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Celiac (and Related Disorders) Research

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Development of autoimmunity to transglutaminase C in children of patients with type 1 diabetes: relationship to islet autoantibodies and infant feeding.

Hummel S, Hummel M, Banholzer J, Hanak D, Mollenhauer U, Bonifacio E, Ziegler AG.

Diabetes Research Institute, Munich, Germany.

AIMS/HYPOTHESIS: Coeliac disease and transglutaminase antibodies are common in patients with type 1 diabetes and their relatives. We investigated the development of transglutaminase antibodies and analysed potential risk factors for coeliac disease autoimmunity in first-degree relatives of patients with type 1 diabetes. METHODS: The study was conducted by prospective observational follow-up from birth of 1,511 children at increased risk of type 1 diabetes or coeliac disease born in Germany between 1989 and 2000. Mean follow-up was to age 7.6 years. Children were tested for transglutaminase and islet autoantibodies. Children were classified as transglutaminase antibody-positive if antibodies were detected by both ELISA and radiobinding assays. RESULTS: The risk of developing transglutaminase antibodies was 4.9% by age 8 years (n=63; 95% CI, 3.7-6.1%). Transglutaminase antibodies developed at an older age than islet autoantibodies (median age, 4.9 vs 2.3 years; p<0.005), and only three children developed both transglutaminase antibodies and islet autoantibodies. Multivariate analysis indicated an increased risk of transglutaminase antibodies in children with the HLA-DRB1*03 allele (hazard ratio for heterozygous DR3, 5.5; 95% CI, 2.9-10.2; hazard ratio for homozygous DR3, 16.2; 95% CI, 6.7-39; p<0.0001) and in children with impaired uterine growth (birth weight < or = 1st percentile, hazard ratio, 3.1; 95% CI, 1.1-7.8, p=0.03). Neither breast-feeding or its duration nor the age of first exposure to gluten was associated with the risk of developing transglutaminase antibodies. CONCLUSIONS/INTERPRETATION: Coeliac disease autoimmunity is initiated later than islet autoimmunity in children who are at risk. An influence of infant nutrition on the development of coeliac disease autoimmunity could not be confirmed in this prospective study.

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Clinical, subclinical and potential autoimmune diseases in an Italian population of children with Celiac disease.

Guariso G, Conte S, Presotto F, Basso D, Brotto F, Vison

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Correction of Celiac Disease After Allogeneic Hematopoietic Stem Cell Transplantation for Acute Myelogenous Leukemia.

Kline RM, Neudorf SM, Baron HI.

aPediatric Division, Comprehensive Cancer Centers of Nevada, Las Vegas, Nevada.

Allogeneic hematopoietic stem cell transplantation has been shown to correct or improve a variety of autoimmune disorders. This has not been reported for celiac disease, but transmission to a hematopoietic stem cell transplantation recipient from a donor with celiac disease has been reported. We report a 12-year-old girl with celiac disease who was diagnosed with acute leukemia and received an allogeneic hematopoietic stem cell transplant. Her celiac disease resolved after the hematopoietic stem cell transplant.

PMID: 17893186 [PubMed - as supplied by publisher]

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Natural history of antibodies to deamidated gliadin peptides and transglutaminase in early childhood celiac disease.

Liu E, Li M, Emery L, Taki I, Barriga K, Tiberti C, Eisenbarth GS, Rewers MJ, Hoffenberg EJ.

Section of Gastroenterology, Hepatology and Nutrition, The Children's Hospital, and Department of Pediatrics, Barbara Davis Center for Childhood Diabetes, University of Colorado at Denver and Health Sciences Center, Denver, CO, USA. edwin.liu@uchsc.edu

INTRODUCTION: Gliadin proteins play a key role in the pathogenesis of celiac disease; however, as a screen for celiac disease, anti-gliadin antibody testing has been replaced by the more sensitive and specific serological assays for transglutaminase autoantibodies (TGAA). A new generation of anti-gliadin antibody assays has been developed to detect synthetic, deamidated homologous gliadin peptides (DGP) with high sensitivity and specificity. METHODS: Sera were collected prospectively from children with an increased risk for celiac disease as part of an ongoing study at Denver, and studied for the development of celiac autoimmunity. We investigated the high-performance DGP antibody assay in 50 TGAA-positive children both before the development of celiac autoimmunity and following the institution of a gluten-free diet to determine the relationship of DGP antibodies to TGAA. TGAA were measured by an in-house radioassay. RESULTS: DGP antibodies and TGAA parallel each other over the period of years children were studied. DGP antibodies resolved sooner than TGAA in subjects on a gluten-free diet. DGP antibodies appeared earlier than TGAA in 9 children. CONCLUSIONS: Measuring DGP antibodies may be more useful than TGAA in monitoring children on a gluten-free diet. DGP antibodies can precede the appearance of TGAA in some at-risk children.

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Subclinical neurological abnormalities in children with celiac disease receiving a gluten-free diet.

Cakir D, Tosun A, Polat M, Celebisoy N, Gokben S, Aydogdu S, Yagci RV, Tekgul H.

Department of Pediatrics, Ege University Medical School, Izmir, Turkey.

OBJECTIVES: Because clinically evident manifestations are frequent in adults with celiac disease (celiac disease), we aimed to investigate whether early neurological abnormalities may be detected in children with celiac disease. METHODS: Electroencephalography, electromyography, and somatosensory evoked potentials were performed in children with celiac disease receiving a gluten-free diet. RESULTS: The neurophysiological tests revealed subclinical neurological abnormalities associated with celiac disease in 3 (11%) of 27 children: 2 had peripheral polyneuropathy documented with electromyography, and 1 had prolonged latencies in somatosensory evoked potential. Magnetic resonance imaging showed abnormalities in 2 (7.4%) of children: pontine demyelinization in 1 and cortical atrophy in the other. CONCLUSIONS: Because the rate of neurological problems is increased in children with celiac disease, neurological abnormalities should be carefully investigated early after the diagnosis of celiac disease is made.

PMID: 17873753 [PubMed - in process]

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