Background & Aims-Serologic tests are frequently used in celiac disease diagnosis. Gliadin antibodies generally lack the accuracy required for proper diagnosis. We evaluated the value of deamidated gliadin antibody measurements in the diagnosis and follow-up of celiac disease and compared their potential usefulness with that of gliadin and tissue-transglutaminase antibodies.
It has become recently apparent that celiac disease, though once thought to be a primarily childhood disease, can affect people of any age. Epidemiologic studies have suggested that a substantial portion of patients are diagnosed after the age of 50. Indeed, in one study, the median age at the diagnosis was just under the age of 50 with one-third of new patients diagnosed over the age of 65. The purpose of this review is to address the prevalence, clinical features, diagnosis and consequences of celiac disease in the elderly. We will also review management strategies for celiac disease and adjust these with emphasis on the particular nutritional and non-nutritional consequences or associations of celiac disease as they pertain to the elderly.
Active delivery of recombinant autoantigens or allergens at the intestinal mucosa by genetically modified Lactococcus lactis (LL) provides a novel therapeutic approach for the induction of tolerance. Celiac disease is associated with either HLA-DQ2 or HLA-DQ8 restricted responses to specific antigenic epitopes of gliadin, and may be treated by induction of antigen-specific tolerance. We investigated whether oral administration of LL-delivered DQ8-specific gliadin epitope induces antigen-specific tolerance.
L. lactis
was engineered to secrete a deamidated DQ8 gliadin epitope (LL-eDQ8d) and the induction of antigen-specific tolerance was studied in NOD AB° DQ8 transgenic mice. Tolerance was assessed by delayed-type hypersensitivity reaction, cytokine measurements, eDQ8d-specific proliferation and regulatory T cell analysis. Oral administration of LL-eDQ8d induced suppression of local and systemic DQ8 restricted T-cell responses in NOD AB° DQ8 transgenic mice. Treatment resulted in an antigen-specific decrease of the proliferative capacity of inguinal lymph node cells and lamina propria cells. Production of IL-10 and TGF-β and a significant induction of Foxp3+ regulatory T-cells were associated with the eDQ8d-specific suppression induced by LL-eDQ8d.
These data provide support for the development of effective therapeutic approaches for gluten-sensitive disorders using orally administered antigen-secreting LL. Such treatments may be effective even in the setting of established hypersensitivity.
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