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Celiac Disease Prevention

Prevention of Celiac Disease in Children at Genetic Risk - Optimized Introduction of Gluten and Follow-up of Immunization

Status
UNKNOWN
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT00617838
Enrollment
168
Registered
2008-02-18
Start date
2007-10-31
Completion date
2014-12-31
Last updated
2013-08-23

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Celiac Disease

Keywords

Celiac disease, genetic risk, gluten introduction, predicting antibodies

Brief summary

Celiac disease is an autoimmune disease induced by wheat gluten. Destruction of epithelial cells and microvilli on gut mucosa is causing a flat mucosa and an absorption defect. The diagnosis is based on typical microscopical finding in biopsy specimens but serum antibodies to tissue transglutaminase and certain gliadin peptides are strongly associated with the pathology. Severe diarrhoea associated with growth disturbance in infancy was historically characterising the disease but is nowadays rare. Clinically more mild forms including silent disease are very common. Studies based on antibody screening and biopsies done in autoantibody positive subjects have confirmed a frequency of about 1-2% in adult population. Undiagnosed disease is associated with deficiencies of nutrients and vitamins leading to various chronic symptoms like anaemia, osteoporosis and general fatigue. It has also been recently found that undiagnosed celiac disease may be associated with general underachievement in society probably associated with common psychological symptoms like fatigue and depression during the adolescence. The disease is treated by complete elimination of wheat, rye and barley in the diet, which is laborious and causing considerable extra costs in nutrition. Much progress has been recently made in understanding of the genetic background and immune markers associated with the disease as well as in understanding those patterns of gluten introduction in infancy, which might be connected to a high disease risk. Our aim in this study is in the first phase to identify children at high genetic risk (around 10%) and in a follow-up study to define: 1. Are the age, dose of gluten and presence of simultaneous breast feeding at the introduction of gluten associated with the risk of celiac disease? 2. Is it possible to decrease the frequency of celiac disease by nutritional counselling? 3. Is it possible to predict development of celiac disease by immunological tests before the development of mucosal lesion If we can confirm, that optimising the conditions at the introduction of wheat gluten in infancy diet significantly reduces the disease incidence, will this have an important effect on the nutritional recommendations concerning the diet in infancy. Combining genetic screening and immunological tests might also offer a way to reduce the frequency of celiac disease and help in early diagnosis and organisation of an adequate treatment

Interventions

OTHEROptimal gluten introduction

Optimization of gluten introduction by nutritional counselling

Sponsors

University of Eastern Finland
CollaboratorOTHER
University of Turku
CollaboratorOTHER
Finnish Institute for Health and Welfare
CollaboratorOTHER_GOV
Päivikki and Sakari Sohlberg Foundation, Finland
CollaboratorOTHER
Kätilöopisto Maternity Hospital
CollaboratorOTHER
Kuopio University Hospital
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
PREVENTION
Masking
SINGLE (Subject)

Eligibility

Sex/Gender
ALL
Age
No minimum to 2 Months
Healthy volunteers
Yes

Inclusion criteria

* Presence of HLA-risk alleles DQA1\*05 and DQB1\*02

Exclusion criteria

* Lack of these HLA risk alleles

Design outcomes

Primary

MeasureTime frame
development of transglutaminase antibodies2-4 year age

Secondary

MeasureTime frame
gliadin peptide antibodies2-4 years
mucosal biopsy in TGA positive childre2-4 years

Countries

Finland

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026