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PubMed2002

Coagulation factor XIII and markers of thrombin generation and fibrinolysis in patients with inflammatory bowel disease.

OBJECTIVE: To relate factor XIII levels and other prothrombotic markers to inflammatory bowel disease and investigate the frequency of valine34leucine and its effect on factor XIII cross-linking activity in patients with inflammatory bowel disease. DESIGN: Fifty patients with active inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), 50 patients with inactive inflammatory bowel disease but no venous thromboembolism (32 with ulcerative colitis, 18 with Crohn's disease), two age- and gender-matched healthy control groups of 100 subjects each were recruited. To further explore the relationship between valine34leucine and inflammatory bowel disease, 21 patients with the disease (13 with ulcerative colitis and eight with Crohn's disease) and venous thromoembolism (male to female ratio = 7 : 14, median age 59.5 years (range, 19-80 years)) were recruited. Two hundred and fifteen control subjects (M : F = 121 : 94, median age 62 years (28-74 years)), with venous thromboembolism (119 with deep venous thrombosis, and 96 with pulmonary embolism) were drawn from the same geographical area as the patients. METHODS: Factor XIII A, B-subunit antigen and A2B2 tetramer levels were measured using an in-house sandwich enzyme-linked immunoassay method. RESULTS: Factor XIII A2B2 tetramer and the A-subunit were significantly decreased in patients with active inflammatory bowel disease compared with controls (59% vs 95%, P < 0.0001 and 75% vs 102%, P < 0.0001, respectively), but not between the inactive inflammatory bowel disease group and controls. The D-dimer and prothrombin 1+2 fragment levels in patients with active inflammatory bowel disease were raised compared with controls (178 (152) vs 109 (84), P = 0.0007 and 82 (43) vs 55 (28), P = 0.0001, respectively). The factor XIII B-subunit and factor XIII cross-linking activity were not significantly different between patients with active or inactive inflammatory bowel disease and controls. There was no significant difference in genotype distribution in inflammatory bowel disease patients with or without venous thromboembolism and respective control subjects. Levels of tissue plasminogen activator antigen were significantly increased in patients with active inflammatory bowel disease when compared to inactive inflammatory bowel disease and controls (8.9 (3.7) vs 6.7 (3.4) vs 6.9 (3.4), P < 0.001). CONCLUSIONS: Active inflammatory bowel disease is associated with activation of coagulation. Factor XIII A and A2B2 tetramer levels were markedly decreased in active inflammatory bowel disease. Variations in the level of factor XIII in patients with inflammatory bowel disease could be multifactorial and in part may result from the increased formation of microthrombi and accelerated turnover of the factor XIII. We found no evidence of association of factor XIII valine34leucine polymorphism and inflammatory bowel disease.

Case-Control Studies↗
PubMed1994

Nutrition support in inflammatory bowel disease.

The mechanisms of nutritional therapy in inflammatory bowel disease have not been thoroughly established. It is likely that a further understanding of the underlying disease process will allow better understanding of these forms of therapy, with a sounder rationale for the construction of specific diet constituents for therapy. Regardless, nutritional therapy is likely to be multidimensional, and various forms may affect different aspects of the disease process. Decreased inflammatory factors, decreased antigenic stimuli, provision of essential nutrients, improved immune function, and other factors may all be of varying importance in different patients with inflammatory bowel disease. Little work has been done on the role of diet therapy in the long-term treatment of patients with inflammatory bowel disease as a method of preventing relapse. Parenteral nutrition and elemental diets appear to have limited roles in this area. Some investigation has been done to see if minor modifications of the normal diet can prolong remission periods. Low-fiber diets are frequently recommended for patients with strictures. Whether this has any significant effect on symptoms, inflammation, or complications is unclear. Heaton et al suggested that a high-fiber, unrefined carbohydrate diet resulted in fewer and shorter hospitalizations. In a prospective follow-up study by Ritchie et al, however, these results were not able to be reproduced. Exclusion diets have also been suggested as a means of reducing relapse rates in patients with Crohn's disease. In a small, randomized, controlled trial of an exclusion diet versus an unrefined carbohydrate, fiber-rich diet, there were significantly fewer relapses among the patients treated with the exclusion diet at 6 months. These diets require intensive patient cooperation, but the potential side effects are minimal. Clearly, these findings need to be reproduced in large, prospective, randomized, controlled studies before widespread use can be advocated. A great deal of data exists on the use of nutritional supplementation in the treatment of inflammatory bowel disease, although little of it is in the form of large, randomized, controlled studies. Nutritional manipulation currently has a limited role in patients with ulcerative colitis; a much broader role exists in patients with Crohn's disease. The mechanisms by which nutritional therapy affects these diseases may include a combination of factors--decreased antigenic exposure, improved immune function, and provision of essential nutrients and calories needed for bowel regeneration.(ABSTRACT TRUNCATED AT 400 WORDS)

Humans↗
PubMedDate not supplied

Risk-benefit assessment of drugs used in the treatment of inflammatory bowel disease.

Although the aetiology of inflammatory bowel disease remains elusive, many agents are available for the control of symptoms and inflammation. Knowledge of drug pharmacology, indications and side effects is essential to ensure the best possible clinical care while minimising toxicity and inappropriate use. Sulfasalazine consists of sulfapyridine linked to mesalazine (5-aminosalicylic acid) via an azobond. Its use is indicated in the treatment of mild to moderately active ulcerative colitis and in the prevention of relapse in patients with quiescent disease. Patients with mild to moderate colonic or ileocolonic Crohn's disease also benefit from this drug, as do a proportion of patients with isolated small bowel disease. Sulfasalazine has not been uniformly effective in preventing relapse in Crohn's disease, although many clinicians continue its use in patients who respond initially. A high incidence of side effects which limit therapy include intolerance, hypersensitivity reactions and impairment of male infertility. The newer aminosalicylates offer targeted delivery of mesalazine to the bowel, with fewer side effects. Topical mesalazine has proved extremely effective in patients with distal ulcerative colitis; oral forms are effective in the treatment of mild to moderately active ulcerative colitis and in relapse. Both types appear to be effective in the treatment of Crohn's disease, and possibly in preventing relapse. There is no current clinical advantage of one mesalazine preparation over another, nor is there an indication for their use in sulfasalazine-treated patients who have satisfactory response without adverse effects. Corticosteroids are indicated for more severe disease activity where the aminosalicylates have limited efficacy-specifically to induce remission in patients with severe or refractory ulcerative colitis or Crohn's disease. They should not be used to maintain disease remission or in the prevention of postoperative recurrence. Topical corticosteroids allow their local use in distal colitis with minimal systemic side effects. Long term use is limited by side effects, many of which are dose related, although alternate-day therapy may lessen the incidence. Immunosuppressive agents are beneficial for the treatment of refractory inflammatory bowel disease unresponsive to other medications, and may also facilitate the withdrawal of steroids in refractory patients. Mercaptopurine has an added benefit in the treatment of Crohn's disease fistulae; the role of cyclosporin in bowel disease has not been established and its use cannot currently be recommended. The potential toxicity of immunosuppressive agents warrants careful consideration of their use by both physician and patient. Metronidazole is indicated for the treatment of mild to moderate Crohn's disease, including perineal disease. Common side effects include peripheral neuropathy and nausea.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex Hormones↗
PubMed1987

Defective memory B cell formation in patients with inflammatory bowel disease following tetanus toxoid booster immunization.

Inflammatory bowel disease patients with mild to inactive disease were studied for their ability to generate pokeweed mitogen responsive anti-tetanus toxoid IgG producing B cells in the peripheral blood 21 days following in vivo tetanus toxoid booster immunization. Compared to normals and disease controls, patients with inflammatory bowel disease had significantly impaired in vitro production of anti-tetanus toxoid antibody during an 8 day pokeweed mitogen stimulated culture period. There was poor correlation between the ratio of helper to suppressor T cells in the peripheral blood and pokeweed mitogen stimulated antibody production. Likewise, there was little correlation between in vitro antibody production and peripheral blood natural killer cell cytotoxic activity. Culture of the patients B cells with normal T cells failed to improve antibody production in vitro. These results indicate that many inflammatory bowel disease patients have an impaired humoral immune response to tetanus toxoid booster immunization. This impaired immune response may be due to an inability to generate B cell precursors of anti-tetanus toxoid IgG producing B cells rather than to abnormal circulating helper or suppressor T cell activity or natural killer cell regulatory activity.

Adult↗
PubMed2003

CCR6 has a non-redundant role in the development of inflammatory bowel disease.

Antigen-loaded tissues such as the intestinal mucosa must simultaneously elicit appropriate immune response to innocuous bacteria and food proteins, and to potentially harmful antigens. Impairment of the mechanisms controlling this response may mediate the excessive immune reaction that can lead to tissue destruction and inflammatory intestinal diseases, including inflammatory bowel disease. The intestinal epithelium influences local immune responses through the expression of adhesion molecules, costimulatory factors, cytokines and chemokines. CCL20, a beta-chemokine expressed in epithelia from colon and other intestinal tissue, plays a role in immune responses of intestinal mucosa, as deduced from the defects in intestinal leukocyte homeostasis shown by mice lacking CCR6, the CCL20 receptor. We studied the response of CCR6-deficient mice in two models of inflammatory bowel disease. The data show that absence of CCR6 resulted in less severe intestinal pathology in animals treated with dextran sodium sulfate. Conversely, CCR6 deficiency alters leukocyte homeostasis and the cytokine environment in the intestinal mucosa; these changes are sufficient to confer susceptibility to trinitrobenzene sulfonic acid-induced intestinal inflammation in the otherwise resistant C57BL/6J mouse strain. These results suggest that the CCR6/CCL20 axis has a critical, non-redundant role in the in vivo control of immune responses in the intestine.

Animals↗
PubMedDate not supplied

Thrombopoietin serum levels in patients with inflammatory bowel disease with and without previous thromboembolic events.

BACKGROUND/AIMS: Patients affected by inflammatory bowel disease frequently suffer from thromboembolic complications and mesenteric microvascular occlusion could be involved in the pathogenesis of inflammatory bowel disease. Increased platelet counts and abnormal platelet function seem to play a crucial role in determining the hypercoagulable state observed in inflammatory bowel disease. Thrombopoietin is considered the primary regulator of thrombopoiesis and recent studies have investigated the role of thrombopoietin in inflammatory bowel disease. However, the available data are not conclusive. The aim of this study was to assess thrombopoietin serum levels in inflammatory bowel disease patients according to platelet counts, disease activity and previous thrombotic events. METHODOLOGY: Seventy-one patients with inflammatory bowel disease [41 with ulcerative colitis and 30 with Crohn's disease] and 30 healthy controls were investigated. Eight (11%) inflammatory bowel disease patients had suffered previous thromboembolic complications, none had active thrombosis. Thrombopoietin serum levels were measured by ELISA. RESULTS: Mean thrombopoietin levels were significantly increased in inflammatory bowel disease patients with active disease compared to both healthy controls and patients with inactive disease. Platelet counts were significantly higher only in patients with active disease with respect to healthy subjects. No correlation was found between thrombopoietin levels and platelet counts in either controls or inflammatory bowel disease patients. No differences were found either in thrombopoietin levels or in platelet counts comparing inflammatory bowel disease patients with and without thromboembolic complications. CONCLUSIONS: Our data show elevated thrombopoietin levels in active inflammatory bowel disease. However, no correlation was found between platelet counts and thrombopoietin levels, supporting the hypothesis that other circulating factors than thrombopoietin interact in determining reactive thrombocytosis. Furthermore, thrombopoietin levels did not differ in inflammatory bowel disease patients with or without previous thromboembolic events. This finding could be probably explained by the lack of patients with active thrombosis at the moment of inclusion in the study.

Adult↗
PubMed2002

Functional relevance of soluble TNF-alpha, transmembrane TNF-alpha and TNF-signal transduction in gastrointestinal diseases with special reference to inflammatory bowel diseases.

As a result of extensive clinical and basic research, the pivotal role of tumour necrosis factor (TNF) in the pathogenesis of chronic inflammatory diseases such as inflammatory bowel disease (IBD) has now generally been acknowledged. This has led to promising clinically effective anti-TNF-strategies. Of note, there is more and more evidence that TNF seems to play a key role in other gastrointestinal diseases including Helicobacter pylori infection, pancreatitis, viral hepatitis and toxic liver damage, too. The action of TNF at the cellular level is mediated by two cell surface receptors, TNF-R1 (p60) and TNF-R2 (p80). The function of these receptors and the downstream intracellular signal transduction pathway have been extensively studied in vitro and it can be expected, that there are critically important steps in TNF-signal transduction that might be dysregulated in these disease states. Their elucidation could lead to a better understanding of the pathogenesis of these diseases, in particular IBD and potentially reveal new, more specific therapeutic targets. Objective of this review is to give an overview about the current knowledge on TNF signal transduction in relationship to selected examples of important gastrointestinal disorders with special focus on IBD. Finally, the implications for future research efforts will be discussed.

Antibodies, Monoclonal↗
PubMed1979

Inflammatory bowel disease in the West Indies.

Inflammatory bowel disease is generally assumed to be rare among negroes and Indians. Over 10 years 34 cases of ulcerative colitis and 14 cases of Crohn's disease were seen in one medical and one surgical unit in Port-of-Spain, Trinidad. Twenty-six patients were Negroes, 18 were Indians, three were of mixed race, and one was Caucasian. In many of these patients the disease was extensive and several of those with Crohn's disease suffered severe complications. The assumption that inflammatory bowel disease is rare among West Indians of African and Indian origin therefore seems to be wrong.

Adolescent↗
PubMed1995

Laparoscopic surgery for inflammatory bowel disease.

In the setting of inflammatory bowel disease (IBD), laparoscopic approaches have been avoided because of the often fragile intestinal tissue, thickened mesentery, malnutrition, immunosuppression, and the presence of dense adhesions. In this article, we report 10 successfully managed laparoscopic cases in IBD patients (five with ulcerative colitis, five with Crohn's Disease). Patients with ulcerative colitis underwent total abdominal colectomies, mucosal proctectomies, J-pouch construction, and diverting ileostomies. Procedures in patients with Crohn's disease included ileocecectomy (3), sigmoid colectomy with takedown of a transverse colonic fistula (1), and stricturoplasty (1). One of the 10 cases was converted to an open technique for technical reasons. Six of the 10 patients were on high dose corticosteroids for disease control. Hospital stay ranged from 6-13 days, with a median of 7 days. The morbidity rate was 20 per cent, and included one case of mild postoperative pancreatitis in a Crohn's disease patient and one delayed peri-ileostomy fistula in an ulcerative colitis patient. There was no mortality. Based on these results, we conclude that laparoscopic intestinal surgery is both feasible and safe in selected patients with inflammatory bowel disease. Use of laparoscopic techniques in these patients may reduce hospital stay, lessen adhesion formation, and improve cosmetic results in this generally young group of patients.

Adolescent↗
PubMed2001

[Value of sonography in the diagnosis and follow-up of patients with cryptogenic inflammatory bowel diseases in current practice: review of a 10-year experience in a community hospital].

Inflammatory bowel diseases (IBD) are chronic inflammatory diseases of the bowel that are of unknown etiology. These diseases either progress with intermittent flare-ups interrupted by periods of remission or on a chronic active progressive mode. IBDs include Crohn disease (CD) and ulcerative colitis (UC). Clinical and imaging diagnosis often is challenging, hence explaining the frequent time delay between onset of disease and initiation of therapy. Clinical evaluation is characterized by three consecutive steps: consider a diagnosis of IBD; exclude other causes of inflammatory bowel disease; differentiate CD from UC since a definitive curative surgical treatment is available for UC. US is non-invasive, widely available, easy to perform, and relatively inexpensive and thus represents a significant advance in the evaluation of these three steps. The role of US in the evaluation of patients with suspected IBD will be reviewed.

Colitis, Ulcerative↗
PubMed1997

Monoclonal antibody therapy of inflammatory bowel disease.

Animal models of inflammatory bowel disease have provided insight in the regulation of mucosal inflammation. This has resulted in novel therapeutic approaches that specifically target a single inflammatory mediator. Monoclonal antibody therapy has been used in steroid refractory Crohn's disease patients. Anti-TNF antibody administration induced complete remissions and few side effects were observed. Although these findings need to be confirmed in controlled and long term treatment studies they may guide the development of specific and effective therapies for these diseases.

Animals↗
PubMed2005

[The importance of nutrition in inflammatory bowel disease in children].

Many children with inflammatory bowel disease, mainly Crohn's disease, suffer from malnutrition and growth retardation. Maintenance of adequate nutrition is extremely important in the management of pediatric patients with Crohn's disease. This can usually be achieved by exclusive elemental formulae and polymeric formulae and rarely necessitates the use of parenteral nutrition. This review presents an update on the nutritional aspects of inflammatory bowel disease in children.

Child↗
PubMed1992

[Chronic inflammatory bowel disease--current status].

Chronic inflammatory bowel disease (IBD) encompasses the disease entities, ulcerative colitis (UC) and Crohn's disease (CD). An aetiologic agent has not yet been defined and the diagnosis is based, therefore, on the sum of clinical, paraclinical, radiologic, endoscopic and histopathologic features. In recent years pathogenetic studies have focused on immune mechanisms, transmissible infectious agents, the potential role of the normal intestinal flora, dietary factors, enzymatic alterations and genetic features, in addition to vascular, neuromotor, allergic and psychologic factors. The prevalence of IBD is increased in first-degree relatives of patients and there is a high rate of disease concordance among monozygotic twins. Thus abnormal genes may encode for one or several immunoregulatory factors, while bacterial wall products seem to activate colonic inflammatory cells in a non-specific way, leading to increased production of cytokines, complement-derived peptides, eicosanoids, platelet activating factor, biogenic amines, kinins, chemotactic oligopeptides, and neuropeptides. The named soluble inflammatory mediators, in addition to free oxygen radicals, are considered responsible for the secondary amplification of the inflammatory process. The corner stones in medical therapy of IBD are still corticosteroids and sulphasalazine (SAZ). The new oral salicylates, which are analogues of SAZ or "slow release" preparations of 5-aminosalicylic acid (mesalazine), have provided a therapeutic progress, because they are tolerated better than SAZ. Immunosuppressive agents, such as azathioprine and 6-mercaptopurine, reduce the requirement for corticosteroids and are effective in refractory CD, but the effect is delayed up to several months. The therapeutic action of cyclosporine A is not sustained, but often associated with side effects. Metronidazole has a beneficial effect on perineal disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Colitis, Ulcerative↗
PubMed2005

Irritable bowel syndrome and inflammatory bowel disease: interrelated diseases?

In the past inflammatory bowel disease (IBD), celiac disease and irritable bowel syndrome (IBS) were regarded as completely separate disorders. Now, with the description of inflammation, albeit low-grade, in IBS, and of symptom overlap between IBS and celiac disease, this contention has come under question. Is there true overlap between these disorders? Despite the limitations of available data one cannot but be struck by some areas of apparent convergence: IBD and celiac disease in remission, lymphocytic colitis and microscopic inflammation in IBS, in general, and, especially, in the post-infectious IBS category. The convergence between latent celiac disease and sub-clinical IBD, on the one hand, and IBS, on the other, appears, based on available evidence, to be somewhat spurious and may largely relate to misdiagnosis, a phenomenon which may also explain the apparent evolution of IBS into IBD in some studies. Similarities between IBS and lymphocytic colitis are more striking and less readily dismissed; as for IBS, well documented instances of progression of lymphocytic colitis to full-blown IBD are infrequent, suggesting a true separation between this disorder and classical IBD. Do IBS and lymphocytic colitis represent different responses to similar triggers? Will some of the 'inflamed' IBS subgroup be reclassified as part of the spectrum of lymphocytic colitis in the future? Will inflammation emerge as a common underlying factor in the pathogenesis of IBS? The answer to these and many questions must await further study of this fascinating area.

Environment↗
PubMed2000

Comparison of iohexol and lactulose-mannitol tests as markers of disease activity in patients with inflammatory bowel disease.

Increased intestinal permeability has been proposed as one aetiological factor for inflammatory bowel diseases (IBD). We have previously found that intestinal permeability of a water-soluble contrast medium, iohexol, correlates with disease activity. The objective was to compare the iohexol test with the lactulose-mannitol ratio, which is a more extensively studied permeability marker, in patients with active IBD. Urinary excretion of iohexol was compared to the lactulose-mannitol ratio in 22 patients with an exacerbation of IBD and in 10 healthy controls. Median intestinal absorption of iohexol was 0.64% (range 0.13-3.8%) in the 22 patients and 0.3% (range 0.15-0.54%) in the controls (p = 0.016), whereas the median lactulose-mannitol ratio was 0.037 (range 0.01-0.260) in patients and 0.03 (range 0.004-0.063) in controls (N.S.). Correlation between urinary excretion of iohexol and lactulose-mannitol ratio was positive (R = +0.41, p = 0.018). The urinary excretion of iohexol correlated positively with endoscopic disease activity (R = +0.74, p < 0.001) and the modified Harvey-Bradshaw index (R = +0.44, p = 0.04). The lactulose-mannitol ratio correlated positively with endoscopic disease activity (R = +0.44, p = 0.05), but correlations with clinical index or c-reactive protein were poor. In conclusion, the iohexol test is a superior activity marker compared to the lactulose-mannitol ratio which probably reflects, instead, some pathogenic property of IBD.

Adult↗
PubMed1993

[Local or systemic treatment of inflammatory bowel diseases?].

Standard therapy of inflammatory bowel disease is based on the treatment with corticosteroids, sulfasalazine and 5-aminosalicylic acid. Depending on localization, extent and activity of the bowel inflammation, these drugs are administered topically, systemically or in combination. The advantage of the topical therapy is the lack of non allergic side effects. Ulcerative proctitis and left-sided colitis should, in the first approach, be treated topically with suppositories or enemas. In severe colitis, a combined systemic and topical therapy is useful. In Crohn's disease topical agents are of minor importance. 5-aminosalicylic acid is efficient in mildly active Crohn's disease and prevents relapse for some patients in remission. In severely active Crohn's disease, systemic corticosteroids have to be administered. Azathioprine, cyclosporin A and metronidazole are considered to be reserve drugs because of significant side effects. The clinical usefulness of new topical corticosteroids showing both high antiinflammatory effect and no systemic side effects is presently investigated.

Administration, Oral↗