Laparoscopic surgery for inflammatory bowel disease.
Laparoscopic surgery for inflammatory bowel disease is an expanding field, which has physical benefits to the patient and economic benefits to the trust and community.
Colectomy↗
SEARCH · PubMed Health
Results for “INFLAMMATORY BOWEL DISEASE”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Projective personality tests of children with inflammatory bowel disease.
15 children with inflammatory bowel disease were given projective tests after initial diagnosis. Analysis of responses suggested affective constriction, abandonment anxiety, and depression. The children were of good intelligence with good object relationships and psychosexual differentiation for their ages. Severe psychopathology and bizarre slippage were absent.
Adolescent↗
Genetics of inflammatory bowel disease.
The etiology of inflammatory bowel diseases, Crohn's disease and ulcerative colitis, is uncertain. Studies of specific environmental factors and immune dysfunction have provided limited insight into disease pathogenesis. There is ample evidence that these diseases are in part the result of genetic predisposition. The early search for candidate genes focused on genes involved in the regulation of immune function. Recent genome-wide searches reported several susceptibility loci for Crohn's disease and ulcerative colitis. The recent identification of the IBD1 gene (NOD2) with mutations that are associated with susceptibility to Crohn's disease will have a major impact on the understanding of the genetics of this disease.
Australia↗
[The malignant side of chronic inflammatory bowel disease].
Patients with chronic inflammatory bowel disease (IBD) have a higher risk of colorectal carcinoma, and present with this malignancy at a younger age than non-IBD individuals. In three patients, two men aged 20 and 36 years and one woman aged 34 years, colorectal cancer developed at a young age, following a long history of ulcerative colitis. Surveillance for colorectal cancer in IBD patients needs to be performed by regular colonoscopy with extensive biopsy sampling for the detection of dysplasia, regarded by many as predictive for colon carcinoma. Whenever a dysplasia-associated lesion or mass or a highgrade dysplasia is identified, there is a strong indication for colectomy. When low-grade dysplasia is found, the findings should be discussed with the patient and it should be decided whether the patient should resume surveillance or opt for colectomy.
Adenocarcinoma↗
[Epstein-Barr virus-related lymphomas in patients with inflammatory bowel disease].
During treatment for inflammatory bowel disease (IBD) 2 men with ulcerative colitis, aged 52 and 38 years, and a 37-year-old man with Crohn's disease developed Epstein-Barr virus (EBV)-related non-Hodgkin's B-cell lymphoma. The first 2 patients underwent proctocolectomy and the use of immunosuppressive agents was discontinued, after which the lymphoma disappeared. The third patient had icterus, hepatosplenomegaly and pancytopenia; he died from multiple organ failure. Azathioprine and 6-mercaptopurine are first choice therapy in the treatment of steroid-refractory IBD. These immunomodulating agents are associated with the development of EBV-positive lymphomas in the setting of solid organ transplantation. This type of lymphoma is a rare complication in IBD, although the incidence in referral centres appears to be increasing. Since azathioprine is an important drug in IBD, there is a need for identification of IBD patients at risk of developing a lymphoma. EBV-DNA in plasma or in faeces may be a candidate tumour marker.
Adult↗
Inflammatory bowel disease in exclusively breast-fed infants.
Inflammatory bowel disease is uncommon in infants. We present the clinical, endoscopic and pathologic findings for two exclusively breast-fed infants with a diagnosis of inflammatory bowel disease. We emphasize that although inflammatory bowel disease is rare in infants, chronic bloody diarrhea must be a sufficiently alarming symptom to consider a differential diagnosis of inflammatory bowel disease in young infants is considered, even when they are exclusively breast-fed.
Anti-Inflammatory Agents, Non-Steroidal↗
Idiopathic pancreatitis associated with inflammatory bowel disease.
The list of extraintestinal manifestations of inflammatory bowel diseases does not classically include pancreatitis and pancreatic insufficiency. We report here six cases of unexplained pancreatitis associated with inflammatory bowel disease (five patients with Crohn's disease, one with indeterminate colitis). None of the classical etiologies for pancreatitis was found in our patients; moreover none of them had duodenal localization of Crohn's disease or sclerosing cholangitis, two conditions in which pancreatitis associated with inflammatory bowel disease has been previously described. Pancreatitis was painless (or was associated with moderate and atypical abdominal pain) in four of our six cases; no pancreatic calcification was found in any case; in three patients a total or subtotal exocrine pancreatic insufficiency was evidenced. Endoscopic retrograde pancreatography performed in four subjects showed normal or minimally altered pancreatic ducts even in those with severe pancreatic insufficiency. These cases emphasize the existence of a probably nonfortuitous association of inflammatory bowel disease with pancreatitis. Its recognition could make a significant contribution in the management of inflammatory bowel disease.
Adolescent↗
Exploring the relationships between inflammatory response and coagulation cascade in inflammatory bowel disease.
BACKGROUND: The inflammatory network and the coagulation cascade are strictly correlated biological systems. Inflammatory Bowel Diseases (IBD) are characterised by a prothrombotic state, a hypercoagulability state and an increased prevalence of thromboembolic events. METHODS: We reviewed the IBD literature in which the relationships between inflammation and coagulation were evaluated. RESULTS: Several risk factors and mechanisms have been suggested to be implicated in determining the increased risk for thrombosis of IBD. Even if IBD may be per se a prothrombotic condition, systemic inflammation and vitamin deficiencies appear to play a relevant role in determining such a risk. CONCLUSIONS: A good and continuous control of the intestinal disease and vitamin supplementation are strongly recommended in order to correct some of the risk factors for thrombosis in IBD patients.
Blood Coagulation↗
Levels of purine, kynurenine and lipid peroxidation products in patients with inflammatory bowel disease.
The factors affecting gut activity in inflammatory bowel disease are unclear, but purines and kynurenines may be involved in the regulation of neuronal activity and therefore gut motility and secretion. We have measured the serum levels of these compounds in patients and in sex- and age-matched controls. Purines and kynurenines were analysed using HPLC. The levels of tryptophan and its metabolites 3-hydroxykynurenine, 3-hydroxyanthranilic acid and xanthurenic acid were unchanged in all patients. However, the levels of kynurenine and kynurenic acid were significantly elevated in patients with inflammatory bowel disease when compared to control subjects. There were no significant differences between patients and controls for any of the purines analysed or for neopterin. In the inflammatory bowel disease patients serum lipid peroxidation products were significantly elevated when compared to control subjects, suggesting the presence of increased oxidative stress consistent with inflammatory activity. The elevated level of kynurenic acid may represent either a compensatory response to elevated activation of enteric neurones, or a primary abnormality, which induces a compensatory increase in gut activity, but may indicate a role for kynurenine modulation of glutamate receptors in the symptoms of inflammatory bowel disease.
Adenosine↗
Cross-cultural variation in disease-related concerns among patients with inflammatory bowel disease.
OBJECTIVE: The aim of this work was to study cross-cultural variations in the impact of inflammatory bowel disease (IBD) on health-related quality of life by an international comparison of disease-related concerns. METHODS: Item and factor scores on the Rating Form of Inflammatory Bowel Disease Patient Concerns and overall mean concern levels were compared by analysis of variance among 2002 IBD patients in eight countries. RESULTS: The overall level of concern varied from 51 out of 100 in Portugal to 19 in Sweden, with intermediate scores for Italy (43), Canada (40), United States (39), France (39), Austria (33), and Israel (25). Having surgery, an ostomy, the uncertain nature of the disease, and medication side effects were each rated among the first five in importance in six countries. Other items varied considerably. For example, concern regarding pain and suffering was high in Israel and low in Portugal, whereas concern over developing cancer was low in Italy. Concern over financial issues and access to high-quality health care were inversely associated with measures of national economic prosperity. CONCLUSIONS: 1) Cross-cultural comparisons of patient concerns related to IBD are feasible using translated scales. 2) Reporting tendencies vary greatly; within Europe, patients from southern countries report greater overall concern. 3) The complications and the variable evolution of disease elicit general concern, but the importance of specific issues varies among countries. 4) The reasons for national differences may have social, cultural, and/or economic determinants with relevance to the patient-physician relationship, patient education, and therapeutic decision making.
Canada↗
Update on the genetics of inflammatory bowel disease.
There is a general consensus that interplay of genetic and environmental factors leads to an overactive mucosal immune response, which mediates the tissue damage in inflammatory bowel disease. Ethnic aggregation of inflammatory bowel disease (particularly, increased incidence and prevalence in the Ashkenazim), familial aggregation of inflammatory bowel disease, and greater concordance for inflammatory bowel disease in monozygotic twins than dizygotic twins are 3 lines of evidence for a central role of genetic factors in the pathogenesis. The genetics of inflammatory bowel disease cannot be explained by simple Mendelian genetics; it is characterized by incomplete penetrance, multiple susceptibility loci and genetic heterogeneity. Unraveling the complex genetics of inflammatory bowel disease is a daunting challenge, but the perseverance of inflammatory bowel disease gene hunters has produced commendable results in recent years. Since 1996, the field of inflammatory bowel disease genetics has progressed from publication of the first systematic genome searches for inflammatory bowel disease susceptibility loci to the identification of Crohn disease-associated genetic variants in CARD15/NOD2. Strategies for finding additional inflammatory bowel disease genes include taking advantage of the greater resolution and power of linkage disequilibrium mapping, mapping by admixture disequilibrium in African-American and Hispanic-American populations, stratifying genetic analyses by genotypes at known inflammatory bowel disease loci, and refining inflammatory bowel disease phenotypes to reduce genetic heterogeneity and simplify the search for additional inflammatory bowel disease genes.
Carrier Proteins↗
Mechanisms of disease: vitamin D and inflammatory bowel disease.
Until recently, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3))-the active form of vitamin D-was thought to function primarily as a regulator of calcium and phosphate metabolism. More diverse functionality was indicated by the discovery of the vitamin D receptor in tissues that are not involved in calcium and phosphate homeostasis. Detection of the vitamin D receptor in monocytes and activated T cells has sparked interest in the immunomodulatory properties of vitamin D. Here, we review the role of vitamin D in regulation of the immune system, and evidence for its involvement in the pathogenesis of inflammatory bowel disease.
Animals↗
Novel signal transduction pathways: analysis of STAT-3 and Rac-1 signaling in inflammatory bowel disease.
Although the precise etiology of inflammatory bowel disease still remains unclear, considerable progress has been made in the identification of novel signal transduction pathways that elucidate the immunopathogenesis involved in the perpetuation of the inflammatory process. Augmented T cell resistance against apoptosis is regarded as a pivotal factor in the pathogenesis, as it impairs mucosal homeostasis and leads to unrestrained accumulation of activated T cells, which subsequently lead to the amplification of the inflammatory response. Therefore novel therapeutic strategies aim at restoring mucosal T cell susceptibility to apoptosis through targeting of signal transduction pathways that are elemental for augmented resistance of T lymphocytes against apoptosis. For example, a newly developed humanized anti-IL-6R monoclonal antibody that induces intestinal T cell apoptosis showed clinical efficacy in patients with active Crohn;s disease. Moreover, recent data that relate the immunosuppressive effects of azathioprine in inflammatory bowel disease to its apoptosis-inducing potential, have important implications for the design of a more specific therapeutic approach. The examination of these novel signal transduction pathways has elucidated the pathogenetic mechanisms involved in inflammatory bowel disease and gives hope for the development of new strategies that may result in a more effective and less toxic therapeutic procedure.
Apoptosis↗
Morphology of colorectal lymphoid aggregates in cancer, diverticular and inflammatory bowel diseases.
The present study compares the characteristics of colorectal lymphoid aggregates in patients with carcinoma, diverticular disease, Crohn's disease, or ulcerative colitis of the large bowel. A total of 77 patients (41 colorectal cancer, 27 diverticular disease, six ulcerative colitis, three Crohn's disease) undergoing colorectal resection were included. Acetic acid staining, hematoxylin and eosin staining, CD3, CD20, and MIB1 immunostaining were employed in order to assess density, diameter, subepithelial or basal location, cellular profile, and proliferation of lymphoid aggregates in normal-appearing and actively inflamed large bowel. In normal-appearing tissue, mean density of lymphoid aggregates was lower in patients with ulcerative colitis and Crohn's disease than in those with colorectal cancer or diverticular disease. A larger mean diameter of aggregates was observed in patients with Crohn's disease. In inflammatory bowel diseases, a marked increase of the mean density of lymphoid aggregates was observed in actively affected specimens. In Crohn's disease more than in ulcerative colitis, the aggregates had a predominant basal or transmural distribution. In diverticular disease, active inflammation determined a less significant increase of subepithelial aggregates harboring a lower proportion of germinal centers. No significant variations of CD3, CD20, and MIB1 were recorded among the four disease groups. The lymphoid aggregate derangements observed not only in the actively affected mucosa but also in the unaffected colorectal lining of patients with Crohn's disease and ulcerative colitis support a relevant involvement of lymphoid aggregate system in the pathogenesis of inflammatory bowel diseases.
Acetic Acid↗
Inflammatory bowel disease in the pregnant woman.
This article discusses fertility and inflammatory bowel disease, the influence of inflammatory bowel disease on pregnancy, the influence of pregnancy on inflammatory bowel disease, the safety of breast-feeding while taking medication for active disease, and abdominal pain in the pregnant woman with inflammatory bowel disease.
Abdomen↗
The current future understanding of inflammatory bowel disease.
Accumulating evidence indicates that the inflammatory bowel diseases result from an activation of immune and inflammatory responses initiated by a stimulation of the luminal flora or their products. Genetically determined variations in key mucosal functions, including cell activation by prototypic bacterial pattern molecules, lead to differential susceptibility to the development of these disorders, probably reflecting an interrelated activation of the innate and adaptive immune responses. The persistence and amplification of inflammation is likely to reflect the continuing presence of the driving stimulus and the complex, self-reinforcing activation of select T-helper subtypes and macrophages and other antigen-presenting cells, mediated by several cytokines. The latter include interleukins-2, 12, and 18 as well as interferon and macrophage migration inhibitory factors. The production of other broadly pro-inflammatory cytokines, most notably tumour necrosis factor and interleukins-1 and 6, enhances related inflammatory processes that eventually lead to many of the clinical manifestations of inflammatory bowel disease. The overall severity of the inflammatory process reflects a balance between leukocyte recruitment and downregulatory mucosal repair processes.
Cytokines↗
A long-term cohort study of nonsteroidal anti-inflammatory drug use and disease activity in outpatients with inflammatory bowel disease.
BACKGROUND AND AIMS: We examined whether use of nonsteroidal anti-inflammatory drugs (NSAIDs) in outpatients with inflammatory bowel disease was associated with increased severity of disease activity. METHODS: Outpatients with Crohn's disease (CD; n = 426) and with ulcerative colitis (UC; n = 203) were seen between November 1997 and April 2002. Patients were questioned at each visit regarding use of prescription or over-the counter NSAIDs and a clinical disease activity index (modified Harvey Bradshaw [MHB] or Lichtiger score) was obtained. RESULTS: For the Crohn's patients, for 1315 visits no NSAIDs were used, on 215 visits low-dose NSAIDs were used, and for 139 visits high-dose NSAIDs were taken. For UC patient visits, 495 used no NSAIDs, 112 low-dose NSAIDs, and 49 high-dose NSAIDs. Average MHB score was 4.07 for the no-NSAID group, 4.24 for low-dose NSAIDs (P = 0.46), and 4.78 for high-dose (P = 0.0072 versus no NSAIDs). For the ulcerative colitis patients corresponding scores were 5.64, 5.46, and 6.20, respectively (P = not significant). The probability of moderately active disease as defined by crossing a threshold MHB or Lichtiger score, however, was not significantly affected by NSAID use. Subgroup analysis indicated the increase in disease activity among CD patients taking high-dose NSAIDs was limited to patients with colonic involvement. CONCLUSIONS: Use of low-dose NSAIDs was not associated with an increase in disease activity for these outpatients with either CD or UC. Use of high-doses of NSAIDs was associated with a higher numerical disease activity index score among CD patients with colonic involvement, but this was not reflected by an increase in significant disease flares.
Anti-Inflammatory Agents, Non-Steroidal↗
Inflammatory bowel disease: a new assessment.
The etiologies of Crohn's disease and inflammatory bowel disease remain undefined. A growing body of evidence suggests that genetic factors play at least a permissive role while a variety of initiating agents, varying from bacteria to viruses, to a vast array of inert antigens have been postulated, but clear-cut cause and effect relationships have not been established. Recently, a resurgence of interest in Mycobacteria paratuberculosis has developed. Regardless of the initiating cause, growing evidence continues to suggest an immunomodulatory role for the immune system in perpetuating the chronicity of these illnesses. Treatment approaches have been directed against possible initiating agents as well as against the elements which may establish chronicity. Thus currently antibiotics and anti-mycobacterial drugs are being utilized. A variety of anti-inflammatory and/or immunosuppressive agents, including prednisolone, cyclosporine, 6-mercaptopurine, as well as many 5-aminosalicylic acid products comprise a growing armamentarium.
Humans↗