13.08.2006, 20:17
kleinen Zöliakie-Patienten
Unten angeführt eine interessante Veröffentlichung, die bei genetischer Disposition zu Zöliakie Antikörper auf Antigliadin und Kuhmilch – Beta-Lactoglobulin bei Kleinkindern untersuchte . Dabei stellte sich heraus, dass sowohl IgG und IgA – Antikörper auf Antigliadin und Beta-Lactoglobulin gefunden wurden. Bei behandelten Kindern allerdings keine Antikörper mehr auf Gliadin ( "Behandlung" bedeutet bei Zöliakie : glutenfreie Ernährung!) aber noch auf Beta- Lactoglobulin!
Sehe ich da meine Vermutung nicht bestätigt, dass >>Milch<< ( hier vor allem Beta-lactoglobulin) mit der „Wegbereiter“ für Zöliakie/ Sprue ist? Und dass die „passagere LI“( = vorübergehende) , wie sie bei Erwachsenen mit Sprue/Zöliakie immer erwähnt wird ( vor allem, dass sie wieder „verschwinden“ würde), nicht das Hauptproblem darstellt, sondern die „Unverträglichkeit“ auf Beta-Lactoglobulin !
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2: Scand J Gastroenterol. 2006 Aug;41(8):919-28.
Effect of HLA DQ2, dietary exposure and coeliac disease on the development of antibody response to gliadin in children.
Ludvigsson JF, Eylert M, Ilonen J, Ludvigson J, Vaarala O.
Division of Paediatrics, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linkoping University, Sweden.
Objective. To study the effect of HLA DQ2, dietary history and development of coeliac disease (CD) on the induction of antibody response to wheat gliadin and cow's milk, beta-lactoglobulin between 1 and 2.5 years of age in children who developed CD and in healthy children.
Material and methods. Infants participating in a birth cohort study (the ABIS study) in Sweden were studied. Thirty-nine ( 39) children developed CD (=cases), confirmed through biopsy, during follow-up until 2.5-5 years of age. A total of 181 healthy control children were matched for duration of exclusive breast-feeding, birth-weight, gender, maternal smoking and season of birth. IgG and IgA antigliadin and anti-beta-lactoglobulin antibodies were measured using enzyme immunoassay (EIA). The effects of HLA-risk genotypes, DQ2 and DQ8, on CD were also considered.
Results. Children who developed CD had higher IgG and IgA antigliadin and anti-beta-lactoglobulin antibody levels at 1 year of age than controls (all comparisons: p<0.001). Similar differences were seen between cases with as yet undiagnosed CD by 1 year of age and controls, and also when cases were compared with HLA-matched controls. Higher levels of IgG and IgA antibodies to beta-lactoglobulin (p=0.003; p=0.001), but not to gliadin, were found in treated cases versus controls at 2.5 years of age. HLA-DQ2-positive healthy children had lower levels of IgG and IgA antigliadin antibodies than HLA-DQ2 negative controls at 1 year of age (p=0.004; p=0.012).
Conclusions. Enhanced humoral response emerging not only to gliadin, but also to other food antigens seems to be primarily associated with CD. Poor induction of antibody response to wheat gliadin in healthy children with the HLA-DQ2 risk molecule could at least partly explain the genetic predisposition to gluten intolerance and CD.
PMID: 16803690
http://www.ncbi.nlm.nih.gov/entrez/query...t=Abstract
Unten angeführt eine interessante Veröffentlichung, die bei genetischer Disposition zu Zöliakie Antikörper auf Antigliadin und Kuhmilch – Beta-Lactoglobulin bei Kleinkindern untersuchte . Dabei stellte sich heraus, dass sowohl IgG und IgA – Antikörper auf Antigliadin und Beta-Lactoglobulin gefunden wurden. Bei behandelten Kindern allerdings keine Antikörper mehr auf Gliadin ( "Behandlung" bedeutet bei Zöliakie : glutenfreie Ernährung!) aber noch auf Beta- Lactoglobulin!
Sehe ich da meine Vermutung nicht bestätigt, dass >>Milch<< ( hier vor allem Beta-lactoglobulin) mit der „Wegbereiter“ für Zöliakie/ Sprue ist? Und dass die „passagere LI“( = vorübergehende) , wie sie bei Erwachsenen mit Sprue/Zöliakie immer erwähnt wird ( vor allem, dass sie wieder „verschwinden“ würde), nicht das Hauptproblem darstellt, sondern die „Unverträglichkeit“ auf Beta-Lactoglobulin !
*********
2: Scand J Gastroenterol. 2006 Aug;41(8):919-28.
Effect of HLA DQ2, dietary exposure and coeliac disease on the development of antibody response to gliadin in children.
Ludvigsson JF, Eylert M, Ilonen J, Ludvigson J, Vaarala O.
Division of Paediatrics, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linkoping University, Sweden.
Objective. To study the effect of HLA DQ2, dietary history and development of coeliac disease (CD) on the induction of antibody response to wheat gliadin and cow's milk, beta-lactoglobulin between 1 and 2.5 years of age in children who developed CD and in healthy children.
Material and methods. Infants participating in a birth cohort study (the ABIS study) in Sweden were studied. Thirty-nine ( 39) children developed CD (=cases), confirmed through biopsy, during follow-up until 2.5-5 years of age. A total of 181 healthy control children were matched for duration of exclusive breast-feeding, birth-weight, gender, maternal smoking and season of birth. IgG and IgA antigliadin and anti-beta-lactoglobulin antibodies were measured using enzyme immunoassay (EIA). The effects of HLA-risk genotypes, DQ2 and DQ8, on CD were also considered.
Results. Children who developed CD had higher IgG and IgA antigliadin and anti-beta-lactoglobulin antibody levels at 1 year of age than controls (all comparisons: p<0.001). Similar differences were seen between cases with as yet undiagnosed CD by 1 year of age and controls, and also when cases were compared with HLA-matched controls. Higher levels of IgG and IgA antibodies to beta-lactoglobulin (p=0.003; p=0.001), but not to gliadin, were found in treated cases versus controls at 2.5 years of age. HLA-DQ2-positive healthy children had lower levels of IgG and IgA antigliadin antibodies than HLA-DQ2 negative controls at 1 year of age (p=0.004; p=0.012).
Conclusions. Enhanced humoral response emerging not only to gliadin, but also to other food antigens seems to be primarily associated with CD. Poor induction of antibody response to wheat gliadin in healthy children with the HLA-DQ2 risk molecule could at least partly explain the genetic predisposition to gluten intolerance and CD.
PMID: 16803690
http://www.ncbi.nlm.nih.gov/entrez/query...t=Abstract