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Salami, F.* ; Lee, H.* ; Freyhult, E.* ; Larsson, H.E.* ; Lernmark, A.* ; Törn, C.* ; TEDDY Study Group (Ziegler, A.-G. ; Beyerlein, A. ; Gavrisan, A. ; Gezginci, C. ; Hummel, M. ; Hummel, S. ; Knopff, A. ; Koletzko, S. ; Stock, J. ; Scholz, M. ; Roth, R. ; Warncke, K. ; Wendel, L. ; Winkler, C.)

Reduction in white blood cell, neutrophil, and red blood cell counts related to sex, HLA, and islet autoantibodies in Swedish TEDDY children at increased risk for type 1 diabetes.

Diabetes 67, 2329-2336 (2018)
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Open Access Green as soon as Postprint is submitted to ZB.
Islet autoantibodies (IAs) precede the clinical onset of type 1 diabetes (T1D); however, the knowledge is limited about whether the prodrome affects complete blood counts (CBCs) in 4- to 12-year-old children with increased genetic risk for T1D. This study tested whether CBCs were altered in 4- to 12-year-old children without (n = 376) or with one or several IAs against insulin, GAD65, or IA-2 (n = 72). CBC was analyzed during longitudinal follow-up in 448 Swedish children enrolled in The Environmental Determinants of Diabetes in the Young (TEDDY) study. A linear mixed-effects model was used to assess potential association between IA and CBC measurements over time. The white blood cell and neutrophil counts were reduced in children with IAs, primarily in boys. In contrast, girls had lower levels of hemoglobin and hematocrit. Positivity for multiple IAs showed the lowest counts in white blood cells and neutrophils in boys and red blood cells, hemoglobin, and hematocrit in girls. These associations were primarily observed in children with the HLA-DR3-DQ2/DR4-DQ8 genotype. We conclude that the reduction in neutrophils and red blood cells in children with multiple IAs and HLA-DR3-DQ2/DR4-DQ8 genotype may signal a sex-dependent islet autoimmunity detected in longitudinal CBCs.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Glutamic-acid Decarboxylase; T-cells; Environmental Determinants; Autoimmune-diseases; Young Teddy; Beta-cells; Progression; Pathogenesis; Susceptibility; Association
ISSN (print) / ISBN 0012-1797
e-ISSN 1939-327X
Journal Diabetes
Quellenangaben Volume: 67, Issue: 11, Pages: 2329-2336 Article Number: , Supplement: ,
Publisher American Diabetes Association
Publishing Place Alexandria, VA.
Reviewing status Peer reviewed