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1.  Celiac disease risk varies between birth cohorts, generating hypotheses about causality: evidence from 36 years of population-based follow-up 
BMC Gastroenterology  2014;14:59.
Background
Celiac disease (CD) is a major public health problem with estimated 1-3% prevalence in the general population. In recent years an increase in CD prevalence has been reported both in Sweden and worldwide. This study aimed at examining the annual incidence rate of biopsy-proven celiac disease among children in Sweden over a 36-year period, to assess variations by age, sex and birth cohort, and to assess the clinical impact of these changes.
Methods
The National Swedish Childhood CD Register was used to identify 9107 children aged 0–14.9 years who were diagnosed with CD during the period 1973 to 2009. From 1973 to 1990 the register covered 15% of the nation, this increased to 40% during 1991–1997; a full national coverage was obtained from 1998 onwards. Estimations for the annual incidence rate, cumulative incidence and clinical impact by age groups, calendar month and birth cohorts were made.
Results
CD incidence is continuing to increase in the child population aged 2–14.9 years. A continued variation in CD incidence was observed in children aged 0–1.9 years, characterized by a marked decrease in most recent years. The median age at diagnosis has increased from 1.0 year in the 1970s to 6.8 years in 2009. The average number of new cases has risen from ~200 during 1973–1983 to ~600 during 2004–2009. In the birth cohorts of 2000–2002 the cumulative incidence even exceeded that of the epidemic cohorts at comparable ages. The highest cumulative incidence was observed in the birth cohorts of 1985–1995 and 2000–2002.
Conclusions
CD risk varies between birth cohorts, suggesting cyclic environmental and/or lifestyle risk factors in CD etiology. More research on underlying risk factors is required in order to move forward with preventive strategies.
doi:10.1186/1471-230X-14-59
PMCID: PMC3977663  PMID: 24693975
Celiac disease; Children; Incidence; Epidemiology
2.  Prevotella jejuni sp. nov., isolated from the small intestine of a child with coeliac disease 
Five obligately anaerobic, Gram-stain-negative, saccharolytic and proteolytic, non-spore-forming bacilli (strains CD3 : 27, CD3 : 28T, CD3 : 33, CD3 : 32 and CD3 : 34) are described. All five strains were isolated from the small intestine of a female child with coeliac disease. Cells of the five strains were short rods or coccoid cells with longer filamentous forms seen sporadically. The organisms produced acetic acid and succinic acid as major metabolic end products. Phylogenetic analysis based on comparative 16S rRNA gene sequence analysis revealed close relationships between CD3 : 27, CD3 : 28T and CD3 : 33, between CD3 : 32 and Prevotella histicola CCUG 55407T, and between CD3 : 34 and Prevotella melaninogenica CCUG 4944BT. Strains CD3 : 27, CD3 : 28T and CD3 : 33 were clearly different from all recognized species within the genus Prevotella and related most closely to but distinct from P. melaninogenica. Based on 16S rRNA, RNA polymerase β-subunit (rpoB) and 60 kDa chaperonin protein subunit (cpn60) gene sequencing, and phenotypic, chemical and biochemical properties, strains CD3 : 27, CD3 : 28T and CD3 : 33 are considered to represent a novel species within the genus Prevotella, for which the name Prevotella jejuni sp. nov. is proposed. Strain CD3 : 28T ( = CCUG 60371T = DSM 26989T) is the type strain of the proposed novel species. All five strains were able to form homologous aggregates, in which tube-like structures were connecting individual bacteria cells. The five strains were able to bind to human intestinal carcinoma cell lines at 37 °C.
doi:10.1099/ijs.0.052647-0
PMCID: PMC3836492  PMID: 23793857
3.  Intestinal T-cell Responses in Celiac Disease – Impact of Celiac Disease Associated Bacteria 
PLoS ONE  2013;8(1):e53414.
A hallmark of active celiac disease (CD), an inflammatory small-bowel enteropathy caused by permanent intolerance to gluten, is cytokine production by intestinal T lymphocytes. Prerequisites for contracting CD are that the individual carries the MHC class II alleles HLA-DQ2 and/or HLA-DQ8 and is exposed to gluten in the diet. Dysbiosis in the resident microbiota has been suggested to be another risk factor for CD. In fact, rod shaped bacteria adhering to the small intestinal mucosa were frequently seen in patients with CD during the “Swedish CD epidemic” and bacterial candidates could later be isolated from patients born during the epidemic suggesting long-lasting changes in the gut microbiota. Interleukin-17A (IL-17A) plays a role in both inflammation and anti-bacterial responses. In active CD IL-17A was produced by both CD8+ T cells (Tc17) and CD4+ T cells (Th17), with intraepithelial Tc17 cells being the dominant producers. Gluten peptides as well as CD associated bacteria induced IL-17A responses in ex vivo challenged biopsies from patients with inactive CD. The IL-17A response was suppressed in patients born during the epidemic when a mixture of CD associated bacteria was added to gluten, while the reverse was the case in patients born after the epidemic. Under these conditions Th17 cells were the dominant producers. Thus Tc17 and Th17 responses to gluten and bacteria seem to pave the way for the chronic disease with interferon-γ-production by intraepithelial Tc1 cells and lamina propria Th1 cells. The CD associated bacteria and the dysbiosis they might cause in the resident microbiota may be a risk factor for CD either by directly influencing the immune responses in the mucosa or by enhancing inflammatory responses to gluten.
doi:10.1371/journal.pone.0053414
PMCID: PMC3541273  PMID: 23326425
4.  A gluten-free diet effectively reduces symptoms and health care consumption in a Swedish celiac disease population 
BMC Gastroenterology  2012;12:125.
Background
A gluten-free diet is the only available treatment for celiac disease. Our aim was to investigate the effect of a gluten-free diet on celiac disease related symptoms, health care consumption, and the risk of developing associated immune-mediated diseases.
Methods
A questionnaire was sent to 1,560 randomly selected members of the Swedish Society for Coeliacs, divided into equal-sized age- and sex strata; 1,031 (66%) responded. Self-reported symptoms, health care consumption (measured by health care visits and hospitalization days), and missed working days were reported both for the year prior to diagnosis (normal diet) and the year prior to receiving the questionnaire while undergoing treatment with a gluten-free diet. Associated immune-mediated diseases (diabetes mellitus type 1, rheumatic disease, thyroid disease, vitiligo, alopecia areata and inflammatory bowel disease) were self-reported including the year of diagnosis.
Results
All investigated symptoms except joint pain improved after diagnosis and initiated gluten-free diet. Both health care consumption and missed working days decreased. Associated immune-mediated diseases were diagnosed equally often before and after celiac disease diagnosis.
Conclusions
Initiated treatment with a gluten-free diet improves the situation for celiac disease patients in terms of reduced symptoms and health care consumption. An earlier celiac disease diagnosis is therefore of great importance.
doi:10.1186/1471-230X-12-125
PMCID: PMC3482575  PMID: 22984893
5.  Delay to celiac disease diagnosis and its implications for health-related quality of life 
BMC Gastroenterology  2011;11:118.
Background
To determine how the delay in diagnosing celiac disease (CD) has developed during recent decades and how this affects the burden of disease in terms of health-related quality of life (HRQoL), and also to consider differences with respect to sex and age.
Methods
In collaboration with the Swedish Society for Coeliacs, a questionnaire was sent to 1,560 randomly selected members, divided in equal-sized age- and sex strata, and 1,031 (66%) responded. HRQoL was measured with the EQ-5D descriptive system and was then translated to quality-adjusted life year (QALY) scores. A general population survey was used as comparison.
Results
The mean delay to diagnosis from the first symptoms was 9.7 years, and from the first doctor visit it was 5.8 years. The delay has been reduced over time for some age groups, but is still quite long. The mean QALY score during the year prior to initiated treatment was 0.66; it improved after diagnosis and treatment to 0.86, and was then better than that of a general population (0.79).
Conclusions
The delay from first symptoms to CD diagnosis is unacceptably long for many persons. Untreated CD results in poor HRQoL, which improves to the level of the general population if diagnosed and treated. By shortening the diagnostic delay it is possible to reduce this unnecessary burden of disease. Increased awareness of CD as a common health problem is needed, and active case finding should be intensified. Mass screening for CD might be an option in the future.
doi:10.1186/1471-230X-11-118
PMCID: PMC3233515  PMID: 22060243

Results 1-5 (5)