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Even small amounts of gluten cause relapse in children with celiac disease
Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Neuroscience and Locomotion, Pathology. Linköping University, Department of Molecular and Clinical Medicine, Medical Microbiology. Linköping University, Faculty of Health Sciences.
Linköping University, Department of Molecular and Clinical Medicine, Pediatrics. Linköping University, Faculty of Health Sciences.
2002 (English)In: Journal of Pediatric Gastroenterology and Nutrition - JPGN, ISSN 0277-2116, E-ISSN 1536-4801, Vol. 34, no 1, 26-30 p.Article in journal (Refereed) Published
Abstract [en]

Background: Previously, a gluten challenge was customary to establish the diagnosis of celiac disease in children. There are no clear recommendations on how to perform this challenge or what markers to rely on for timing the biopsy after the challenge. The authors' aim was to monitor gluten intake, clinical symptoms, and antibody kinetics to evaluate the influence of gluten exposure during the challenge.

Methods: Twenty-five children under investigation for suspected celiac disease were challenged. One child was excluded because blood samples, food records, or biopsy was lacking. Median age at the postchallenge biopsy was 3.8 (2.7-8.8) years. The families kept daily records of the children's gluten intake and of symptoms that occurred. Blood samples were taken monthly for analysis of antigliadin and endomysium antibodies and total immunoglobulin A (IgA). A third biopsy was performed when clinical symptoms suggested a relapse.

Results: All 24 children showed deterioration of the mucosa or elevated antibodies during gluten challenge. Median duration of the challenge was 13 (5-51) weeks, and mean gluten intake was 1.7 (0.2-4.3) g/d and 0.1 (0.02-0.26) g/kg daily.

Conclusions: Gluten intake during the challenge varied widely, and the parents were unable to give their children the recommended amount. Despite the small amounts given, all children showed signs of relapse at a clinical, laboratory, or histologic level. Much smaller amounts of gluten than previously suggested seem sufficient to cause relapse during gluten challenge in children.

Place, publisher, year, edition, pages
2002. Vol. 34, no 1, 26-30 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-26463DOI: 10.1097/00005176-200201000-00007Local ID: 11011OAI: oai:DiVA.org:liu-26463DiVA: diva2:247012
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2012-09-20Bibliographically approved
In thesis
1. Clinical and epidemiological aspects of childhood celiac disease
Open this publication in new window or tab >>Clinical and epidemiological aspects of childhood celiac disease
2002 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Background: Celiac disease (CD) is one of the most common chronic diseases in childhood in many countries. It is a small intestinal disease, caused by gluten in genetically predisposed individuals, but underlying immunological mechanisms are not exactly known. Gluten is found in wheat, rye and barley, and possibly in oats. The clinical presentation of CD varies from overt to no symptoms at all. Treatment with gluten free diet (GFD) heals the mucosa and symptoms disappear. The varying clinical presentation makes the evaluation of the "true" prevalence difficult. When screening with serum antibodies, similar prevalence is found in several countries. The reported increase of clinically detected cases among Swedish children in the mid 1980s attracted much interest and was publicly debated. Infant feeding changes was focused on, but new diagnostic tools were also introduced during this period.

Aims: To describe epidemiological changes in the county of Östergötland from 1980 to 2001. To analyse the possible influence of diagnostic activity and accuracy and the possible influence of certain infant feeding patterns on disease occurrence. To study gluten intake, clinical, histological and immunological parameters during gluten challenge. To evaluate the practical usefulness of the nitric oxide (NO) analysis in CD.

Material and methods: All children (0-17.9 years) investigated for suspected CD in the county of Östergötland 1980-2001 were studied regarding disease occurrence, diagnostic activity and accuracy. Data on infant feeding were analysed in 72 CD children and 288 agematched referents. During gluten challenge 25 children were studied regarding gluten intake, serum antibodies, NO products in the urine, clinical symptoms and mucosal histology. NO products were also measured at different stages of CD investigation in !37 children.

Results: The incidence rate of CD in small children has fluctuated over the study period. How, or whether, infant feeding and/or diagnostic tools have influenced this is not known.

CD children were significantly shorter breastfed, more seldom breastfed at gluten introduction, and started more often with follow-up formula than porridge. This could be interpreted in two ways. Breastfeeding per se could protect against CD, but it is also known that a breastfed baby consumes lower amounts of gluten at the time of introduction. The lower exposure can make symptoms more vague in early childhood and thus postpone the diagnosis.

Gluten intake during challenge varied a lot. Some CD children reacted to minute amounts of gluten. Despite the small amounts given, all children showed signs of relapse at a clinical, serological, or histological level.

CD children on a gluten containing diet have significantly higher levels of NO products in the urine, compared to reference children and to CD children on a GFD. NO products increased during gluten challenge, and doubled within four weeks of challenge. This is probably caused by iNOS activation and increased NO production in the diseased intestinal mucosa.

Conclusions: How, or whether, changes in infant feeding and/or new diagnostic tools influenced the fluctuating incidence of the disease is not known. Very small amounts of gluten caused relapse in CD children. NO products in the urine were elevated in CD children on a gluten diet, and doubled within four weeks of gluten challenge. NO analysis is simple and non-traumatic for the child, and could be of value as a diagnostic tool in celiac disease.

Abstract [en]

Bakgrund: Celiaki (glutenintolerans) är en av de vanligaste kroniska sjukdomarna hos barn, både i Sverige och i andra länder. Celiaki är en tunntarmssjukdom som orsakas av gluten hos personer med ärftlig benägenhet. Gluten finns i vete, råg, korn och kanske också i havre. Den bakomliggande immunologiska mekanismen är fortfarande inte helt känd. Celiaki kan ge varierande symptom, alltifrån kraftiga magtarmsymtom tiH nästan inga symtom alls. Om patienten håller glutenfri diet (GFD) läker tarmen och symtomen försvinner. Livslång GFD innebär fördelaktiga hälsoeffekter både på kort och på lång sikt.

Sjukdomens varierande symtomatologi gör det svårt att uppskatta den "sanna" förekomsten. Vid screening med serumantikroppar hittas ungefar samma förekomst av sjukdomen i olika länder. I mitten av 1980-talet ökade antalet kliniskt upptäckta fall bland svenska barn kraftigt. Detta rönte stort intresse och debatterades livligt, även i pressen. Förändringar i spädbarnsuppfödningen diskuterades som orsak, men nya diagnostiska metoder infördes också under perioden.

Mål: Att beskriva förändringar i förekomst av celiaki hos barn i Östergötland under åren 1980 till 2001. Att analysera eventuellt inflytande av träffsäkerhet och intensitet i diagnostiken samt spädbarnsuppfödning på sjukdomens förekomst. Att studera glutenintag, kliniska, immunologiska och histologiska parametrar under glutenprovokationen. Att utvärdera den praktiska nyttan av att mäta kvävemonoxid (NO)-metaboliter i urinen hos celiakibarn,

Material och metod: Alla barn (0-17 .9 år) som undersökts för misstänkt celiaki i Östergötland under åren1980-2001 registrerades. De studerades med avseende på sjukdomsförekomst samt träffsäkerhet och intensitet i diagnostiken. Uppfödningsdata från 72 celiakibam och deras 288 åldersmatchade kontroller analyserades. Under glutenprovokationen studerades glutenintag, kliniska symtom, NO-metaboliter i urinen, tarmslemhinnans histologi och serumantikroppar. På 137 bam under olika skeden i celiakiutredningen mättes också NO-metaboliter.

Resultat: Antalet nyinsjuknade småbarn varierade mycket kraftigt under de 22 år vi studerat. Huruvida förändrad spädbarnsuppfådning, och/eller fårbättrade diagnostiska metoder har påverkat sjukdomens förekomst går ej att avgöra.

Celiakibam hade ammats kortare tid, ammades mer sällan vid glutenintroduktionen och fick oftare börja med välling än med gröt. Det kan tolkas antingen som att amning i sig skyddar mot celiaki, men det är också känt att ett barn som ammas får i sig mindre mängder gluten vid introduktionen. Denna lägre exponering skulle kunna ge lindrigare symtom, och på så sätt försvåra och fårsena diagnosen.

Mängden gluten som barnen åt under provokationen varierade kraftigt. Vissa barn reagerade på ytterst små mängder. Trots de små mängder barnen fick i sig visade alla tecken på återfall i sjukdomen, antingen kliniskt, serologiskt eller histologiskt.

Hos celiakibam som åt g!uten uppmättes signifikant högre värden av NO-metaboliter i urinen än hos kontrollbarn och celiakibarn som inte åt gluten. Det beror antagligen på enzymaktivcring med ökad NO-produktion i den sjuka tarmslemhinnan. Under glutenprovokationen fördubblas NO-mctabolitema inom fyra veckor.

Sammanfattning: Huruvida fårändringar i spädbarnsuppfödningen och/eller förbättrade diagnostiska metoder har påverkat den varierande förekomsten av celiaki hos småbarn i Sverige går ej att avgöra. Mycket små glutenmängder var tillräckliga för att orsaka återfall under provokationen. NO-metaboliter i urinen var signifikant högre hos celiakibarn som åt gluten, än hos kontrollbarn och celiakibarn som åt glutenfritt Under provokationen stiger värdena till det dubbla inom f)rra veckor. NO-analysen är enkel, billig och dessutom skonsam för barnet. Den skulle därfår kunna utgöra ett värdefullt tillskott i den diagnostiska arsenalen.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2002. 104 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 746
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-26660 (URN)11226 (Local ID)91-7373-188-9 (ISBN)11226 (Archive number)11226 (OAI)
Public defence
2002-10-18, Berzeliussalen, Hälsouniversitetet, Linköping, 09:00 (Swedish)
Opponent
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2012-09-20Bibliographically approved

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Laurin, PiaFälth-Magnusson, Karin

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