The spectrum of celiac disease: epidemiology, clinical aspects and treatment

Department of Gastroenterology and Hepatology, VU University Medical Center, P. O. Box 7057, 1007 MB Amsterdam, The Netherlands.
Nature Reviews Gastroenterology &#38 Hepatology (Impact Factor: 12.61). 03/2010; 7(4):204-13. DOI: 10.1038/nrgastro.2010.23
Source: PubMed


Celiac disease is a gluten-sensitive enteropathy that affects people of all ages worldwide. This disease has emerged as a major health-care problem, as advances in diagnostic and screening methods have revealed its global prevalence. Environmental factors such as gluten introduction at childhood, infectious agents and socioeconomic features, as well as the presence of HLA-DQ2 and/or HLA-DQ8 haplotypes or genetic variations in several non-HLA genes contribute to the development of celiac disease. Growing insight into the variable clinical and histopathological presentation features of this disease has opened new perspectives for future research. A strict life-long gluten-free diet is the only safe and efficient available treatment, yet it results in a social burden. Alternative treatment modalities focus on modification of dietary components, enzymatic degradation of gluten, inhibition of intestinal permeability and modulation of the immune response. A small group of patients with celiac disease (2-5%), however, fail to improve clinically and histologically upon elimination of dietary gluten. This complication is referred to as refractory celiac disease, and imposes a serious risk of developing a virtually lethal enteropathy-associated T-cell lymphoma.

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    • "Celiac disease occurs in genetically predisposed people and affects approximately 1% of the population in Western countries [13] [14] [15]. Many pathological conditions such as malignancy have been reported as a possible association with CD [16] [17] [18] [19] [20] [21] [22]. "
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    ABSTRACT: Background and Aims. Hepatic hemangioma (HH) has a widely ranging prevalence. The etiology is unclear; however, associations with autoimmune disorders have been described. We aimed at evaluating the prevalence of HH in celiac disease. Methods. Ninety-seven consecutive patients with celiac disease (18 M, 79 F, median age 41, and range 17-84 years) underwent liver ultrasound between January 2011 and 2012. The findings were compared with those of 1352 nonceliac patients (581 M, 771 F, median age 50, and range 16-94 years), without liver disease or previously detected HH, who underwent US in the same period. Results. Ultrasonographic findings consistent with HH were observed in 14 celiac patients (14.4%), a prevalence significantly higher than in controls (69 cases, 5.1%) (P = 0.0006). Subgroup analysis showed that, among women, the prevalence of HH was 16.4% in the celiac disease group (13/79) compared with 5.9% in controls (46/771) (P = 0.002). In celiac setting, HH had a median diameter of 1.3 cm and presented as a single lesion in 12 cases (86%). Conclusions. Our findings are consistent with a significantly higher prevalence of HH in celiac patients. Although mechanisms underlying this association remain unclear, autoimmune and metabolic processes, as well as alterations of gut-liver axis equilibrium, could play a role.
    Gastroenterology Research and Practice 01/2015; 2015:1-6. DOI:10.1155/2015/749235 · 1.75 Impact Factor
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    • "Celiac disease (CD) is one of the most prevalent affections in the current society [1]. It is characterized by a permanent intolerance to wheat, barley, rye and even oat gluten, mainly. "
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    ABSTRACT: This contribution pursues the goal of achieving an optical fibre-based platform to detect anti-gliadin antibodies (AGAs), in order to early diagnose celiac disease. To this purpose, the generation of lossy mode resonances (LMRs) in several evanescent field optical structures was studied both theoretically and experimentally. LMRs were obtained by adsorbing a polymeric thin-film onto the optical structures using the layer-by-layer assembly technique. The LMR shape depends on the geometry of the optical structure and its attenuation was controlled just by tuning the length of the device. The best performance was obtained with tapered single-mode optical fibres, which provided more than a 50% reduction in the spectral width of the LMR by using a shorter device. This improvement was successfully applied to detect anti-gliadin antibodies (AGAs) in 5 ppm concentration, what can be used to diagnose celiac disease, and shows the potential of this technology to address biosensing applications.
    Sensors and Actuators B Chemical 09/2014; 200:53–60. DOI:10.1016/j.snb.2014.04.017 · 4.10 Impact Factor
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    • "However, a severe complication occurs in a small proportion of CD patients who become unresponsive to the GFD and develop refractory celiac disease (RCD). RCD is defined by the identification of malabsorption and persisting duodenal villous atrophy, despite adherence to a GFD and absence of other enteropathies [4], [5]. A subgroup of RCD patients, denoted as type II, have aberrant populations of T cells lacking the surface expression of CD3 rendering these patients at high risk to develop an enteropathy-associated T-cell lymphoma (EATL) [6]. "
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    ABSTRACT: Celiac disease (CD) is an intestinal inflammation driven by gluten-reactive CD4(+) T cells. Due to lack of selective markers it has not been determined whether defects in inducible regulatory T cell (Treg) differentiation are associated with CD. This is of importance as changes in numbers of induced Treg could be indicative of defects in mucosal tolerance development in CD. Recently, we have shown that, after encounter of retinoic acid during differentiation, circulating gut-imprinted T cells express CD62L(neg)CD38(+). Using this new phenotype, we now determined whether alterations occur in the frequency of natural CD62L(+)Foxp3(+) Treg or mucosally-imprinted CD62L(neg)CD38(+)Foxp3(+) Treg in peripheral blood of CD patients. In particular, we compared pediatric CD, aiming to select for disease at onset, with adult CD. Cell surface markers, intracellular Foxp3 and Helios were determined by flow cytometry. Foxp3 expression was also detected by immunohistochemistry in duodenal tissue of CD patients. In children, the percentages of peripheral blood CD4(+)Foxp3(+) Treg were comparable between CD patients and healthy age-matched controls. Differentiation between natural and mucosally-imprinted Treg on the basis of CD62L and CD38 did not uncover differences in Foxp3. In adult patients on gluten-free diet and in refractory CD increased percentages of circulating natural CD62L(+)Foxp3(+) Treg, but normal mucosally-imprinted CD62L(neg)CD38(+)Foxp3(+) Treg frequencies were observed. Our data exclude that significant numeric deficiency of mucosally-imprinted or natural Foxp3(+) Treg explains exuberant effector responses in CD. Changes in natural Foxp3(+) Treg occur in a subset of adult patients on a gluten-free diet and in refractory CD patients.
    PLoS ONE 07/2013; 8(7):e68432. DOI:10.1371/journal.pone.0068432 · 3.23 Impact Factor
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