Class of 2008 Abstract / Objectives: To assess pharmacists’ and celiac patients’ knowledge and awareness about gluten in medications. Methods: People diagnosed with celiac disease were eligible to participate in the study. Patient questionnaires were administered at two of the quarterly Southern Arizona Celiac Support group meetings. Patients were surveyed regarding how to check the gluten-free status of prescription medications. Pharmacists from Tucson and Phoenix were included in the study. They were contacted by e-mail and invited to participate in the website questionnaire. Pharmacists were surveyed regarding their knowledge and comfort level of gluten content in medications. Both the patient questionnaires and pharmacist questionnaires utilized a rating scale of 0 to 5 (0=not at all, 5=very much). All other questions were multiple-choice. Results: Patient questionnaires were completed by 20 patients diagnosed for <5 years and 19 patients diagnosed ≥5 years. Seventy percent of patients reported that one of the ways they determine a medications’ gluten content is by asking a pharmacist which was significantly higher than any other method reported (p ≤ .010). Pharmacist questionnaires were completed by 40 clinical/hospital pharmacists and 25 community pharmacists. There were no significant differences in the two pharmacist groups’ reported level of knowledge (2.0±1.4 and 2.2±1.3, p=0.50), confidence in counseling (1.6±1.3 and 1.9 ±1.5 p= 0.41), or willingness to determine gluten content in medications (3.4±1.4 and 3.5±1.5). Conclusions: Celiac patients rely on pharmacists to determine the gluten content in medications. Pharmacists are willing to help patients determine gluten content, but are unconfident in their ability to do this.

Background: Celiac disease affects 1% of the population and the only treatment for CD is life-long adherence to a gluten-free diet, this affects every aspect of life including emotional, social, physical and psychological which in turn has an effect on patient quality of life. Objective: This pilot study is an effort in understanding the quality of life in the pediatric CD population and is a guide for a future, large sample research study. Design & Methods: Thirteen children diagnosed with CD by intestinal biopsy (mean 6 months) and their parent pair were asked to complete a generic QoL questionnaire (EQ-5D-CY) and a disease-specific questionnaire (TACQoL-CD). Results: The overall QoL was higher on the generic questionnaire, while the effects of CD and the GFD resulted in a lower quality of life as determined by the TACQoL-CD. Future research with a large sample at multiple timepoints is imperative.

No description available.

Celiac disease, an inflammatory disease of small bowel caused by sensitivity to dietary gluten and related protein, affects approximately 0.5-1% of the population in the Western world. Extra-intestinal symptoms and associated diseases are increasingly recognized including diabetes mellitus type 1, thyroid disease, dermatitis herpetiformis and ataxia. There have also been a number of reports of various types of renal involvement in patients with celiac disease including diabetes nephropathy, IgA nephropathy, membranous nephropathy, membranoproliferative glomerulonephritis, nephrotic syndrome related to malabsorption, oxalate nephropathy, and associations of celiac disease with chronic kidney disease and end-stage kidney disease. This review aims to present the current literature on possible pathologic mechanisms underlying renal disease in patients with celiac disease.

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Celiac disease (CD) is an immune-mediated enteropathy caused by permanent intolerance to dietary gliadin in wheat gluten and related prolamines in barley and rye. The pathogenesis of CD is still unknown and several different environmental factors have been associated with CD, such as dysbiosis of the microflora. In this translational study we investigated the immune status and the interplay of T-cells and Tregs in the mucosa of children with CD and controls, as well as the immune status in treated CD patients, provoked by either dietary oats, CD associated bacteria or gluten. The major findings in the studies were: First, indicators of extrathymic T-cells maturation (ETCM), i.e., the RAG1 enzyme required for recombination of the T cell receptor (TCR) genes and the preTα-surrogate chain in the immature TCR, were both expressed at lower levels in CD patients compared to controls. In addition, IELs expressing RAG1 were less abundant in CD patients compared to controls. The levels of these two indicators stayed low in treated CD patients as well, suggesting that impaired capacity of ETCM is an inherent feature of CD patients. Second, IL-17A, a cytokine involved in both inflammation and anti-bacterial responses was increased in active CD. The major cellular source was CD8+IELs. Furthermore, ex vivo challenge of biopsies from treated CD patients with gluten and with CD-associated bacteria induced an IL-17A response. The CD-associated bacteria also influenced the magnitude of the IL-17A response to gluten. Third, we investigated the effect of dietary oats on local immune status in the intestinal mucosa by comparing CD patients receiving GFD with and without oats. 22 different mRNAs for immunity effector molecules and tight junction proteins were analyzed. We found that expression of two down-regulatory cytokines, two activating NK-receptors and the tight-junction protein claudin-4 normalized in patients on a standard GFD while they did not normalize in patients on a GFD with oats. Fourth, we analyzed the expression level of mRNAs for chemokines, cytotoxic effector molecules, NK-receptors and their ligands in IELs and epithelial cells. Expression levels of several of these genes follow disease activity, suggesting massive recruitment of immune cells by both cell types accompanied by increased IEL-mediated cytotoxicity in the epithelium of inflamed mucosa. In this thesis we have identified three potential risk factors for development of CD: 1) an inherent lower level of ETCM in the small intestinal mucosa than in controls. This could lead to decreased generation of regulatory T cells and less capacity to tolerate gluten and adapt to the local milieu in the mucosa. 2) Dysbiosis of the resident microbiota with increased IL-17A production that could promote local inflammation and immune cell infiltration as well as antibacterial reactions. 3) Dietary oats may provoke a local immune response in a sub-population of CD patients. These patients should probably avoid oats in their GFD but larger studies are needed.

No description available.

Zöliakie ist durch eine dysregulierte Immunreaktion auf die in Getreiden enthaltene Proteinfraktion Gluten charakterisiert. Die Assoziation der Erkrankung mit Polymorphismen in immunregulatorischen Genen weist auf eine Rolle von regulatorischen T-Zellen im Krankheitsgeschehen hin. Foxp3+ regulatorische T-Zellen haben eine essentielle Bedeutung für die Aufrechterhaltung der intestinalen Immunhomöostase und die Limitierung von Autoimmunität. In der vorliegenden Arbeit wurde eine 2005 bis 2010 diagnostizierte Gruppe von 51 Kindern und Jugendlichen mit Zöliakie untersucht. Diese Gruppe wurde mit 51 geschlechts- und altersadaptierten Kontrollen ohne Zöliakie verglichen. Es wurden anamnestische, paraklinische und histologische Daten mit der Verteilung von CD3+Foxp3+ regulatorischen T-Zellen in der Dünndarmschleimhaut untersucht. Patienten mit Zöliakie wiesen eine leichte Anämie, jedoch keine signifikante Wachstums- und Gewichtsentwicklung auf, was die oligosymptomatische Verlaufsform in der Gesamtkohorte unterstreicht. Es konnte gezeigt werden, dass CD3+Foxp3+ regulatorische T-Zellen bei Zöliakie-Patienten vermehrt in der Dünndarmschleimhaut akkumulieren. Weiterhin korreliert die Häufigkeit CD3+Foxp3+ regulatorischer T-Zellen sowohl mit dem Schweregrad der Schleimhaut-schädigung (gemessen an der Marsh-Oberhuber-Klassifikation, dem Zotten-Krypten Verhältnis oder der Zahl der intraepithelialen Lymphozyten) als auch mit den Titern Zöliakie-spezifischer Antikörper. Die Akkumulation CD3+Foxp3+ regulatorischer T Zellen lässt sich partiell als Folge einer Anreicherung von CD4+ T-Zellen auf Kosten CD8+ T-Zellen erklären. Die Daten weisen darauf hin, dass Foxp3+ regulatorische T Zellen sekundär als Folge des gluteninduzierten Entzündungsprozesses in der Schleimhaut akkumulieren, diesen offensichtlich aber nicht effektiv begrenzen. Die mögliche Assoziation der Immundysregulation der Zöliakie mit Foxp3+ regulatorischen T-Zellen ist damit nicht durch eine numerische Reduktion sondern wahrscheinlich durch partielle funktionelle Defekte bedingt.

No description available.

Diss. (sammanfattning) Umeå : Umeå universitet, 2006. / Härtill 4 uppsatser.