The New Epidemiology of Celiac Disease

Journal of Pediatric Gastroenterology and Nutrition (Impact Factor: 2.63). 07/2014; 59 Suppl 1:S7-S9. DOI: 10.1097/01.mpg.0000450393.23156.59
Source: PubMed


The prevalence of celiac disease (CD) varies greatly, but several reports have shown that CD is increasing in frequency in different geographic areas. The increase in prevalence can be partially attributed to the improvement in diagnostic techniques and disease awareness; however the equally well documented rise in incidence in the last 30-40 years cannot be so easily explained. The new epidemiology of CD is now characterized by an increase of new cases in the historical CD areas (northern Europe and the United States) and more interestingly in a spread of the disease in new regions (Asian countries). A significant change in diet habits, particularly in gluten consumption as well as in infant feeding patterns are probably the main factors that can account for these new trends in CD epidemiology.

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    • "The role of gluten in other conditions is increasingly emphasized, as many diseases, the autoimmune ones in particular, are associated with CelD, including type 1 diabetes mellitus (DM1) and chromosomal abnormalities , such as Down syndrome (DS) [2,4–6]. In several countries (including Brazil), the prevalence of CelD in DM1 varies from 3.0% to 16.0% [2,5,7–12] and in DS from 4.0% to 17.0% [2,6,13–17], being considerably higher compared with the overall population (0.5–1.0%) [1] [2] [18]. From the clinical point of view, most individuals with DM1 and DS are believed to exhibit the silent form of CelD [2] [7] [14]. "
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    ABSTRACT: The objective of this study is to investigate the occurrence of gastrointestinal (GI) and extraintestinal symptoms in children and adolescents with type 1 diabetes mellitus (DM1) and Down syndrome (DS) and their association with specific antibodies and histopathology of celiac disease (CelD), representing its clinical forms in the iceberg. Cross-sectional study (November 2009-December 2012) conducted at an outpatient care facility in Northeast Brazil including patients [DM1 (n = 111); DS (n = 77)] aged 10 months-18 years old. Measurement of anti-endomysial (EmA) and anti-tissue transglutaminase (anti-tTG) IgA antibodies was performed, as was that of anti-tTG-IgG in the cases with low serum IgA. The patients with antibody positivity were subjected to small intestine biopsy. GI symptoms occurred in 53.7% of the sample, extraintestinal symptoms in 4.3%, and antibody positivity in 28.2% (n = 53). Of those who underwent biopsy (n = 40), histopathological findings of CelD were found in 37.5% [DM1 = 5/111 (4.5%), DS = 10/77 (13.0%)]. GI symptoms were associated with antibody positivity, but not with the histopathology. The GI (32.5%), silent (5.0%), and potential (62.5%) forms of disease were detected. The prevalence of GI symptoms was high in groups DM1 and DS, and the occurrence of such symptoms was associated with antibody positivity. The lack of association between the symptoms and histopatholological findings points to the inconsistency of the former as indicators of CelD. Although the GI form predominated among the cases with active CelD, its contribution to the celiac iceberg was smaller compared with the potential form, which determined the large and submerged base of the iceberg representing the high-risk groups investigated.
    Scandinavian Journal of Gastroenterology 09/2015; 51(2):1-8. DOI:10.3109/00365521.2015.1079645 · 2.36 Impact Factor
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    ABSTRACT: Type 1 Diabetes (T1D) is a pro-inflammatory autoimmune disorder leading to β-cells destruction and insulin deficiency. Its prevalence of 1:300 is increasing and cannot be explained only by HLA DR4-DQ8 and DR3-DQ2 predisposition. Environmental factors seem to have a crucial role in its development through microbiota modulation. The aim of this study was to determine the HLA risk prevalence and to compare the fecal microbiota structure of Mexican children with T1D at onset and after treatment for more than 2 years. A case-control study was conducted in Mexican mestizo children, aged 7-18 years (8 newly diagnosed, 13 controlled T1D cases after 2 years treatment and 8 healthy controls). Predisposing haplotypes were typed and the fecal DNA was extracted; the V4 region of the 16S rRNA gene was amplified and pyrosequenced. All of the T1D cases had at least one HLA risk allele, principally the DQA1*0301. The newly diagnosed T1D cases had high levels of the genus Bacteroides (p<0.004), whereas the control group had a gut microbiota dominated by Prevotella. Children with T1D treated for 蠅2 years had levels of Bacteroides and Prevotella tending to those of the control group. The gut microbiota of newly diagnosed T1D cases is altered, but involving of causes or consequences remains unclear.
    The FASEB Journal 04/2014; 28(1):S1118.3. · 5.04 Impact Factor
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    ABSTRACT: Abstract Immediately following birth, the gastrointestinal tract is colonized with a complex community of bacteria, which helps shape the immune system. Under conditions of health, the immune system is able to differentiate between innocuous antigens, including food protein and commensals, and harmful antigens such as pathogens. However, patients with celiac disease (CD) develop an intolerance to gluten proteins which results in a pro-inflammatory T-cell mediated immune response with production of anti-gluten and anti-tissue transglutaminase antibodies. This adaptive immune response, in conjunction with activation of innate inflammatory cells, lead to destruction of the small intestinal mucosa. Overall 30% of the global population has genetic risk to develop CD. However, only a small proportion develop CD, suggesting that additional environmental factors must play a role in disease pathogenesis. Alterations in small intestinal microbial composition have recently been associated with active CD, indicating a possible role for the microbiota in CD. However, studies demonstrating causality are lacking. This review will highlight the recent data on the potential role of the microbiota in CD pathogenesis, the potential mechanisms, and discuss future research directions.
    Gut Microbes 09/2014; 5(5). DOI:10.4161/19490976.2014.969635
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