Inflammatory Bowel Disease

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Guenter J. Krejs - One of the best experts on this subject based on the ideXlab platform.

  • Anti-Cardiolipin Antibodies in Patients with Inflammatory Bowel Disease
    Digestive Diseases and Sciences, 1999
    Co-Authors: Berendt W. Aichbichler, Wolfgang Petritsch, Gerhard Reicht, Heimo H. Wenzl, Andreas J. Eherer, Thomas A. Hinterleitner, Piet Auer-grumbach, Guenter J. Krejs
    Abstract:

    Elevated levels of anti-cardiolipin antibodies are associated with an increased risk for venous and arterial thrombosis. In patients with Inflammatory Bowel Disease thrombosis is a well known complication. We determined the prevalence of elevated anti-cardiolipin antibodies in 136 patients with Inflammatory Bowel Disease compared with 136 healthy controls and analyzed thromboembolic complications in patients with increased anti-cardiolipin antibody levels. Anti-cardiolipin antibody titers were significantly elevated in patients with Crohn's Disease (5.7 units/ml) and ulcerative colitis (5.3 units/ml) compared to the control group (2.5 units/ml). We found no correlation between Disease activity and anti-cardiolipin antibody levels. Seven patients had deep venous thrombosis in their history, in three of them this was complicated by pulmonary embolism. In only two of the seven patients with deep venous thrombosis were anti-cardiolipin antibody levels increased. In conclusion, anti-cardiolipin antibody titers were significantly increased in patients with Inflammatory Bowel Disease. Elevated anti-cardiolipin antibody levels appear to play no role in the pathogenesis of thromboembolic events in patients with Inflammatory Bowel Disease.

Antonio Picarelli - One of the best experts on this subject based on the ideXlab platform.

  • anti tissue transglutaminase antibodies in Inflammatory Bowel Disease new evidence
    Clinical Chemistry and Laboratory Medicine, 2004
    Co-Authors: Marco Tola, L. Sabbatella, Maria Chiara Anania, R Caprilli, P Paoluzi, Angelo Viscido, Roberta Pica, Antonio Picarelli
    Abstract:

    Anti-tissue transglutaminase, previously held to be identical to anti-endomysial antibodies in celiac sprue, has been reported in Inflammatory Bowel Disease patients. To investigate these data further, we evaluated serum and intestinal anti-tissue transglutaminase in Inflammatory Bowel Disease patients, with respect to the Crohn's Disease activity index and the integrated Disease activity index. Study population comprised: 49 patients with Crohn's Disease and 29 patients with ulcerative colitis; 45 patients with celiac sprue and 85 autoimmune patients as Disease controls; and 58 volunteers as healthy controls. Immunoglobulin A (IgA) anti-recombinant human tissue transglutaminase and anti-endomysial antibody detection in sera and fecal supernatants were performed. Adsorption of positive sera with recombinant human tissue transglutaminase were also performed. Marked increased anti-tissue transglutaminase concentrations were found in celiac sprue, while low-positive values were also found in Crohn's Disease and ulcerative colitis. Anti-endomysial antibodies were detectable only in celiac sprue. Antigen adsorption resulted in a significant reduction of the anti-tissue transglutaminase either in celiac sprue or Inflammatory Bowel Disease sera. A significant correlation between anti-tissue transglutaminase and Crohn's Disease activity index or integrated Disease activity index scores was found. Anti-tissue transglutaminase was also detectable in fecal supernatants from Inflammatory Bowel Disease patients. Data highlight that both circulating and intestinal anti-tissue transglutaminases are detectable in Inflammatory Bowel Disease, and that they are related to Disease activity. These features underline that, in addition to anti-tissue transglutaminase, an anti-endomysial antibody test is necessary in the diagnostic work-up of celiac sprue, especially in patients with known Inflammatory Bowel Disease.

Randall Schrager - One of the best experts on this subject based on the ideXlab platform.

  • Nutritional management of Inflammatory Bowel Disease.
    The Surgical clinics of North America, 1991
    Co-Authors: Stanley J. Dudrick, Rifat Latifi, Randall Schrager
    Abstract:

    The etiology and specific treatment of Crohn's Disease and ulcerative colitis are unknown, and the treatment strategy for patients with Inflammatory Bowel Disease is essentially symptomatic and supportive. The malnutrition that frequently accompanies Inflammatory Bowel Disease is a manifestation of intestinal failure and should be vigorously corrected with total parenteral nutrition, elemental diets, or both. Evidence exists for the value of total parenteral nutrition and elemental diets as primary therapy for Inflammatory Bowel Disease in selected patients. Judicious nutritional therapy remains a cornerstone in the adjunctive management of these patients.

William D. Leslie - One of the best experts on this subject based on the ideXlab platform.

  • Review article: Osteoporosis and Inflammatory Bowel Disease.
    Alimentary pharmacology & therapeutics, 2004
    Co-Authors: Charles N. Bernstein, William D. Leslie
    Abstract:

    Studies using dual-energy X-ray absorptiometry have suggested a high prevalence of osteoporosis in Inflammatory Bowel Disease. However, population-based data on fracture incidence suggest only a small increased risk of fracture amongst patients with Inflammatory Bowel Disease compared with the general population. Therefore, it would be helpful to identify patients with Inflammatory Bowel Disease at particularly high risk for fracture so that these risks might be modified or interventions might be undertaken. The data on calcium intake as a predictor of bone mineral density are conflicting. Although there are data suggesting that a one-time survey to determine current calcium intake will not help to predict bone mineral density in Inflammatory Bowel Disease, persistently reduced calcium intake does appear to lead to lower bone mineral density. In the general population, body mass is strongly correlated with bone mineral density, which also appears to be true in Crohn's Disease. Hence, subjects with Inflammatory Bowel Disease and considerable weight loss, or who are obviously malnourished, could be considered for bone mineral density testing, and the finding of a low bone mineral density would suggest the need for more aggressive nutritional support. Although vitamin D is undoubtedly important in bone health, vitamin D intake and serum vitamin D levels do not correlate well with bone mineral density. Sex hormone deficiency can also adversely affect bone health, although a well-developed strategy for sex hormone measurements in patients with Inflammatory Bowel Disease remains to be established. Ultimately, the determination of genetic mutations that accurately predict fracture susceptibility may be the best hope for developing a simplified strategy for managing bone health in Inflammatory Bowel Disease. The therapy of osteoporosis in Inflammatory Bowel Disease has been adapted from other osteoporosis settings, such as post-menopausal or corticosteroid-induced osteoporosis. To date, there remains no therapy proven to be efficacious in Inflammatory Bowel Disease-related osteoporosis; however, calcium and vitamin D supplementation and bisphosphonates have their roles.

Richard J. Grand - One of the best experts on this subject based on the ideXlab platform.

  • Pediatric Inflammatory Bowel Disease.
    Current opinion in gastroenterology, 2004
    Co-Authors: Helen M. Pappa, Gaith Semrin, Thomas R. Walker, Richard J. Grand
    Abstract:

    PURPOSE OF THIS REVIEW The prevalence of early-onset Inflammatory Bowel Disease has been on the rise, with children and adolescents currently accounting for approximately 30% of all patients with this condition. Remarkable new advances in diagnostic modalities and therapy for adults with Inflammatory Bowel Disease, and further information about the role of genetics in determining susceptibility to Disease make the review of the recent literature in pediatric Inflammatory Bowel Disease more timely than ever. RECENT FINDINGS In the area of genetics, new studies provide strong evidence for genetic susceptibility to Disease, and match genotype with phenotypic presentation. A few studies examine the use of noninvasive diagnostic modalities, such as MRI, and biomarkers (fecal lactoferrin) in pediatric Inflammatory Bowel Disease. Remarkable new agents in therapy for adults with Inflammatory Bowel Disease have been empirically administered to children with Inflammatory Bowel Disease. The first attempts to systematically study the effects of these agents in children and adolescents are reviewed here. Furthermore, new studies revise our notion of surgical outcomes in pediatric Inflammatory Bowel Disease. SUMMARY Although premature for clinical practice application, the role of genetic testing in determining Disease susceptibility and assisting with prognosis and course of therapy is clearly evolving and needs further study. As new therapeutic agents join the available treatments of Inflammatory Bowel Disease it is imperative to include pediatric patients in clinical trials. The goals of future studies will be to alter the natural history of early-onset Inflammatory Bowel Disease, reduce the frequency of recurrences, and perhaps reduce requirements for surgical intervention.