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PubMed2005

Is interferon-alpha therapy safe and effective for patients with chronic hepatitis C and inflammatory bowel disease? A case-control study.

BACKGROUND: Hepatitis C virus infection is more common in patients with inflammatory bowel disease than in general population. Limited data are available as to the safety and efficacy of alpha-interferon therapy for chronic active hepatitis C in patients with concomitant inflammatory bowel disease. AIM: To evaluate the efficacy and safety of alpha-interferon monotherapy in patients with chronic active hepatitis C and inactive or mildly active inflammatory bowel disease. METHODS: A total of 513 consecutive inflammatory bowel disease patients at a single centre were tested for antibodies to hepatitis C virus (anti-hepatitis C virus) between 1995 and 2000. Twenty-one patients had detectable anti-hepatitis C virus Ab and were hepatitis C virus-RNA positive with histologically proved chronic active hepatitis. Each of these patients, whose inflammatory bowel disease was in clinical remission or mildly active, was sex- and age-matched to three controls with similar histological grade and stage of chronic hepatitis C virus but without inflammatory bowel disease; and all were treated with human leucocyte alpha-interferon 6 million units given thrice weekly for 12 months. Responses to treatment were classified as follows: complete response--persistently normal alanine aminotransferase and viral clearance (hepatitis C virus-RNA-ve) at the end-of-treatment, incomplete response--alanine aminotransferase normalization without viral clearance (hepatitis C virus-RNA+ve), and sustained response--alanine aminotransferase normalization and hepatitis C virus clearance 12 months after the end-of-treatment. RESULTS: Twenty-one patients with chronic active hepatitis C and inflammatory bowel disease (10 with Crohn's disease and 11 with ulcerative colitis) and 63 sex- and age-matched controls with chronic hepatitis C virus alone received alpha-interferon monotherapy. Response rates to interferon were similar for inflammatory bowel disease patients compared with controls [CR 42% vs. 35% and SR 24% vs. 18% (P, not significant), respectively]. None of the 21 inflammatory bowel disease patients had severe adverse effects and the mild ones observed were comparable with those seen in the control group. No patients developed an inflammatory bowel disease relapse during the interferon treatment period or in the 12 months thereafter. CONCLUSIONS: The biochemical and virological response to a 12-month human leucocyte alpha-interferon treatment in patients with chronic active hepatitis C are similar to that observed in matched controls with chronic hepatitis C virus without inflammatory bowel disease. Adverse effects are similar in both groups of patients and unrelated to the underlying inflammatory bowel condition. This provides hepatologists with evidence that alpha-interferon can be safely administered to patients with chronic hepatitis C virus and inflammatory bowel disease provided that the inflammatory bowel condition is in clinical remission.

Adult↗
PubMed1986

[Role of nutrition in acute and long-term therapy of chronic inflammatory bowel diseases].

The clinical picture and course of inflammatory bowel disease are influenced by nutritional abnormalities and malnutrition. Interest at present concentrates on high-fibre low-refined sugar diets, elimination diets with identification of specific food intolerance and low-residue diets. All three failed to show significant positive effects on the course of the disease, need for hospitalisation, surgical procedures required or post-operative recurrence. Only a low lactose diet seems to be justified, since we found lactose intolerance in 25-35% of patients with inflammatory bowel disease, as compared with 5-10% in the normal population. In 25 patients with Crohn's disease (CD) a reduction in inflammatory activity and improvement of nutritional status was obtained with parenteral nutrition (PN). Nevertheless, longer follow up periods revealed no additional benefit in comparison with conventional therapies. Furthermore, the combination of PN and total bowel rest resulted in the same improvement as with PN alone. 25 patients with CD manifesting an acute phase of the condition were treated with tube feeding (TF) as primary therapy. TF reduced CD activity and improved nutritional status in 15 patients with small bowel disease, whereas the patients with colonic disease and extraintestinal manifestations did not react. A comparison of the effect of PN and TF in 10 patients with CD showed no significant difference with regard to clinical course and objective parameters. In view of the high costs and risks of complications of PN, TF is recommended as primary therapy for the acute phase of CD. The importance of substitution therapy, especially of vitamin D, is documented.

Colitis, Ulcerative↗
PubMed2006

Inflammatory bowel disease.

Twenty five per cent of inflammatory bowel disease presents in childhood. Growth and nutrition are key issues in the management with the aim of treatment being to induce and then maintain disease remission with minimal side effects. Only 25% of Crohn's disease presents with the classic triad of abdominal pain, weight loss, and diarrhoea. Most children with ulcerative colitis have blood in the stool at presentation. Inflammatory markers are usually although not invariably raised at presentation (particularly in Crohn's disease). Full investigation includes upper gastrointestinal endoscopy and ileocolonoscopy. Treatment requires multidisciplinary input as part of a clinical network led by a paediatrician with special expertise in the management of the condition.

Adolescent↗
PubMed2005

Nucleotide-binding-oligomerization domain proteins and toll-like receptors: sensors of the inflammatory bowel diseases' microbial environment.

PURPOSE OF REVIEW: Chronic inflammatory bowel diseases appear to result from inappropriate immune responses driven by apparently normal intestinal microflora in genetically susceptible hosts. This review focuses on recently described mechanisms balancing toll-like receptor and nucleotide-binding-oligomerization domain activation in the face of ubiquitous enteric flora. RECENT FINDINGS: Toll-like receptor and nucleotide-binding-oligomerization domain signaling plays an integral role in the close collaboration between the intestinal epithelial cell monolayer and adjacent mucosal immune cells. Pathways activated by functional cytosolic nucleotide-binding-oligomerization domain proteins appear to interact with those mediated by membrane-associated toll-like receptors in the innate and adaptive immune defense against intra-and extracellular pathogens. Nucleotide-binding-oligomerization domain-mediated signaling may also control toll-like receptor-induced proinflammatory pathways. SUMMARY: Intersections between toll-like receptor and nucleotide-binding-oligomerization domain pathways may exist to refine the host immune response to pathogens and prevent undesired immune stimulation driven by the intestinal microbiota. Deficient toll-like receptor and nucleotide-binding-oligomerization domain function due to genetic variability is associated with an increased susceptibility to the development of inflammatory bowel disease.

Bacteria↗
PubMed1990

Platelet count, platelet function, coagulation activity and fibrinolysis in the acute phase of inflammatory bowel disease.

Twenty two patients with exacerbation of inflammatory bowel disease (19 with Crohn's disease, 3 with ulcerative colitis) and thrombocytosis were tested for possible activation of the coagulation and platelet system. Fifteen patients had abnormal platelet function i.e. unphysiologically high sensitivity in vitro towards ADP 2 mumol/l aggregation induction. In 81.8% of the patients we found enhanced fibrinogen concentrations. In 22.7% of the patients thrombin-antithrombin III values exceeded the upper limit of the reference range, and in 68.2% of the patients the D-Dimer concentration exceeded the upper reference limit as a result of reactive fibrinolysis. The altered platelet count and function, and the increased levels of fibrinogen and thrombin-antithrombin III with reactive fibrinolysis activation indicate the presence of prethrombotic factors in patients with exacerbation of inflammatory bowel disease. The presence of enhanced fibrinolysis in these patients might have consequences for the therapeutic treatment.

Adult↗
PubMed1997

[Thromboembolic complications in inflammatory bowel disease].

Thromboembolic complications during the course of inflammatory bowel disease are infrequent but are mainly found in young patients and are associated with a high morbimortality. The etiopathogenesis of these complications has been widely debated and the existence of coagulation alterations and fibrinolysis have been suggested. Nonetheless, the mechanism must be complex since not only do not all the patients with these alterations present this complication but neither do all the patients with thromboembolism have recognized coagulation disorders. The most common clinical presentation is deep vein thrombosis with pulmonary embolism with arterial thrombosis being rare. Five patients with Crohn's disease and two with ulcerative colitis who presented a total of new thromboembolic episodes, six arterial (1 in primitive iliac artery, 1 in common femoral artery, 1 in humeral-axillary artery, 2 in internal carotid and 1 in superior mesenteric artery) and three of venous localization (1 in brachyocephalic-subclavian trunk, 1 axillary and 1 iliac-femoral/pulmonary thromboembolism) are reported. An updated review of the etiopathogenesis, presentation, treatment and prophylaxis of the thromboembolic complications of inflammatory bowel disease is presented.

Adult↗
PubMed2003

Nutritional and metabolic issues in inflammatory bowel disease.

PURPOSE OF REVIEW: This article describes the clinical papers published in 2002 and early 2003 on nutritional and metabolic derangement in inflammatory bowel disease. RECENT FINDINGS: Insulin-like growth factor 1 and Insulin-like growth factor binding protein 3 are decreased in inflammatory bowel disease, and disease therapy hardly reverses this situation. There are promising data on recombinant human growth hormone therapy in paediatric inflammatory bowel disease. Several papers have added some fuel to the debate on the prevalence and pathogenesis of metabolic bone disease in inflammatory bowel disease. Articles have been published investigating the role of dietary fat in the therapeutic action of enteral feeding in Crohn's disease. Low-fat diets are particularly useful, and adding medium-chain triglycerides does not impair the effectiveness of these diets. Balanced amounts of saturated, monounsaturated and polyunsaturated fat should probably be used. Relevant contributions on the usefulness of probiotic preparations (VSL#3) in the treatment and prevention of pouchitis have been published. Other papers deal with the effects of medical and surgical therapy on body composition and metabolism in the inflammatory bowel disease, the treatment of oxidative stress of these patients, and the possible role of some vitamin deficiencies on thrombotic risk in the condition. SUMMARY: Inflammatory bowel disease therapy hardly reverses growth hormone-insulin-like growth factor 1 disturbances of patients. The role of inflammation and steroid therapy of metabolic bone disease in inflammatory bowel disease is still controversial. Low-fat diets, with added amounts of medium-chain triglycerides, are useful in decreasing gut inflammation in the condition. The search for the optimal dietary fatty acid composition deserves further investigations. The use of probiotics and prebiotics opens new therapeutic perspectives for the disease.

Adult↗
PubMed2002

Complementary practitioners' views of treatment for inflammatory bowel disease.

A substantial number of patients with inflammatory bowel disease use complementary therapies to manage their disease, including chiropractic and herbal therapies. The objective of this study was to explore whether providers of these therapies see patients with inflammatory bowel disease and recommend therapies, and to determine their opinions about the treatments that they recommend. The study sample comprised 66 chiropractors, 19 pharmacists, 16 herbalists and 15 health food store employees in Calgary, Alberta. A structured questionnaire containing two patient scenarios (a patient with active ulcerative colitis and a patient with inactive Crohn's disease) was completed either by an in-person interview or by a mailed questionnaire. Most respondents had seen patients with ulcerative colitis, and at least 80% of each group except pharmacists (only 10%) would treat these patients or recommend treatment. Almost all chiropractors used spinal manipulation, whereas herbalists and health food store employees suggested a wide range of different treatments. Chiropractors rated their treatment as moderately effective; herbalists and health food store employees viewed their recommendations as very effective. The results with respect to the second scenario were very similar. The wide range of treatment recommendations by practitioners, who differ greatly in terms of skills, knowledge and experience, has important implications for physician-patient communication, information provision and education regarding complementary and alternative therapies.

Adult↗
PubMed1985

Nutritional management of inflammatory bowel disease.

Malnutrition and growth failure are frequent complications of inflammatory bowel disease in childhood owing to inadequate dietary nutrient intakes, excessive intestinal losses, malabsorption, and increased nutrient requirements. Aggressive nutritional therapy is indicated for primary and supportive management of disease activity, drug nutrient interactives, individual nutrient abnormalities, and the overall complications of inflammatory bowel disease, malnutrition, and growth failure. The prevention of nutritional disorders in inflammatory bowel disease is accomplished by monitoring anthropometric and biochemical indices and by instituting appropriate enteral or parenteral nutritional therapy when indicated.

Adolescent↗
PubMed2003

Experimental models of inflammatory bowel disease.

The etiology and pathogenesis of inflammatory bowel disease (IBD) remains unsolved, but improved experimental models of enterocolitis have led to progress. Intestinal inflammation and experimental IBD can be induced by chemical or dietary factors or by microbial products. Many animal models of IBD can be used to evaluate new anti-inflammatory drugs. These models, however, usually demonstrate acute, self-limiting colitis. The spontaneous colitis models developed in the cotton-top tamarin monkey and the C3H/HeJBir mouse mimic more features of human IBD. Inflammation is chronic and is under genetic control. The differential genetic susceptibility of inbred rat strains to chronic inflammation have been exploited. Lewis rats injected with bacterial products, peptidoglycan polysaccharide or indomethicin develop chronic relapsing enterocolitis, whereas closely related Buffalo or Fisher rat strains develop only transient inflammation. These models are also useful to test the specific inhibition of inflammatory mediators and target molecules. Over-expression (transgenic) or deletion (knockout) of specific genes have led to the development of rodent models of spontaneous colitis. Inflammation arises from a number of mutations of immunomodulatory molecules, supporting the concept of genetic heterogeneity for IBD. The results obtained from experimental models have generated new hypotheses, expanded human studies, and suggested novel forms of therapy for IBD patients.

Animals↗
PubMed2001

Chemiluminescence in inflammatory bowel disease patients: a parameter of inflammatory activity.

BACKGROUND: Reactive oxygen species (ROS) are produced in excess in the inflamed mucosa and peripheral blood of patients with inflammatory bowel disease. These species have emerged as a common pathway of tissue injury in a wide variety of inflammatory and other disease processes. The present study was conducted to assess ROS production and to correlate this with parameters of inflammatory activity. METHODS: In 25 patients with Crohn's disease (CD), 20 patients with ulcerative colitis (UC) and 65 age- and sex-matched healthy volunteers ROS production was measured using the whole blood luminol enhanced chemiluminescence assay (LECA). Disease activity was assessed using the Crohn's disease activity index and the Ulcerative Colitis Symptoms Score (UCSS) for CD and UC, respectively. Furthermore, the effect of various scavengers, enzymes and enzyme inhibitors on LECA was studied to assess the contribution of different ROS. RESULTS: LECA was significantly higher in CD and UC patients compared with healthy controls (7.1+/-4.7 and 9.8+/-6 vs. 5.2+/-2.8 x 10(3) counts per minute (cpm), p<0.05 and <0.001). In CD, relative LECA (patient/control) was correlated with the Crohn's disease activity index and C-reactive protein (CRP) (r=0.54, p=0.001 and r=0.51, p=0.01). In UC, CRP but not LECA was correlated with the Ulcerative Colitis Symptoms Score (C-reactive protein: r=0.42, p=0.01). Addition of azide, superoxide dismutase, deferoxamine and dimethylthiourea resulted in a decrease of LECA values. CONCLUSION: Whole blood LECA is increased in patients with CD and UC. This parameter is correlated with disease activity in CD. The observed chemiluminescence is probably due to generation of superoxide and the hydroxyl radical.

Adult↗
PubMed1990

A comparison of serum mucoprotein with serum alpha 1 acid glycoprotein, haptoglobin, and alpha 1 antitrypsin assays in monitoring inflammatory bowel disease.

Serum mucoprotein level is a monitor for inflammatory bowel disease activity although its method of measurement is laborious. An easier assay of alpha 1 acid glycoprotein is described. The ability of the two proteins to differentiate active from non-active cases was evaluated and the results compared with acute inflammatory reactants such as alpha 1 antitrypsin and haptoglobin. Amongst 79 patients with inflammatory bowel disease linear discriminant analysis was used to segregate overlapping ranges for patients with and without active disease and thus enabling the evaluation of sensitivity and specificity of each test. Predictive values of 78.6% for mucoprotein and 76.7% for alpha 1 acid glycoprotein were achieved and were due to the fact that there is a very strong linear correlation between these two proteins (r = 0.83, p less than 0.01). Furthermore the mucoprotein fraction is predominantly comprised of alpha 1 acid glycoprotein by as much as 91.5%. alpha 1 antitrypsin and haptoglobin showed poor predictive values. Pairing up all the proteins each with mucoprotein improved the sensitivity, specificity, and predictive value slightly. As a single test alpha 1 acid glycoprotein gave highest specificity, proved easy to assay and was automatable. It was therefore recommended as a substitute for serum mucoprotein in routine assays and as an effective monitor and predictor of inflammatory bowel disease.

Colitis, Ulcerative↗
PubMed1991

Decrease in two intestinal copper/zinc containing proteins with antioxidant function in inflammatory bowel disease.

Oxygen derived radicals contribute to tissue injury in inflammatory bowel disease. We measured the content of superoxide dismutase and metallothionein (two endogenous copper and zinc containing proteins involved in radical scavenging) in intestinal resection specimens from 29 patients with Crohn's disease and 12 patients with ulcerative colitis and compared the concentrations with those obtained in the normal mucosa of a control group of 18 patients with colorectal cancer. The superoxide dismutase content was similar in control mucosa and non-inflamed mucosa from patients with inflammatory bowel disease (mean (SEM) 2.13 (0.10) and 2.24 (0.10) mg/g protein, respectively) but was decreased in inflamed mucosa (1.87 (0.08) mg/g protein, p less than 0.005 v non-inflamed mucosa). The metallothionein content was decreased in non-inflamed inflammatory bowel disease mucosa compared with control mucosa (0.23 (0.03) and 0.36 (0.04) mg/g protein, respectively, p less than 0.02) and a further decrease was found in inflamed mucosa (0.17 (0.02) mg/g protein, p less than 0.001 v control mucosa). No differences were found between Crohn's disease and ulcerative colitis and no significant effect of medication or tissue localisation was noted. These findings might indicate a decreased endogenous intestinal protection against oxygen derived radicals in inflammatory bowel disease which could contribute to the pathogenesis of the disease.

Adolescent↗
PubMed1990

Cow's milk protein sensitivity during infancy in patients with inflammatory bowel disease.

Seventy-eight patients with inflammatory bowel disease (35 with Crohn's disease and 43 with ulcerative colitis) and a control population of 36 children without organic disease were surveyed to determine the frequency of symptoms compatible with cow's milk-protein sensitivity during infancy. The incidence of a history compatible with cow's milk sensitivity was 8.5% (3/35) in patients with Crohn's disease and 2.8% (1/36) in controls. Patients with ulcerative colitis had a significantly greater prevalence of symptoms, compared with the other patient groups (20.9%, 9/43; p less than 0.03). In addition, patients with a history of cow's milk allergy, who subsequently developed ulcerative colitis, did so at an earlier age (6.68 +/- 2.05 yr vs. 10.62 +/- 0.74 yr: p less than 0.02) than those without a history of cow's milk sensitivity. Thus, there appears to be a potential relationship between early cow's milk sensitivity and the development of ulcerative colitis.

Adolescent↗
PubMed2003

Campylobacter jejuni enterocolitis presenting as inflammatory bowel disease.

We report a case of Campylobacter jejuni enterocolitis presenting as inflammatory bowel disease in a 19-year old woman. After a useless course of corticosteroids, ceftazidime and metronidazole, she was successfully treated with erythromicin. Campylobacter species represent an important cause of gastroenteritis in children and adults. The rate of Campylobacter isolation is 5-6 per 100,000 persons. This rate, however, grossly understimates the actual number of Campylobacter infections. In most cases, Campylobacter enteritis is a self-limiting disease, rarely associated with severe complications. Our case demonstrates the difficulty in distinguishing inflammatory bowel disease (Crohn's disease or ulcerative colitis) at onset from atypical infectious colitis. Unfortunately, corticosteroids (necessary for the treatment of inflammatory bowel disease) may exacerbate infectious etiologies. Campylobacter jejuni should be ruled out when assessing inflammatory bowel diseases at onset (as during flare-ups), especially if corticosteroids or immunosuppressive therapies are required.

Adult↗
PubMed2002

Review article: oxidative stress as a pathogenic factor in inflammatory bowel disease--radicals or ridiculous?

Virtually all inflammatory mediators investigated to date seem to be dysregulated in the inflamed intestinal mucosa of patients with inflammatory bowel disease. However, which of these are actually involved in the initiation and perpetuation of intestinal tissue damage is still not fully understood. Amongst these mediators are the reactive oxygen metabolites, produced in large amounts by the massively infiltrating leucocytes. These reactive oxygen metabolites are believed to constitute a major tissue-destructive force and may contribute significantly to the pathogenesis of inflammatory bowel disease. This paper provides a concise overview of reactive oxygen metabolite biochemistry, the types of cell and tissue damage potentially inflicted by them, and the endogenous antioxidants which should prevent these harmful effects. An up-to-date summary of the available human experimental data suggests that reactive oxygen metabolite-mediated injury is important in both the primary and downstream secondary pathophysiological mechanisms underlying intestinal inflammation. Nonetheless, how the individual components of the mucosal antioxidant enzymatic cascade respond to inflammatory conditions is a neglected area of research. This particular aspect of intestinal mucosal oxidative stress therefore merits further study, in order to provide a sound, scientific basis for the design of antioxidant-directed treatment strategies for inflammatory bowel disease patients.

Antioxidants↗
PubMedDate not supplied

Macronutrients and bioactive molecules: is there a specific role in the management of inflammatory bowel disease?

The effect of bioactive nutrient molecules on inflammatory response has an archetype in Inflammatory Bowel Disease. The exacerbated inflammatory response in such conditions can be nutritionally modified by 2 ways: changing the response of the host, or changing the composition of the intestinal ecosystem. Host response can be modified by changing the cell structure and function which is nutrient dependent. Nutrient deprivation will lead to a situation where there is not enough building material for cell replacement and the synthesis of mediators (enzymes, hormones, etc). However, this may occur even in a situation where there is no quantitative nutrient deprivation but only qualitative changes. In Inflammatory Bowel Disease, changes in the sources of some nutrients such as lipids or carbohydrates (CHO) can modify the inflammatory response. Lipids, by changing cell membrane composition, may modify the pattern of eicosanoid synthesis, intracellular signal transmission and activation of nuclear transcription factors, which modify the expression of some genes-that is, changing the host response. On the other hand, certain sources of carbohydrates, by undergoing anaerobic bacterial fermentation, drop the pH in the intestinal lumen favoring the growth of certain strains of bacteria which act favorably in maintaining tolerance in the bowel. In addition, as a consequence of CHO fermentation, short-chain fatty acids are produced which, especially butyrate, may act in 2 ways: by providing energy to the epithelial cells, but also as anti-inflammatory substrate-that is, modifying at least 1 of the mechanisms triggering the inflammatory response enhancement. However, it should not be forgotten that the cellular response to dietary modifications will depend on the individual genome, as has been recently observed. This may explain why some individuals do and others do not show a similar response to dietary interventions.

Animals↗