with IBD in this study show abnormalities of the trace elements which is probably a result of inadequate intake, reduced absorption, increased intestinal loss due to impairment of the absorption as a result of the inflammatory process. The reduced free radical scavenging action of zinc and selenium as a result of their deficiency may contribute to the continued inflammatory process of IBD. The recommendation of the supplementation of these trace elements in IBD is further supported by the findings of this study in children.

Child↗

Comparison of inflammatory bowel disease at younger and older age.

OBJECTIVE: In a substantial number of patients inflammatory bowel disease develops past the age of 40 years. However, data about the clinical presentation and disease behaviour in this age group are scarce. METHODS: The following parameters were evaluated retrospectively in 191 consecutive patients with inflammatory bowel disease: Gender, age at diagnosis, leading symptoms, disease localization and behaviour (e. g. fistulizing, fibrostenotic or inflammatory), extraintestinal manifestations, medication, smoking habits, dysplasia, cancer and mortality. RESULTS: In 16 % of patients inflammatory bowel disease had been diagnosed past the age of 40 years. In elderly patients with ulcerative colitis male gender was predominant. Diarrhea, abdominal pain and anaemia were observed more frequently in younger patients, whereas the remainder of parameters showed an equal distribution in both age groups. CONCLUSIONS: Younger patients are frequently afflicted by symptoms which potentially impair the quality of life. However, in this retrospective single center evaluation the disease localization and behaviour of inflammatory bowel disease in elderly patients was comparable to young adults. Due to a potential referral bias, these data await confirmation in larger prospective multicenter trials.

Adult↗

Prevalence and mechanism of nonsteroidal anti-inflammatory drug-induced clinical relapse in patients with inflammatory bowel disease.

BACKGROUND & AIMS: It has been variably suggested that nonselective NSAIDs and cyclooxygenase (COX)-2 selective inhibitors aggravate or ameliorate clinical disease activity in patients with inflammatory bowel disease. We assessed the effect of these drugs in patients with inflammatory bowel disease (n = 209) and the possible mechanisms. METHODS: First, patients with quiescent Crohn's disease and ulcerative colitis received the non-NSAID analgesic acetaminophen (n = 26) and the conventional NSAIDs naproxen (n = 32), diclofenac (n = 29), and indomethacin (n = 22) for 4 weeks. The Harvey-Bradshaw index was used to define relapse. Second, to assess the mechanism of relapse, intestinal inflammation was quantitated (fecal calprotectin) before and during treatment (20 patients/group) with acetaminophen, naproxen (topical effect, COX-1 and -2 inhibitor), nabumetone (COX-1 and -2 inhibitor), nimesulide (selective COX-2 inhibitor), and low-dose aspirin (selective COX-1 inhibition). RESULTS: Nonselective NSAIDs were associated with a 17%-28% relapse rate within 9 days of ingestion. No patient had an early relapse on acetaminophen, nimesulide, or aspirin, whereas those on naproxen and nabumetone (20%) experienced relapse. These clinical relapses were associated with escalating intestinal inflammatory activity. CONCLUSIONS: NSAID ingestion is associated with frequent and early clinical relapse of quiescent inflammatory bowel disease, and the mechanism appears to be due to dual inhibition of the COX enzymes. Selective COX-2 inhibition with nimesulide and COX-1 inhibition with low-dose aspirin appear to be well-tolerated in the short-term.

Acetaminophen↗

Inflammatory bowel disease in children and adolescents: mental health and family functioning.

BACKGROUND: Inflammatory bowel disease in children and adolescents often leads to an extremely complex somatic and psychiatric situation. The psychological effect of inflammatory bowel disease warrants further investigation, especially concerning salutogenetic factors that may lead to good mental health despite bad somatic conditions. METHODS: These studies used a multimethod design comprising both semiquantitative measures, such as rating scales and questionnaires, and qualitative in-depth interviews with both the child and his or her parents. Clinical comparison groups of matched children with diabetes and chronic tension headaches and matched children without chronic physical disease were examined. RESULTS: Inflammatory bowel disease often leads to psychiatric sequelae. Emotional disorders, especially depression and anxiety symptoms, were found to be common. Self-esteem was lowered. A subgroup of children with good mental health despite bad somatic conditions was found. They exhibited certain characteristics, including good knowledge of the disease, an internal locus of control, a good family climate, and an open social network. CONCLUSIONS: This study shows that the well-being of a chronically ill child depends not only on the course of the physical disease but also on the psychological and social complications that often seem to accompany a disease of this kind. The importance of taking good care of the psychosocial aspects of inflammatory bowel disease within the comprehensive treatment program is discussed.

Adolescent↗

The effect of inflammation severity and of treatment on the production and release of TNFalpha by colonic explants in inflammatory bowel disease.

BACKGROUND: Despite its pivotal role in mucosal inflammation, data on TNFalpha levels in inflammatory bowel diseases have been contradictory. AIM: To examine TNFalpha production in relation to the type and severity of inflammation and therapy, using colonic explant cultures. MATERIALS AND METHODS: Rectal mucosal biopsies from 271 paediatric patients (178 inflammatory bowel disease, 27 inflammatory controls, 66 normal) were cultured for 4 or 18 h. Basal TNFalpha tissue content and release into the medium were measured by ELISA and compared to histological severity and clinical parameters. RESULTS: TNFalpha release as well as tissue-associated TNFalpha levels were significantly increased in rectal biopsies from involved inflammatory bowel disease tissue. The amount of TNFalpha correlated with inflammation severity scores. TNFalpha levels were higher at 18 compared to 4 h in all groups, whether inflamed or not. TNFalpha released from rectal biopsies was lower among treated patients at 18 h. The presence of proximal colonic involvement was associated with higher TNFalpha release by uninvolved Crohn's disease rectal biopsies compared to patients with ileitis alone. CONCLUSIONS: TNFalpha production and release is increased in involved rectal explants from inflammatory bowel disease. Anti-inflammatory treatment diminishes this response.

Adolescent↗

Factor V Leiden and prothrombin gene mutation in inflammatory bowel disease in a Mediterranean area.

BACKGROUND: Thromboembolism has been reported to be associated with inflammatory bowel disease. AIM: To evaluate the association of factor V Leiden and prothrombin gene mutation with inflammatory bowel disease in a population of patients with thromboembolic events and inflammatory bowel disease and in a control population of patients with inflammatory bowel disease without thromboembolic events. PATIENTS AND METHODS: A series of 18 patients with inflammatory bowel disease and a history of arterial or venous thrombosis and 45 patients with inflammatory bowel disease without thromboembolic events were evaluated for the presence of factor V Leiden and prothrombin gene mutation. Frequency of gene mutation was compared with its occurrence in 100 healthy controls. RESULTS: One patient with inflammatory bowel disease without thromboembolic events was heterozygous for factor V Leiden mutation. whereas no patient with a thromboembolic event had factor V Leiden mutation. No patients (either cases or controls) had prothrombin gene mutation. In the healthy population the frequency of factor V Leiden and prothrombin mutation was 5% and 2%, respectively. CONCLUSIONS: Data emerging from the present study do not support any role of factor V Leiden and prothrombin gene mutation as the cause of thromboembolism in inflammatory bowel disease.

Colitis, Ulcerative↗

Microflora in inflammatory bowel diseases: a pediatric perspective.

Several lines of evidence link inflammatory bowel diseases to modifications of intestinal microflora. Epidemiologic and clinical data suggest a triggering role for select agents in ulcerative colitis and in Crohn disease. Experimental evidence indicates that intestinal microorganisms are needed for developing intestinal inflammation in IL-10 knockout mice, and this is associated with an increased number of adherent clostridia and a decrease of lactobacilli and bifidobacteria. It may be hypothesized that a host-agent-specific relationship leads to an abnormal immune response, which may be genetically driven in select inflammatory bowel diseases. However, different from adults, the pattern of intestinal microflora undergoes profound changes during the early stage of life, contributing to the development of the immune system. A close relationship exists between microbiologic and immunologic imprinting. The microbiologic imprinting in neonates may be modified using bacterial probiotics that colonize the intestine, modify the immune response, and decrease the risk for atopy. Probiotics may decrease the recurrences of inflammatory bowel diseases. Preliminary evidence of intestinal antiinflammatory effects has been detected in children with cystic fibrosis. Overall these data provide the rationale to investigate the interaction between intestinal microflora and the local and general immune response in children with, or at risk for, inflammatory bowel diseases. This approach may be a key for understanding the pathophysiology of intestinal inflammation and may disclose novel strategies to educate better the immune system, particularly during its developmental stage.

Animals↗

Inflammatory bowel disease--environmental modification and genetic determinants.

Inflammatory bowel disease (IBD) is a complex disease, controlled by multiple risk factors that evolve and interact together. In a genetically susceptible host, there are multiple processing steps controlled by the host and the environment, from environmental exposure to the clinical and biological expression of IBD-related phenotypes. This article discusses the recent genetic discoveries, along with the proposed environmental risk factors that have been implicated in IBD. Technical advances of the HapMap project and the promise of whole genome association scans have given hopes for clarifying gene-environmental interactions in IBD that ultimately lead to a clearer understanding of the pathogenesis.

Child↗