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At least 505 records · Page 28Linked to original sources
PubMed1999

Ultrasound measurements of calcaneus for estimation of skeletal status in patients with inflammatory bowel disease.

BACKGROUND: Patients with inflammatory bowel disease (IBD) are at risk of developing metabolic bone disease. In diagnosing osteoporosis, bone mineral density (BMD) measurements play a key role. Our aims in this study were to assess the skeletal status with quantitative ultrasound (QUS) and to evaluate the ability of this method to predict BMD as measured by dual-energy X-ray absorptiometry (DXA) in IBD patients. METHODS: Altogether 53 patients with Crohn disease (CD) and 57 with ulcerative colitis (UC) were studied by using a Lunar Achilles ultrasound bone densitometer. The ultrasound variables are broadband ultrasound attenuation (BUA) and speed of sound (SOS). The lumbar spine, femoral neck, and total body BMD were measured with DXA. The age- and sex-adjusted values (Z-scores) were obtained by comparison with age- and sex-matched normal values. RESULTS: In CD patients Z-scores for both BUA and SOS were significantly less than zero, and Z-score for SOS was significantly lower than that for UC patients. Z-scores for BMD measured with DXA were significantly lower at all measurements in patients with CD. QUS and DXA measurements were significantly correlated. However, the agreement between the measurements in each individual patient was poor. Body mass index (BMI) was a major determinant for both BUA and SOS. In CD patients low QUS variables were associated with corticosteroid therapy, and both CD and UC patients with previous fractures had low SOS values. CONCLUSIONS: Our study indicates that QUS and DXA are not interchangeable methods for estimation of bone status. QUS variables are insufficient to provide accurate prediction of BMD values and should therefore not be recommended as a screening test for osteoporosis in IBD patients.

Absorptiometry, Photon↗
PubMed2005

Involvement of IL-6 in the pathogenesis of inflammatory bowel disease and colon cancer.

Inflammatory bowel disease (IBD), which consists of Crohn's disease and ulcerative colitis, is defined as a chronic inflammation of the gastrointestinal tract. The etiopathogenetic mechanisms underlying the development of IBD are still not completely understood, and the therapeutic strategies used thus far have been limited to mostly evidence-based principles. There is growing evidence that the pro-inflammatory cytokine interleukin (IL)-6 plays a crucial part in the uncontrolled intestinal inflammatory process, which is a main characteristic of IBD. There is elevated production of IL-6 and its soluble receptor (sIL-6R) by intestinal macrophages and CD4+T-cells. The increased formation of IL-6-sIL-6R complexes that interact with gp130 on the membrane of CD4+T-cells (trans-signaling) lead to an increased expression and nuclear translocation of STAT3, which causes the induction of anti-apoptotic genes, such as Bcl-xl. This leads to an augmented resistance of lamina propria T-cells to apoptosis. The ensuing T-cell expansion contributes to the perpetuation of chronic intestinal inflammation. This understanding concerning the predominant pathogenic role of an IL-6-dependent inflammatory cascade may lead to the development of new therapeutic strategies in the treatment of this disease. Recent studies have also suggested a potential role of IL-6-sIL-6R in the pathogenesis of colon cancer and, therefore, imply a possible novel therapeutic strategy targeting the sIL-6R and ensuing IL-6 trans-signaling.

Animals↗
PubMed2001

Anti-inflammatory peptides and proteins in inflammatory bowel disease.

Current therapy of inflammatory bowel disease, ie, ulcerative colitis and Crohn's disease, is neither sufficient nor disease-modifying. Long-term treatment with non-specific antiinflammatory drugs aminosalicylates, corticosteroids and immunosuppressants is often accompanied with undesirable and potentially serious side effects. Novel biologically-driven therapies are targeted to specific pathophysiological processes, offering the potential for better treatment outcomes. Among other antiinflammatory peptides and proteins, monoclonal antibodies directed against TNFalpha and adhesion molecule alpha4beta7 integrin, recombinant anti-inflammatory cytokines IL-10 and IL-11, as well as colony-stimulating factors and peptide growth factors, are in the most advanced stages of clinical development for IBD.

Animals↗
PubMed2001

Genetic determinants of IL-6 expression levels do not influence bone loss in inflammatory bowel disease.

Bone loss in inflammatory bowel disease (IBD) is presumed to be mediated by inflammation. Increased levels of the multifunctional cytokine IL-6 in inflammatory diseases have been proposed to be the link in such "inflammation-mediated osteopenia." A recently described G/C polymorphism with an effect on transcription rate and plasma levels of IL-6 suggests a genetically determined difference in the degree of the IL-6 response to stressful stimuli between individuals. This study aimed to assess the frequency of genotypes and haplotypes of the G/C polymorphism of IL-6 in IBD patients. A further aim was to assess whether carriage of the potentially protective CC genotype is favorable with respect to the development of bone disease in IBD. The IL-6 polymorphism was typed in 105 IBD patients and 113 healthy controls. Bone mineral density was evaluated at baseline and after a prospective 2-year-follow-up. The favorable CC genotype with decreased IL-6 release was not underrepresented in IBD patients compared to healthy controls. Carriage of this genotype was not protective with respect to the development of bone disease, either for the bone mineral density at baseline or for the prospectively observed bone loss. Within the subgroup of patients who did not receive steroids during follow-up, the prospectively observed bone loss was even slightly higher in CC carriers, but differences did not reach significance. Genetically determined differences in the degree of the IL-6 response to stressful stimuli are no major predictors for the degree of bone disease in IBD patients.

Adult↗
PubMed1998

Reduced bone mineral density and unbalanced bone metabolism in patients with inflammatory bowel disease.

Patients with chronic inflammatory bowel diseases (IBD) are at increased risk to develop osteopenia and osteoporosis. New parameters for the assessment of bone formation and especially bone resorption have significantly improved the diagnostic procedures to characterize bone metabolism. Biochemical characterization of bone turnover in IBD patients may provide important information about the pathogenesis of osteoporosis in this patient population. A cross-sectional study was performed. One hundred forty-nine patients (77 men, 52 premenopausal, and 20 postmenopausal women) with IBD (104 with Crohn's disease [CD] and 45 with ulcerative colitis [UC]) underwent clinical, osteodensitometric, and metabolic bone assessment. Bone mineral density was determined by dual energy X-ray absorptiometry. Bone formation (bone alkaline phosphatase), bone resorption (N-terminal telopeptide of type-I collagen, free desoxypyridinoline, total pyridinoline, and desoxypyridinoline), vitamin D, and parathyroid hormone were assessed. Thirty-six percent of patients with CD and 32% with UC showed osteopenia, 15% with CD and 7% with UC showed osteoporosis. Bone resorption was significantly increased in IBD patients compared to normal controls, whereas bone formation did not show a compensatory increase. Bone formation was even more suppressed in the subset of patients currently treated with corticosteroids. Our data confirm the high prevalence of osteopenia and osteoporosis reported in IBD patients. Furthermore, we provide evidence for an increased bone resorption accompanied by low bone formation in IBD patients. This imbalance of bone metabolism is likely to be one of the reasons for increased bone loss in IBD patients.

Absorptiometry, Photon↗
PubMed1993

Thromboembolism in inflammatory bowel disease: role of platelets.

Patients with inflammatory bowel disease are susceptible to thromboembolism and recently small vessel thrombosis has been implicated as an aetiological factor in Crohn's disease. This study therefore investigated platelet function in 104 patients with inflammatory bowel disease of whom eight had previous thromboembolism. Thirty five patients had reproducible spontaneous platelet aggregation of more than 30% (0 in controls) (p < 0.0001). A further 20 patients showed hypersensitivity of platelets to low concentrations of aggregating agents (p < 0.001). Plasma thromboxane B2 and beta thromboglobulin levels were significantly higher than controls (p < 0.001 and p < 0.001), but platelet lifespan studies were normal. There was no correlation with disease activity. Patients with inflammatory bowel disease have abnormal platelet activity, which may contribute to the inflammatory process.

Adult↗
PubMed1990

Epidemiology of inflammatory bowel disease.

Epidemiologic studies of inflammatory bowel disease indicate that these disorders occur in susceptible individuals, possibly due to genetic abnormalities, resulting in disturbance of bowel wall function. Environmental factor(s) exerting a primary effect at an early age, in most patients, cause the disease to manifest usually in teenagers or young adults. Secondary environmental factors may alter disease expression, severity, or influence relapse. Studies in identical twins provide the best evidence for the role of genetic factors in the cause of Crohn's disease. Changing trends in disease incidence (seen in many countries) provide strong support for environmental factors as playing a major influence in disease expression. We now require further laboratory and epidemiologic studies in family members at risk of disease, in migrants who move from low incidence areas to high incidence areas, and in area where Crohn's disease particularly is starting to appear. The clinician can play an important role by performing careful observations in patients with a view to uncovering new clues to disease etiology.

Contraceptives, Oral↗
PubMed2003

Progress in searching for susceptibility gene for inflammatory bowel disease by positional cloning.

Inflammatory bowel disease (IBD) includes two clinical subtypes: Crohn disease (CD) and ulcerative colitis (UC). The general prevalence is about 1.0-2.0 % in Western countries. It is predominantly regarded as a multifactorial disorder involving environmental factors and polygenic defects. The view was confirmed by a lot of evidences from clinical attributions and animal models, especially from epidemiological investigations. So the etiological study of IBD has been focused on searching for susceptibility genes by positional cloning, which consists of two steps: linkage analysis and association analysis. Linkage analysis has been an important method of searching for susceptibility genes to polygenic diseases as well as single-gene disorders. IBD, as a polygenic disease, has been widely investigated by linkage analysis for susceptibility gene since 1996. The paper reviewed 38 articles, which covered almost all original researches in relation to IBD and linkage analysis. So far, several loci, such as 16q, 12q, 6p and 3p, have been identified by the studies. The most striking is 16q12 (IBD1), which linked only with CD not UC in the majority of studies. Association analysis, as one essential step for positional cloning, is usually carried out by genotyping candidate genes selected by means of linkage analysis or other methods, for figuring out the frequencies of alleles and comparing the frequencies between IBD group and healthy control group to identify the specific allele. It has been established that IBD is implicated in immune disorder. So the studies were centered on the genes of NOD2/CARD15, HLA-II, cytokine, cytokine receptor and adhesion molecule. This paper reviewed 14 original articles on association between NOD2 and IBD that have been published since 2001. All results, with the exception of one report from a Japanese group, provide evidences that the three kinds of variants of NOD2 are susceptibility factors for IBD. This article also comprehensively analyzed 18 original researches of HLA gene polymorphism in IBD. We found extensive discrepancy among the conclusions and a novel hypothesis was put forward to explain the discordance. Most studies published recently on association between IBD and cytokine gene polymorphism were reviewed.

Carrier Proteins↗
PubMed2002

Role of infections in the manifestation or reactivation of inflammatory bowel diseases.

The etiology of inflammatory bowel disease (IBD) is unknown. In addition to genetic and environmental factors, microorganisms have been discussed as possibly playing an important role. Recent reports in the literature do not suggest that a specific persistent infection causes IBD, but indicate that enteric pathogens could cause initial onset of IBD and are associated with reactivation of quiescent disease. Despite their self-limited character, these infections initiate a cascade of inflammatory events leading to chronic, relapsing disease in a genetically susceptible host ("hit-and-run" hypothesis). Epidemiological and microbiologic studies suggest that enteropathogenic microorganisms play a substantial role in the clinical initiation and relapses of IBD. However, similar to traveler's diarrhea, the frequency of infections in the first manifestation and in relapses of IBD is probably understated, due to the problems in detecting enteric pathogens. Thus microbiologic screening is helpful in patients with flares of IBD for optimal medical treatment.

Bacterial Infections↗
PubMed2005

Alicaforsen therapy in inflammatory bowel disease.

Current understanding of inflammatory bowel disease (IBD) has resulted in the development of new treatments that antagonise the pathological pathways associated with T lymphocytes and inflammatory cytokines. Intercellular adhesion molecules (ICAMs) contribute to leukocyte adhesion and migration, local lymphocyte stimulation, and are responsible for T lymphocyte trafficking in the intestine. ICAMs are constitutively expressed by enterocytes and are upregulated in the presence of inflammation. Mobile T lymphocytes in the circulatory system are key to the deleterious inflammatory response resulting in IBD. Alicaforsen, a human ICAM-1 antisense oligonucleotide, blocks ICAM-1 production by disabling target RNA molecules and blocking the translation of protein. This alters the local inflammatory reaction in the intestinal wall. Alicaforsen has been evaluated in both Crohn's disease and ulcerative colitis. The role of the immune system in IBD is reviewed and the responses to treatment with alicaforsen are discussed.

Cell Adhesion Molecules↗
PubMed2005

Effects of dietary fiber on inflammatory bowel disease.

The chronic idiopathic inflammatory bowel diseases (IBDs), namely Crohn's disease and ulcerative colitis, appear to be derived from an inappropriate reaction towards a luminal agent, most probably driven by the intestinal microflora, which upregulates the synthesis and release of different pro-inflammatory mediators, thus contributing to tissue damage that characterizes these intestinal conditions. Several studies have reported that IBD is associated with impairment in short-chain fatty acid (SCFA) production, mainly acetate, propionate, and butyrate. They are produced in the large bowel by anaerobic bacterial fermentation of undigested dietary carbohydrates and fiber polysaccharides, with butyrate being considered as the major fuel source for colonocytes. These SCFAs have been proposed to play a key role in the maintenance of colonic homeostasis. Therefore, it is reasonable to consider therapeutic approaches that increase colonic SCFA production, as it can be achieved by administration of dietary fiber to IBD patients. Unfortunately, there is quite limited documentation of efficacy of dietary fiber in properly designed trials. This review discusses the rationale, available evidence for the use of dietary fiber and its mechanisms of action in the treatment and prevention of IBDs.

Animals↗
PubMed2003

Evaluation of new therapies for inflammatory bowel disease.

The pathophysiology of inflammatory bowel disease (IBD) is gradually being unravelled and new therapies are being developed to target the disturbed biological processes. This article outlines the clinical features of IBD, its current therapy and pathogenesis. The difficulties for clinical pharmacologists and gastroenterologists associated with designing, executing and interpreting clinical trials in IBD are then discussed. The final section reviews methods that can used to demonstrate the pharmacological actions of new treatments in patients with IBD. It is emphasized that proof of the therapeutic efficacy of a novel agent with a specific mechanism of action yields not only clinical benefit to patients with IBD, but also indicates the importance of the targeted biochemical pathway in the pathogenesis of the disease.

Biopsy↗
PubMed1999

Inflammatory bowel disease in the elderly.

Inflammatory bowel disease exhibits a bimodality in age-specific incidence rates, with the second peak occurring from 60 to 70 years of age. In the elderly, both ulcerative colitis and Crohn's disease tend to involve the left side of the colon. The course of disease and the basic principles of management in geriatric populations do not differ from those in younger patients; however, elderly patients do pose distinct problems in differential diagnosis and in therapy choice.

Aged↗
PubMed1983

Studies of antibodies to lipid A and Tamm-Horsfall in patients with inflammatory bowel disease.

Sera from patients with inflammatory bowel disease, ulcerative colitis (UC), or Crohn's disease (MC) were analysed for antibodies to lipid A and Tamm-Horsfall protein (TH), Escherichia coli O antigens, and food antigens, using enzyme-linked immunosorbent assay, indirect haemagglutination, and thin-layer immunoassay, respectively. C-reactive protein (CRP), an indicator of acute inflammation, was also studied. The MC and UC groups were not separated by any of the factors tested. The extent of the disease, however, seemed to influence the IgG antibody response to lipid A and TH. Patients with extended inflammatory areas in the intestine had decreased anti-lipid-A levels during the active phase of the disease compared with patients with less inflammation. In contrast, the IgG anti-TH levels were increased in these patients during both the active and inactive phases compared with less affected patients. Compared with healthy individuals, MC or UC patients showed decreased IgG anti-lipid-A levels. Both IgG and IgA anti-TH and total anti-O levels were increased compared with controls. Antibodies to cow's milk were lower in patients with inflammatory bowel disease than in the control group. CRP was increased in patients with active inflammatory bowel disease compared with inactive.

Adolescent↗
PubMed2000

Enteric bacteria, lipopolysaccharides and related cytokines in inflammatory bowel disease: biological and clinical significance.

Ulcerative colitis (UC) and Crohn's disease (CD) [inflammatory bowel disease (IBD)] are both characterized by an exaggerated immune response at the gut associated lymphoreticular tissue level. Such an abnormal and dysregulated immune response may be directed against luminal and/or enteric bacterial antigens, as also supported by murine models of inflammatory bowel disease (IBD) caused by organisms such as Citrobacter rodentium and Helicobacter hepaticus. Bacterial endotoxins or lipopolysaccharides (LPS) have been detected in the plasma of IBD patients and an abnormal microflora and/or an increased permeability of the intestinal mucosa have been invoked as cofactors responsible for endotoxemia. At the same time, the evidence that phagocytosis and killing exerted by polymorphonuclear cells and monocytes and the T-cell dependent antibacterial activity are decreased in IBD patients may also explain the origin of LPS in these diseases. In IBD, pro-inflammatory cytokines and chemokines have been detected in elevated amounts in mucosal tissue and/or in peripheral blood, thus suggesting a monocyte/macrophage stimulation by enteric bacteria and/or their constituents (e.g. LPS). On these grounds, in experimental models and in human IBD, anti-cytokine monoclonal antibodies and interleukin receptor antagonists are under investigation for their capacity to neutralize the noxious effects of immune mediators. Finally, the administration of lactobacilli is beneficial in human IBD and, in murine colitis, this treatment leads to a normalization of intestinal flora, reducing the number of colonic mucosal adherent and translocated bacteria.

Animals↗
PubMedDate not supplied

Pregnancy and inflammatory bowel disease.

Overall, around 25% of women with inflammatory bowel disease will conceive during their disease. Most of the women with inflammatory bowel disease will have a normal pregnancy and healthy children. However, specific problems may arise related to these pregnancies. This paper reviews what is known on fertility, risk of disease transmission, effect of the disease on the pregnancy and the reverse, delivery, medical follow up and treatment as well as breastfeeding in the setting of inflammatory bowel disease.

Disease Transmission, Infectious↗
PubMed2005

Functional symptoms in inflammatory bowel disease and their potential influence in misclassification of clinical status.

BACKGROUND: Functional symptoms occur in inflammatory bowel disease probably more than in the general population. Existing disease indices rely heavily on symptoms that may be organic or functional. This may explain inconsistencies between recent therapeutic trials in inflammatory bowel disease. Clinically, misinterpretation can lead to over-treatment of functional symptoms with potent agents, and to under-treatment of inflammatory bowel disease when inflammatory features are more subtle. AIM: To assess functional symptoms in inflammatory bowel disease and to devise simple means of their evaluation. METHODS: Patients with Crohn's disease, ulcerative colitis, and irritable bowel syndrome completed questionnaires, generating inflammatory bowel disease and irritable bowel syndrome indices. Data from outliers selected as exemplars were employed to create a new index. RESULTS: One hundred and ninety patients completed questionnaires. Overall, Crohn's and irritable bowel syndrome patients had similar functional features. The new scoring system was based on the eight apparently discriminant symptoms. Prospective evaluation in a separate cohort of 180 inflammatory bowel disease patients yielded scores that are independent of established indices, inflammatory markers and psychometric scores. CONCLUSIONS: Patients with Crohn's report comparable rates of apparently functional symptoms to those with irritable bowel syndrome. A new score has been developed to help in their identification. This has the potential to guide therapeutic decisions and optimize future trial recruitment.

Adult↗