Coeliac disease in The Netherlands

Leiden University, Leyden, South Holland, Netherlands
Scandinavian Journal of Gastroenterology (Impact Factor: 2.36). 05/2004; 39(4):359-64. DOI: 10.1080/00365520310008503
Source: PubMed


The prevalence of adult coeliac disease in The Netherlands was studied in the Dutch Coeliac Disease Society and in blood donors but not in the general population. We therefore studied the prevalence of recognized and unrecognized coeliac disease in a large cohort, representative of the adult Dutch general population. Blood samples were available for anonymous research, as well as data on dietary habits, self-reported physical characteristics, health problems, quality of life and socio-economic circumstances.
Subjects included 50,760 individuals who had previously participated in two large population-based studies on health status in relation to lifestyle factors. Recognized coeliac disease was studied in all subjects by identification of self-reported adherence to a gluten-free diet and subsequent confirmation of the diagnosis of coeliac disease. Unrecognized coeliac disease was studied in a random sample of 1440 out of the 50,760 subjects through serologic screening and human lymphocyte antigen (HLA) typing.
The prevalence of recognized coeliac disease was 0.016% (95% confidence interval 0.008-0.031) and of unrecognized coeliac disease 0.35% (95% confidence interval 0.15-0.81). Menarcheal age was higher in women with recognized coeliac disease than in women without coeliac disease.
The prevalence of adult recognized coeliac disease in The Netherlands is one of the lowest in Europe, while the prevalence of unrecognized coeliac disease is comparable with that in other European countries. Adult coeliac disease is strongly under diagnosed in The Netherlands. The higher menarcheal age in women with recognized coeliac disease may be explained by diagnostic delay.

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    • "Large-scale screening studies have shown a CD prevalence of nearly 0.5–1.0% in both adults and children [5] [6] [7], but a considerable number of patients remain unrecognized and thus untreated. This is partly due to the variable clinical presentation of CD, which can vary from a typical malabsorption syndrome or extraintestinal manifestations to a clinically silent disease, often detected by serological screening of those subjects at risk. "
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    ABSTRACT: IgA antibodies against tissue-transglutaminase (anti-tTG-IgA) and IgA and IgG antibodies against deamidated gliadin peptides (anti-DGP-IgA and anti-DGP-IgG) are considered specific for celiac disease (CD) whereas, patients with chronic liver disorders have an increased risk of latent CD development. We investigated the prevalence and clinical significance of anti-DGP-IgA, anti-DGP-IgG and anti-tTG-IgA in a large cohort of patients with chronic liver diseases. 668 patients without gastrointestinal symptoms (426 viral hepatitis, 94 autoimmune liver diseases, 61 alcoholic disease, 46 non-alcoholic fatty liver disease, 41 with other liver disorders) were investigated by ELISAs (INOVA Diagnostics). Patients positive for at least one autoantibody invited for a small-intestinal biopsy and HLA-DQ typing. Anti-DGP-IgA were detected in 8.5%, anti-DGP-IgG in only one (0.15%, P<0.001) and anti-tTG-IgA in 5.8% of patients (P=0.05). Fifty-two were anti-DGP-IgA(+)/anti-tTG-IgA(-), 34 anti-DGP-IgA(-)/anti-tTG-IgA(+), and 5 anti-DGP-IgA(+)/anti-tTG-IgA(+). Anti-DGP-IgA positivity was associated with older age (P<0.05), cirrhosis (P<0.05) and increased IgA (P<0.05) whereas, anti-tTG-IgA only with cirrhosis (P<0.05). Histology and HLA-typing compatible with CD was revealed in 4/14 anti-DGP-IgA(+)/anti-tTG-IgA(-), 0/13 anti-DGP-IgA(-)/anti-tTG-IgA(+) and 2/2 anti-DGP-IgA(+)/anti-tTG-IgA(+). All 6 patients diagnosed with CD were anti-DGP-IgA(+) and only 2 anti-tTG-IgA(+). Although a significant number of patients had detectable CD-related autoantibodies, anti-DGP-IgA test seems better than anti-tTG-IgA for unmasking occult forms of CD in patients with chronic liver disorders. The known good performance for CD diagnosis of anti-DGP-IgG test was not confirmed in this specific group of patients.
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    ABSTRACT: Celiac disease is an intolerance to dietary gluten in genetically predisposed individuals, leading to alterations of the small bowel mucosa. The treatment consists of a life-long, gluten-free diet. The aims of this thesis were to measure some of the environmental factors considered to play a role in the prevention of celiac disease. For that purpose breast milk was studied on the presence of glutenpeptides and a food frequency questionnaire was developed and validated to quantify gluten intake in young infants. Furthermore, the current treatment at different ages and the ability to develop gluten tolerance were studied. It became clear that the nutrient intake of adolescents on a gluten-free diet can be ameliorated, and that the rather new naturally gluten-free cereal tef is frequently used by Dutch celiac patients and a wide majority of them can consume tef without clinical symptoms. Therefore tef can be a valuable addition to their diet. Although celiac disease is considered to be a permanent condition, we made an attempt to find patients who have become tolerant to gluten. We found 2 of these exceptional patients and found that one of them had HLA-typing different from HLA-DQ2/DQ8, suggesting that genetic factors may play a role in the development of tolerance. The underlying mechanisms leading to prevention, disease development or tolerance to gluten are complex and need to be further studied.
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    ABSTRACT: Screening studies indicate a prevalence of coeliac disease (CD) of up to 1% in populations of European ancestry, yet the majority of cases remain undiagnosed. Serological markers for CD now available have high sensitivity and specificity, offering the option of mass population screening. The principles of disease screening as set out by Wilson and Jugner can be applied to CD to predict whether this is appropriate. CD is an important health problem for the individual and the community because of high prevalence, associated specific and non-specific morbidity, and long-term complications of which the most important are gut malignancy and osteoporosis. However, recent studies indicate that the prevalence of malignancy and the health impact of osteoporosis are much less than previously supposed, so the prophylactic benefits of early diagnosis through screening may be low. While CD has an accepted and effective treatment, dietary gluten exclusion, this is difficult for the individual and asymptomatic cases may be poorly motivated to comply. Diagnosis of CD is by histological confirmation on duodenal biopsy. We now recognise milder degrees of gluten sensitive enteropathy without villous atrophy (Marsh I, II lesions) and the benefits to the individual by identifying these early lesions through screening is unknown: whether to treat such individuals needs to be agreed before programmes commence. Screening with serum antibodies is relatively non-invasive but may have to be repeated during each individual's lifetime. HLA typing beforehand to identify the 30% of the population with DQ2 or DQ8, who are at potential risk of CD, will allow one-off exclusion of a large percentage of the population but like all genetic testing has ethical implications. The economic costs of screening and treatment versus morbidity prevented have not been calculated.
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