29 results on '"Bingley, P. J."'
Search Results
2. Worth the wait: type 1 diabetes prospective birth cohort studies enter adolescence
- Author
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Williams, A. J. K., primary and Bingley, P. J., additional
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- 2012
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3. An increased frequency of NK cell receptor and HLA-C group 1 combinations in early-onset type 1 diabetes
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Mehers, K. L., primary, Long, A. E., additional, van der Slik, A. R., additional, Aitken, R. J., additional, Nathwani, V., additional, Wong, F. S., additional, Bain, S., additional, Gill, G., additional, Roep, B. O., additional, Bingley, P. J., additional, and Gillespie, K. M., additional
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- 2011
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4. Diabetes mellitus among young adults in Sri Lanka—role of GAD antibodies in classification and treatment: The Sri Lanka Young Diabetes study
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Katulanda, P., primary, Shine, B., additional, Katulanda, G. W., additional, Silva, A., additional, Asfir, E. L., additional, Sheriff, R., additional, Somasundaram, N., additional, Long, A. E., additional, Bingley, P. J., additional, McCarthy, M. I., additional, Clark, A., additional, and Matthews, D. R., additional
- Published
- 2008
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5. Autoantibodies to islet antigen-2 are associated with HLA-DRB1*07 and DRB1*09 haplotypes as well as DRB1*04 at onset of type 1 diabetes: the possible role of HLA-DQA in autoimmunity to IA-2
- Author
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Williams, A. J. K., primary, Aitken, R. J., additional, Chandler, M. A.-M., additional, Gillespie, K. M., additional, Lampasona, V., additional, and Bingley, P. J., additional
- Published
- 2008
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6. GAD autoantibodies and epitope reactivities persist after diagnosis in latent autoimmune diabetes in adults but do not predict disease progression: UKPDS 77
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Desai, M., primary, Cull, C. A., additional, Horton, V. A., additional, Christie, M. R., additional, Bonifacio, E., additional, Lampasona, V., additional, Bingley, P. J., additional, Levy, J. C., additional, Mackay, I. R., additional, Zimmet, P., additional, Holman, R. R., additional, and Clark, A., additional
- Published
- 2007
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7. An association analysis of the HLA gene region in latent autoimmune diabetes in adults
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Desai, M., primary, Zeggini, E., additional, Horton, V. A., additional, Owen, K. R., additional, Hattersley, A. T., additional, Levy, J. C., additional, Walker, M., additional, Gillespie, K. M., additional, Bingley, P. J., additional, Hitman, G. A., additional, Holman, R. R., additional, McCarthy, M. I., additional, and Clark, A., additional
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- 2006
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8. Type 1 diabetes risk assessment: improvement by follow-up measurements in young islet autoantibody-positive relatives
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Achenbach, P., primary, Warncke, K., additional, Reiter, J., additional, Williams, A. J. K., additional, Ziegler, A. G., additional, Bingley, P. J., additional, and Bonifacio, E., additional
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- 2006
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9. The prevalence of insulin autoantibodies at the onset of Type 1 diabetes is higher in males than females during adolescence
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Williams, A. J. K., primary, Norcross, A. J., additional, Dix, R. J., additional, Gillespie, K. M., additional, Gale, E. A. M., additional, and Bingley, P. J., additional
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- 2003
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10. Three generations of autoimmune diabetes: an extended family study
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Douek, I. F., primary, Gillespie, K. M., additional, Dix, R. J., additional, Bingley, P. J., additional, and Gale, E. A. M., additional
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- 2003
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11. Mortality from heart disease in a cohort of 23,000 patients with insulin-treated diabetes
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Laing, S. P., primary, Swerdlow, A. J., additional, Slater, S. D., additional, Burden, A. C., additional, Morris, A., additional, Waugh, N. R., additional, Gatling, W., additional, Bingley, P. J., additional, and Patterson, C. C., additional
- Published
- 2003
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12. —to: Pani MA, Van Autreve J, Van der Auwera BJ, Gorus FK, Badenhoop K (2002) Non-transmitted maternal HLA DQ2 or DQ8 alleles and risk of Type 1 diabetes in offspring: the importance of foetal or post partum exposure to diabetogenic molecules. Diabetologia 45:1340–1343
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Lambert, A. P., primary, Gillespie, K. M., additional, Bingley, P. J., additional, and Gale, E. A. M., additional
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- 2003
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13. Diabetes in the parents of children with Type I diabetes
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Douek, I. F., primary, Gillespie, K. M., additional, Bingley, P. J., additional, and Gale, E. A. M., additional
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- 2002
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14. A comparison of the prevalence of islet autoantibodies in children from two countries with differing incidence of diabetes
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Marčiulionytė, D., primary, Williams, A. J. K., additional, Bingley, P. J., additional, Urbonaitė, B., additional, and Gale, E. A. M., additional
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- 2001
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15. Safety of high-dose nicotinamide: a review
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Knip, M., primary, Douek, I. F., additional, Moore, W. P. T., additional, Gillmor, H. A., additional, McLean, A. E. M., additional, Bingley, P. J., additional, and Gale, E. A. M., additional
- Published
- 2000
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16. Islet autoantibody markers in IDDM: risk assessment strategies yielding high sensitivity
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Bonifacio, E., primary, Genovese, S., additional, Braghi, S., additional, Bazzigaluppi, E., additional, Lampasona, Y., additional, Bingley, P. J., additional, Rogge, L., additional, Pastore, M. R., additional, Bognetti, E., additional, Bottazzo, G. F., additional, Gale, E. A. M., additional, and Bosi, E., additional
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- 1995
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17. Slow metabolic deterioration towards diabetes in islet cell antibody positive patients with autoimmune polyendocrine disease
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Wagner, R., primary, Genovese, S., additional, Bosi, E., additional, Becker, F., additional, Bingley, P. J., additional, Bonifacio, E., additional, Miles, K. A., additional, Christie, M. R., additional, Bottazzo, G. F., additional, and Gale, E. A. M., additional
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- 1994
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18. Presentation and progress of childhood diabetes mellitus: a prospective population-based study
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Pinkney, J. H., primary, Bingley, P. J., additional, Sawtell, P. A., additional, Dunger, D. B., additional, and Gale, E. A. M., additional
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- 1994
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19. Nicotinamide and insulin secretion in normal subjects
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Bingley, P. J., primary, Caldas, G., additional, Bonfanti, R., additional, and Gale, E. A. M., additional
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- 1993
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20. Loss of regular oscillatory insulin secretion in islet cell antibody positive non-diabetic subjects
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Bingley, P. J., primary, Matthews, D. R., additional, Williams, A. J. K., additional, Bottazzo, G. F., additional, and Gale, E. A. M., additional
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- 1992
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21. Progression to type 1 diabetes in islet cell antibody-positive relatives in the European Nicotinamide Diabetes Intervention Trial: the role of additional immune, genetic and metabolic markers of risk.
- Author
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Bingley, P. J. and Gale, E. A. M.
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DIABETES ,CLINICAL trials ,DISEASE risk factors ,GENETIC disorders ,GLUTAMATE decarboxylase ,PHOSPHATASES - Abstract
Aims/hypothesis: To examine the role of additional immune, genetic and metabolic risk markers in determining risk of diabetes in islet cell antibody (ICA)-positive individuals with a family history of type 1 diabetes recruited into the European Nicotinamide Diabetes Intervention Trial. Methods: Five hundred and fortynine first-degree relatives with confirmed ICA levels ≥20 Juvenile Diabetes Foundation units (mean age 15.9 years; interquartile range 10.4–33.7 years) were recruited from 20 countries. OGTTs and IVGTTs were performed at baseline, antibodies to glutamate decarboxylase (GADA), protein tyrosine phosphatase (IA-2A) and insulin (IAA) were determined by RIA, and HLA class II genotyping was performed by PCR of sequence-specific oligonucleotides. Results: One hundred and fifty-nine participants developed diabetes within 5 years. Univariate analysis showed that the cumulative risk of development of diabetes within 5 years varied according to age, relationship to the proband, positivity for IAA, IA-2A and GADA, number and combination of islet antibodies, HLA class II genotype, baseline glucose tolerance, and first-phase insulin secretion, but not gender or incidence of childhood type 1 diabetes in the background population. Children aged ≤10 years had a 59% risk of diabetes within 5 years, compared with 11% in those ≥25 years (p<0.0001). Using multivariate analysis, independent determinants were age, first-phase insulin response, baseline glucose tolerance and number of additional antibody markers, but not antibody type or genotype. Individuals <25 years with two or more additional antibodies at baseline had a 62% risk of diabetes within 5 years and these combined criteria identified 81% of the cases in the whole cohort. Conclusions/interpretation: We suggest that screening and recruitment for future intervention trials should be limited to family members aged <25 years, and should be based on islet autoantibodies alone. [ABSTRACT FROM AUTHOR]
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- 2006
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22. Islet autoantibodies, nationality and gender: a multinational screening study in first-degree relatives of patients with Type I diabetes.
- Author
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Williams, A. J. K., Bingley, P. J., Moore, W. P. T., and Gale, E. A. M.
- Subjects
DIABETES ,GENDER ,CITIZENSHIP ,INSULIN ,AUTOANTIBODIES ,ISLANDS of Langerhans ,ENDOCRINOLOGY ,AUTOIMMUNITY - Abstract
Aims/hypothesis: First-degree relatives of patients with Type I (insulin-dependent) diabetes mellitus diagnosed at 20 years of age or under were screened for islet cell antibodies (ICA) in the course of recruitment to an international diabetes prevention trial. Our aim was to evaluate the influence of age, gender, proband characteristics and nationality on the prevalence of ICA and co-existence of autoantibodies to GAD, IA-2 and insulin. Methods: A central laboratory screened samples from 10 326 non-diabetic relatives who were aged less than 40 years, from eight European countries for ICA. Antibodies to GAD and IA-2 were measured in all samples with ICA of 10 JDF units or more. Results: Overall, 8.9 % of relatives had ICA of 10 JDF units or more, 3.8 % with ICA of 20 JDF units or more. Of 921 relatives with ICA of 10 JDF units or more, 29 % had co-existing antibodies to GAD or IA-2 or both. ICA of 10 JDF units or more were more prevalent in males (10.8 %) than females (7.3 %). ICA with GAD or IA-2 antibodies or both were also more common in males (3.4 %) than females (1.9 %) and in relatives under 20 years of age (3.5 % vs 1.5 %). Multiple regression analysis showed nationality to be a determinant of ICA of 10 JDF units or more but not of ICA of 20 JDF units or more or of ICA with co-existing islet antibodies, and confirmed the importance of age and gender as determinants of islet autoimmunity. Conclusions/interpretation: Relatives from different European countries have similar rates of islet autoimmunity despite wide variation in the background incidence of childhood diabetes, and male excess is equally evident in all populations. The male excess of ICA and islet autoimmunity over 10 years of age reflects the higher male incidence of Type I diabetes in this age group, and suggests that boys may be more likely than girls to develop islet autoimmunity during adolescence. [Diabetologia (2002) 45: 217–223] [ABSTRACT FROM AUTHOR]
- Published
- 2002
23. A comparison of the prevalence of islet autoantibodies in children from two countries with differing incidence of diabetes.
- Author
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Marčiulionyt&adot;, D., Williams, A. J. K., Bingley, P. J., Urbonait&adot;, B., and Gale, E. A. M.
- Subjects
AUTOANTIBODIES ,IMMUNOGLOBULINS ,DIABETES in children ,DIABETES ,PEDIATRIC endocrinology ,METABOLIC disorders in children - Abstract
Aims/Hypothesis. To examine the prevalence of subclinical islet autoimmunity in children from two countries with a twofold to threefold difference in incidence of childhood Type I (insulin-dependent) diabetes mellitus.¶Methods. Sera were collected from 2860 English and 3053 Lithuanian non-diabetic schoolchildren according to the same protocol. Occult diabetes was excluded by blood glucose measurement. Antibodies to GAD and the protein tyrosine phosphatase IA-2 were measured with standardised radiobinding assays in a single laboratory. Islet cell antibodies and insulin autoantibodies were additionally measured in all samples with GAD and/or IA-2 antibody levels above the 97.5
th centile of the English schoolchildren.¶Results. Of Lithuanian schoolchildren 2.7 % had GAD antibodies above the 97.5th centile of the English schoolchildren but only 0.2 % had antibodies to IA-2 above this threshold (p < 0.001). Islet cell and/or insulin autoantibodies above the 97.5th centile were found in 22 Lithuanian and 16 English schoolchildren and the overall prevalence of two or more antibodies on or above the 97.5th centile was similar [0.7 % (0.5–1.1) vs 0.6 % (0.4–1.0)] in the two cohorts.¶Conclusion/interpretation. The prevalence of multiple antibody markers was similar in the cohorts from the two populations, despite the two to three-fold difference in incidence of diabetes. The unexpectedly high prevalence of subclinical islet autoimmunity suggests that the incidence of diabetes in Lithuania is likely to increase in the near future. [Diabetologia (2001) 44: 16–21] [ABSTRACT FROM AUTHOR]- Published
- 2001
24. 35th Annual Meeting of the European Association for the Study of Diabetes
- Author
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Melander, A., Olsson, J., Lindberg, G., Salzman, A., Howard, T., Stang, P., Lydick, E., Emslie-Smith, A., Boyle, D. I. R., Evans, J. M. M., Macdonald, T. M., Bain, J., Sullivan, F., Juhl, C., Pørksen, N., Sturis, J., Hollingdal, M., Pincus, S., Veldhuis, J., Dejgaard, A., Schmitz, O., Kristensen, J. S., Frandsen, K. B., Bayer, Th., Müller, P., Dunning, B. E., Paladini, S., Gutierrez, C., Deacon, R., Valentin, M., Grunberger, G., Weston, W. M., Patwardhan, R., Rappaport, E. B., Sargeant, L. A., Wareham, N. J., Khaw, K. T., Zethelius, Björn, Lithell, Hans, Hales, C. Nicholas, Berne, Christian, Lakka, H.-M., Oksanen, L., Tuomainen, T.-P., Kontula, K., Salonen, J. T., Dekker, J. M., de Boks, P., de Vegt, F., Stehouwer, C. D. A., Nijpels, G., Bouter, L. M., Heine, R. J., Bruno, G., Cavallo-Perin, P., Bargero, G., D’Errico, N., Borra, M., Macchia, G., Pagano, G., Newton, R. W., Ruta, D. A., New, J. P., Wallace, C., Roxburgh, M. A., Young, R. J., Vaughan, N. J. A., Elliott, P., Brennan, G., Devers, M., MacAlpine, R., Steinke, D., Lawson, D. H., Decallonne, B., Casteels, K., Gysemans, C., Bouillon, R., Mathieu, C., Linn, Thomas, Strate, Christine, Schneider, Kerstin, Funda, D. P., Jirsa, M., Kozáková, H., Kaas, A., Kofronová, O., Tlaskalová-Hogenová, H., Buschard, K., Wanka, H., Hartmann, A., Kuttler, B., Rasmussen, S. B., Sørensen, T. S., Markholst, H., Petersen, J. S., Karounos, D., Dyrberg, T., Mabley, J. G., Haskó, G., Szabó, C., Seissler, J., Nguyen, T. B. T., Steinbrenner, H., Scherbaum, W. A., Cipriani, R., Gabriele, A., Sensi, M., Guidobaldi, L., Pantellini, F., Cerrito, M. G., Scarpa, S., Di Mario, U., Morano, S., Ceolotto, G., Iori, E., Baritono, E., Del Prato, S., Semplicini, A., Trevisan, R., Zerbini, G., Meregalli, G., Asnaghi, V., Tentori, F., Maestroni, A., Mangili, R., Marescotti, C., Vedovato, M., Tiengo, A., Tadjieva, J., Mankovsky, B. N., Van Aken, S., Raes, A., Vande Walle, J., Matthys, D., Craen, M., Hansen, H. P., Lund, S. S., Rossing, P., Jensen, T., Parving, H.-H., Andersen, S., Tarnow, L., Hansen, B. V., Trautner, C., Haastert, B., Ennenbach, N., Willich, S., Tabák, Á. Gy., Orchard, T. J., Spranger, J., Preissner, K. T., Schatz, H., Pfeiffer, A., Cantón, A., Burgos, R., Hernández, C., Lecube, A., Mesa, J., Segura, R. M., Mateo, C., Simó, R., Fathallah, L., Greene, D. A., Obrosova, I., Gilbert, R. E., Kelly, D. J., Cox, A. J., Berka-Wilkinson, J. L., Taylor, H. R., Panagiotopoulos, S., Lee, V., Jerums, G., Cooper, M. E., Hitman, G. A., Aganna, E., Ogunkolade, W. B., Rema, M., Deepa, R., Shanthi-Rani, C. S., Barakat, K., Kumarajeewa, T. R., Cassell, P. G., McDermott, M. F., Mohan, V., Ways, K., Bursell, S., Devries, T., Woodworth, J., Alatorre, C., King, G., Aiello, L. P., Karisen, A. E., Pavlovic, D., Nielsen, K., Jensen, J., Andersen, H. U., Pociot, F., Mandrup-Poulsen, T., Eizirik, D. L., Nerup, J., Lortz, S., Tiedge, M., Lenzen, S., Lally, F. J., Bone, A. J., Darville, M. I., Ho, Y.-S., Sternesjö, J., Sandler, S., Chen, M.-C., Schuit, F., Pipeleers, D. G., Merezak, S., Hardikar, A., Hoet, J. J., Remacle, C., Reusens, B., Bréant, B., Garofano, A., Czernichow, P., Kubota, N., Terauchi, Y., Miki, H., Tamemoto, H., Yamauchi, T., Nakano, R., Komeda, K., Eto, K., Tobe, K., Kimura, S., Kadowaki, T., Ide, T., Murakami, K., Tsunoda, M., Mochizuki, T., Ozanne, S. E., Nave, B. T., Wang, C. L., Dorling, M. W., Petry, C. J., Koopmans, S. J., van der Bent, C., Que, I., Radder, J. K., Sebokova, E., Sana, A. K., Klimes, I., Ruderman, N., Morviducci, L., Pastore, L., Morelli, S., Sagratella, E., Zorretta, D., Buongiomo, A., Tamburrano, G., Giaccari, A., Martinenghi, Sabina, De Angelis, Gabriella Cusella, Ravasi, Flavio, Bifari, Francesco, Bordignon, Claudio, Falqui, Luca, Kessler, A., Dransfeld, O., Sasson, S., Tomas, E., Zorzano, A., Eckel, J., Thorsby, P., Rosenfalck, A. M., Kjems, L., Hanssen, K. F., Madsbad, S., Birkeland, K. I., Hamilton-Wessler, M., Markussen, J., Bergman, R. N., Melki, V., Hanaire-Broutin, H., Bessières-Lacombe, S., Tauber, J.-P., Home, P. D., Lindholm, A., Riis, A., Rosenstock, J., Schwartz, S., Clark, C., Edwards, M., Donley, D., Swift, P., Mortensen, H. B., Lynggaard, H., Hougaard, P., Cull, C. A., Neil, H. A. W., Frighi, V., Manley, S. E., Holman, R. R., Turner, R. C., Steiner, G., Davis, W. A., Weeraratna, T., Bruce, D. G., Davis, T. M. E., Vergès, B., Duvillard, L., Pont, F., Florentin, E., Gambert, Ph., Benko, B., Ljubić, S., Turk, Z., Granić, M., März, W., Wollschläger, H., Klein, G., Neiss, A., Wehling, M., Huxtable, S. J., Saker, P. J., Walker, M., Frayling, T. M., Levy, J. C., O’Rahilly, S., Hattersley, A. T., McCarthy, M. I., Orecchio, A., Giacchini, A., Dominici, R., Canettieri, G., Trinti, B., Zani, M., Andreoli, M., Sciacchitano, S., de Silva, A. M., Whitecross, K., Pasco, J., Kotowicz, M., Nicholson, G., Zimmet, P., Boyko, E. J., Collier, G. R., Frittitta, L., Pizzuti, A., Argiolas, A., Graci, S., Goldfine, I. D., Bozzali, M., Ercolino, T., Costanzo, B., Iacoviello, L., Tassi, V., Trischitta, V., Wauters, M., Rankinen, T., Mertens, I., Chagnon, M., Bouchard, C., Van Gaal, L., Sivenius, K., Valve, R., Hakkarainen, V., Niskanen, L., Laakso, M., Uusitupa, M., Beridze, N., Japaridze, M., Kurashvili, R., Dundua, M., Kebuladze, G., Kazakhashvili, N., Offley-Shore, B., Thomas, B., Ghebremeskel, K., Crawford, M., Lowy, C., Eriksson, Ulf J., Martin Simán, C., Wisse, Bert, Gittenberger-de Groot, Adriana C., Wentzel, P., Eriksson, U. J., Wender-Ożegowska, E., Drews, K., Biczysko, R., Bronisz, A., Rość, D., Graczykowska-Koczorowska, A., Kotschy, M., Sokup, A., Kohnert, K. D., Besch, W., Strese, J., Frick, U., Zander, E., Kemer, W., Škrha, J., Kvasnička, J., Kalvodová, B., Hilgertová, J., Schatteman, K., Goossens, F., Scharpé, S., De Leeuw, I., Hendriks, D., Legakis, I. N., Panayiotou, D., Mountokalakis, Th. D., Enderle, M. D., Beckmann, P., Balletshofer, B., Rittig, K., Maerker, E., Volk, A., Meisner, C., Jacob, S., Matthaei, S., Häring, H. U., Rett, K., Ueda, K., Nakagawa, T., Shimajiri, Y., Kokawa, M., Matsumoto, E., Sasaki, H., Sanke, T., Nanjo, K., McKinnon, Caroline M., Macfarlane, Wendy M., Docherty, Kevin, Furukawa, N., Shirotani, T., Kishikawa, H., Kaneko, K., Araki, E., Shichiri, M., Prentki, M., Roduit, R., Susini, S., Buteau, J., Ejrnæs, A. M., Andersen, N. Aa., Osterhoff, M., Möhlig, M., Ortmann, J., Bikashaghi, F., Mayer, C., Bikashagi, F., Ackermans, M. T., Pereira Arias, A. M., Bisschop, P. H. L. T., Endert, E., Sauerwein, H. P., Romijn, J. A., Gastaldelli, A., Baldi, S., Pettiti, M., Natali, A., Frascerra, S., Camastra, S., Toschi, E., Ferrannini, E., Stingl, H., Krssak, M., Bischof, M. G., Krebs, M., Fürnsinn, C., Nowotny, P., Waldhäusl, W., Roden, M., Neeft, M., Meijer, A. J., Båvenholm, P., Pigon, J., Efendic, S., Kästenbauer, T., Sauseng, S., Sokol, G., Auinger, M., Irsigler, K., Abbott, C. A., Carrington, A. L., Faragher, B., Kulkarni, J., Van Ross, E. R. E., Boulton, A. J. M., Armstrong, D. G., Hadi, S., Nguyen, H. C., Harkless, L. B., Jirkovská, A., Kasalicky, P., Hosová, J., Skibova, J., Uccioli, L., Caselli, A., Giacomozzi, C., Macellari, V., Giurato, L., Lardieri, L., Menzinger, G., Pham, H. T., Rosenblum, B. I., Lyons, T. E., Giurini, J. M., Smakowski, P., Chrzan, J. S., Habershaw, G. M., Veves, A., Foster, A. M., Bates, M., Doxford, M., Edmonds, M. E., Kecha, O., Winkler, R., Martens, H., Collette, J., Lefèbvre, P. J., Greiner, D., Geenen, V., Atlan-Gepner, C., Naspetti, M., Valéro, R., Barad, M., Lepault, F., Vialettes, B., Naquet, P., de Galan, B., Netea, M. G., Hancu, N., Smits, P., Van der Meer, J. W. M., Osterbye, T., Jørgensen, K. H., Tranum-Jensen, J., Fredman, P., Høy, M., Bokvist, K., Olsen, H. L., Horn, T., Gromada, J., Laub, R., Lohmann, T., Hahn, H. J., Adler, T., Emmrich, F., Rabuazzo, A. M., Lupi, R., Dotta, F., Patanè, G., Marselli, L., Realacci, M., Piro, S., Del Guerra, S., Santangelo, C., Navalesi, R., Purrello, F., Marchetti, P., de Vos, P., Visser, L., de Haan, B. J., Klok, P., van Schilfgaarde, R., Poppema, S., Juang, J.-H., Kuo, C.-H., Hsu, B. R.-S., Nacher, V., Pérez, M., Biarnés, M., Raurell, M., Soler, J., Montanya, E., Ritzel, R., Maubach, J., Büsing, M., Becker, T., Klempnauer, J., Hücking, K., Schmiegel, W. H., Nauck, M. A., Bouček, P., Saudek, F., Adamec, M., Kožitarová, R., Jedináková, T., Vlasáková, Z., Skibová, J., Bartoš, V., Maffi, P., Bertuzzi, F., Aldrighetti, L., Taglietti, M. V., Castelnuovo, A., Pozza, G., Di Carlo, V., Secchi, A., Renier, G., Mamputu, J.-C., Gillespie, J. S., McMaster, D., Mercer, C., Trimble, E. 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L., Srivatsa, A., Anderson, S. G., Cruikshank, J. K., Florkowski, C. M., Scott, R. S., Graham, P. J., Moir, C. L., Flores, C., Ruggenenti, P., Dodesini, A. R., Vasile, B., Gaspari, F., Arnoldi, F., Ferrari, S., Ciocca, I., Spalluzzi, A., Remuzzi, G., Delvigne, C., Ballaux, D., Bosman, D. R., Winkler, A. S., Marsden, J., Watkins, P. J., Strutton, D., Erbey, J. R., Jacobsen, P., Rossing, K., Jensen, J. S., Mansfield, M. W., Kowalska, I., Telejko, B., Bachórzewska-Gajewska, A., Prokop, J., Kochman, W., Musiał, W., Naskręt, D., Oleksa, R., Zozulińska, D., Sowiński, J., Wierusz-Wysocka, B., Klamann, A., Jonas, M., Müller-Lung, U., Heuser, L., Launhardt, V., Valensi, P., Pariès, J., Torremocha, F., Brulport, V., Sachs, R. N., Vanzetto, G., Levy, M., Lormeau, B., Halimi, S., Perfornis, A., Boumal, D., Zimmermann, C., Bernard, Y., Sabbah, A., Meneveau, N., Gautier, S., Bassand, J. P., Anděl, M., Kraml, P., Potočková, J., Dvořáková, H., Trešlová, L., Nuttall, S. L., Martin, U., Kendall, M. J., Schiaffini, R., Pantaleo, A., Battocletti, T., Vaccari, V., Brufani, C., Martuscelli, E., Gargiulo, P., Nieszner, E., Posa, I., Kocsis, E., Préda, I., Pogatsa, G., Koltai, M. Z. S., Stefanidis, A., Manoussakis, S., Handanis, S., Zairis, M., Vitalis, D., Dadiotis, L., Fiorina, P., La Rocca, E., Astorri, E., Rossetti, C., Lucignani, G., Giudici, D., Castoldi, R., Mazarakis, N., Giagiakou, E., Karavidas, A., Agellou, A., Karamani, O., Matsakas, E., Caviezel, F., Morricone, L., Ranucci, M., Denti, S., Cazzaniga, A., Enrini, R., Isgrò, G., González de Molina, F. J., Sala, J., Masià, R., Marrugat, J., Kruszewski, P., Wolnik, B., Bieniaszewski, L., Świerblewska, E., Semetkowska-Jurkiewicz, E., Krupa-Wojciechowska, B., Vasilikos, P. G., Alaveras, A. E. G., Anastasopoulos, N. G., Chala, E., Sidira, M., Christakopoulos, P. D., Poulsen, P. L., Hansen, K. W., Ebbehøj, E., Knudsen, S. T., Mogensen, C. E., Ramu, Y., Vidyullatha, Y., Strojek, K., Gorska, J., Morawin, E., Ritz, E., Ciavarella, A., Malini, P. L., Strocchi, E., Fiumi, N., Ambrosioni, E., Idzior-Waluś, B., Stevens, L., McEneny, J., O’Kane, M. J., Moles, K. W., McMaster, C., Young, I. S., Leonhardt, W., Konstadelou, E., Gürlek, Alper, Soedamah-Muthu, S., Taskinen, M. R., Ehnholm, C., Wägner, A., Bayen, Laia, Rigla, M., Ortega, E., Caixàs, A., Mestrón, A., Ordóñez, J., Pérez, A., Sotiropoulou, G., Servais, P. L., Bertolotto, A., Pilo, M., Suchánková, G., Andratschke, S., Tschöp, M., Strasburger, C.-J., Rizzo, L., Aerts, P., Vinckx, M., Ansquer, J. C., Ryan, M., Buter, H., Navis, G. J., de Jong, P. E., de Zeeuw, D., Carreras, G., Giménez, G., Pou, J. M., Howorka, K., Gabriel, M., Pumprla, J., Köves, A., Bhowmik, N. B., Haque, A., Rahman, A., Paleari, F., Gamba, P., Mauri, G., Rovaris, G., Giannattasio, C., Piatti, M. L., Zincone, A., Cavaletti, G., Mancia, G., Lan, S., Arezzo, J., Gerber, R. A., Klioze, S. S., Saponara, C., Tartaglione, T., Cercone, S., Caputo, S., Meloni, T., Brunetti, D., Di Lazzaro, V., Xu, G., Jiang, H. Y., Shy, M. E., Sugimoto, K., Zhang, W.-X., Kuchmerovskaya, T., Donchenko, G., Shymansky, I., Kuchmerovsky, N., Pakyrbaeva, L., Cameron, N. E., Keegan, A., Cotter, M. A., Mirrlees, D., Smale, S. E., Biessels, G. J., Duis, S. E. J., Kamal, A., Gispen, W. H., Carrington, A., Carman, S., Smiarowski, H., Lavoie, D., Sawicki, D., Sabetta, A., Litchfield, J., Van Zandt, M., Sredy, J., Smirnova, V., Strokov, I., Ivanova, L., Ichunina, A., Nakamura, J., Nakayama, M., Hamada, Y., Chaya, S., Kato, K., Kasuya, Y., Mizubayashi, R., Miwa, K., Yasuda, Y., Kamiya, H., Hotta, N., Bíró, K., Kukorelli, T., Szilágyi, N., Kürthy, M., Komáromy, A., Mogyorosi, T., Nagy, K., Çakir, M., Baskal, N., Güllü, S., Elhan, A. H., Erdogan, G., Ziegler, D., Piolot, R., Neubauer, J., Senesi, B., Bonetti, R., Napolitano, A., Canepa, F., Ottonello, P., Schabmann, A., Giménez-Pérez, G., Arroyo, J. A., López, T., Ponz, E., Mauricio, D., Diem, P., Zanchin, L., Suter, S. L., Lefrandt, J. D., Smit, A., van Roon, A. M., Dullaart, R., Voita, D., Mackevics, V., Vitols, A., Lengyel, Cs., Farkas, Gy., Török, T., Légrády, P., Várkonyi, T. T., Kardos, A., Gingl, Z., Kempler, P., Rudas, L., Lonovics, J., Marchand, M., Stevens, L. K., Tarnás, Gy., Estrella, F., Christensen, N. J., Keresztes, K., Barna, I., Hermányi, Zs., Vargha, P., Bonnevie, L., Chanudet, X., Larroque, P., Tutuncu, N. Bascil, Deger, A., Batur, M. K., Yildirir, A., Onalan, O., Aksöyek, S., Kabakçι, G., Erbaş, T., Galicka-Latała, D., Surdacki, A., Gerritsen, J., TenVoorde, B. J., Heethaar, R. M., Tagawa, T. S., Kodama, M., Yoshioka, R., Yamasaki, Y., Didangelos, T., Athyros, V., Kontopoulos, A., Papageorgiou, A., Karamitsos, D., Lacigová, S., Rušavý, Z., Kárová, R., Perrild, H., Kay, L., Jørgensen, T., Bień, A. I., Witek, P., Geraldes, Elizabete, Rodrigues, D., Pereira, L., Doménech, A., Leitão, P., Anagnostopoulos, D., Foster, A. V. M., Nag, S., Barsoum, M., Lewis, G., Dunlop, N., Connolly, V., Bilous, R., Kelly, W., Chantelau, E., Gede, A., Sharman, D., O’Halloran, D., Best, C., Abbas, Z. G., Lutale, J., Gill, G. V., Jarvis, W. R., Archibald, L. K., Corcoran, S., Mansell, J., Pibworth, L., Terada, H., Shiba, T., Utugi, N., Utugi, T., Blum, M., Strobel, J., Höffken, K., Razvi, F. M., Kritzinger, E. E., Taylor, K., Jones, S., Illahi, W., Grüβer, M., Hartmann, P., Hoffstadt, K., van Leiden, H. A., Moll, A. C., Polak, B. C. P., Pietragalla, G. B., Maurino, M., Montanaro, M., Karadeniz, Ş., Tommasini, P., Quadrini, C., Demiraj, V., Rispoli, E., Ota, A., Takama, H., Saito, N., Hemández, C., Lepore, D., Antico, L., Giardina, B., Franconi, F., Michoud, E., Chamot, S., Riva, Ch., Hammes, H.-P., Renner, O., Breier, G., Lin, J., Alt, A., Betzholtz, C., Bretzel, R. G., Manti, R., Gallo, M., Molinar Hin, A., Brignardello, E., Boccuzzi, G., Li, Shanfang, Xiang, Kunsan, Zhang, Rugeng, Shangguan, Xinhong, Wu, Jianrong, Donnan, P. T., Broomhall, J., Hunter, K., Morris, A. D., Ioannidis, G., Peppa, M., Rontogianni, E., Kallifronas, M., Lekatsas, I., Chrysanthopoulou, G., Anthopoulos, L., Kesse, M., Thalassinos, N., Neves, C., Medina, J. L., Lopes, F., Yılmaz, M., Güvener, N., Güvener, M., Kocagöz, T., Böke, E., Paşaoglu, I., Bascil Tutuncu, N., Oto, A., Karvonen, M. K., Koulu, M., Pesonen, U., Mercuri, M., Rauramaa, R., Rutter, M. K., Kestevan, P., McComb, J. M., Marshall, S. M., Sobieska, M., Wiktorowicz, K., Kanters, S. D. J. M., Banga, J. D., Algra, A., Frijns, C. J. M., Beutler, J. J., Fijnheer, R., Nicoloff, G., Baydanoff, S., Stanimirova, N., Petrova, Ch., Lario, S., Campistol, J. M., Cases, A., Clària, J., Iñigo, P., Esmatjcs, E., Sármán, B., Tóth, M., Kocsis, I., Somogyi, A., Bumbure, A., Jachimowicz, K., Samson, J., Tomasiak, M., Sobol, A., Stańczyk, L., Watala, C., Stradina, P., Wiśniewska-Jarosińska, M., Marciniak, D., Więcławska, B., Watała, C., Golański, J., Zinnat, R., Mahmud, I., Büyükasik, Yahya, Demiroğlu, H., Szczepanik, A., Skowroński, M., Murawska, A., Meeking, D. R., Allard, S., Munday, J., Chowienczyk, P., Shaw, K. M., Cummings, M. H., Šimková, R., Jirsa, M., Hadoke, P. W. F., McIntyre, C. A., Jones, G. C., Williams, B. C., Elliott, A. I., McKnight, J. A., Pernow, J., Bombonato, G. C., Finucci, G. F., Zotta, L., Senses, V., Ozyazgan, S., Ince, E., Tunçdemir, M., Oztürk, M., Sultuybek, G., Akkan, A. G., Özyazgan, S., Unlücerci, Y., Bekpınar, S., Meyer, M. F., Lee, B. C., Shore, A. C., Humphreys, J. M., Tooke, J. E., Dell’Omo, G., Giovannitti, G., Caricato, F., Mariani, M., Pedrinelli, R., Kiviet-Boehm, C., Schwelling, V., Matthäei, S., Pfohl, M., McInerney, D., Itoh, H., Ohno, T., Katoh, N., Baumgartner-Parzer, S., Artwohl, M., Graier, W., Ludwig, C., Tachi, Y., Bannai, C., Shinohara, M., Shimpuku, H., Ohura, K., Bertacca, A., Sasvári, M., Szaleczki, E., Pusztai, P., Boes, U., Klaus, E., Dittrich, P., Wagner, Z., Wittmann, I., Pótó, L., Wagner, L., Mazák, I., Nagy, J., Feletto, F., Taboga, C., Tonutti, L., Lizzio, S., Russo, A., Selmo, V., Ceriello, A., Lekakis, J., Papamichael, C. M., Stamatelopoulos, K., Stamatelopoulos, S., Yillar, D. O., Gay, M., Lillaz, E., Passaro, A., Vanini, A., Calzoni, F., D’Elia, K., Carantoni, M., Zuliani, G., Fellin, R., Solini, A., Chwatko, G., Bald, E., Dramais, A.-S., Wallemacq, P. E., Vandeleene, B., Ciaria, M. V., Ariano, M., Strom, R., Gibney, J., Weiss, U., Turner, B., O’Gorman, P., Watts, G., Powrie, J., Crook, M., Shaw, K., and Cummings, M.
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- 1999
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25. Diabetes Antibody Standardization Program: evaluation of assays for insulin autoantibodies.
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Schlosser M, Mueller PW, Törn C, Bonifacio E, and Bingley PJ
- Subjects
- Area Under Curve, Autoantibodies blood, Case-Control Studies, Consensus Development Conferences as Topic, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 immunology, Humans, Insulin immunology, Insulin Antibodies blood, Laboratory Proficiency Testing, Program Development, ROC Curve, Radioimmunoassay standards, Reference Standards, Sensitivity and Specificity, Autoantibodies analysis, Diabetes Mellitus, Type 1 diagnosis, Diagnostic Techniques, Endocrine standards, Insulin Antibodies analysis
- Abstract
Aims/hypothesis: Insulin autoantibodies (IAA) are important in type 1 diabetes risk assessment. However, their determination varies more between laboratories than other diabetes autoantibodies. The Diabetes Antibody Standardization Program (DASP) aims to improve and standardise measurement of autoantibodies associated with type 1 diabetes. We report the results of measurement of IAA from DASP workshops in 2002, 2003 and 2005., Methods: Up to 32 laboratories in 14 countries participated in each workshop. Aliquots of coded sera from 50 patients with newly diagnosed type 1 diabetes and 100 blood donor controls were circulated to participating laboratories. Reported results were analysed using receiver operator characteristic (ROC) curves. We compared concordance of antibody levels by ranking, IAA and insulin antibody (IA) indices and units derived from an IA standard curve., Results: In all three workshops IAA assay performance had improved compared with DASP 2000. The median area under the ROC curve was 0.73 in DASP 2002, 0.78 in 2003 and 0.80 in 2005 (p = 0.0012), and median laboratory-assigned sensitivity was 26% in 2002, 36% in 2003 and 45% in 2005 (p < 0.0001). There was, however, marked variation between assays. The range of AUC was 0.36-0.91 and that of laboratory-assigned sensitivity was 22-57%. Concordance of ranking of patient serum samples was related to AUC (p < 0.001). Using an index related to common IAA and IA-positive or -negative control sera improved the concordance between assays (p < 0.0001)., Conclusions/interpretation: The overall performance of IAA assays has improved but there is still wide variation between laboratories. Concordance between assays would be improved by the use of a common reference reagent.
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- 2010
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26. Diabetes Antibody Standardization Program: evaluation of assays for autoantibodies to glutamic acid decarboxylase and islet antigen-2.
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Törn C, Mueller PW, Schlosser M, Bonifacio E, and Bingley PJ
- Subjects
- Diabetes Mellitus blood, Glutamate Decarboxylase metabolism, Humans, ROC Curve, Receptor-Like Protein Tyrosine Phosphatases, Class 8 metabolism, Sensitivity and Specificity, Autoantibodies blood, Diabetes Mellitus immunology, Glutamate Decarboxylase immunology, Receptor-Like Protein Tyrosine Phosphatases, Class 8 immunology
- Abstract
Aims/hypothesis: Islet autoantibodies are important in diabetes classification and risk assessment, and as endpoints in observational studies. The Diabetes Autoantibody Standardization Program (DASP) aims to improve and standardise measurement of autoantibodies associated with type 1 diabetes. We report results for glutamic acid decarboxylase autoantibodies (GADA) and islet antigen-2 autoantibodies (IA-2A) from three DASP workshops (2002--2005)., Methods: Up to 60 laboratories in 18 countries participated in each workshop. Participants received coded serum aliquots from 50 patients with newly diagnosed type 1 diabetes (median age 18 years, range 9-35 years) and 100 blood donor controls. Results were analysed using receiver operator characteristic (ROC) curves with sensitivity adjusted to 95% specificity in workshop controls., Results: GADA assays performed well in all three workshops (median area under the ROC curve [AUC] 0.94; interquartile range 0.91-0.95) and performance was similar to DASP 2000. Performance of IA-2A assays improved over the workshop programme. Median AUC was 0.81 (interquartile range 0.79-0.83) in DASP 2002, 0.82 (interquartile range 0.78-0.84) in 2003, and 0.85 (interquartile range 0.82-0.87) in 2005 (p < 0.0001). Performance of GADA ELISA improved between 2002 and 2005, and, in DASP 2005, achieved higher median AUC and adjusted sensitivity than RIA. IA-2A ELISA improved and, in DASP 2005, achieved AUCs equivalent to in-house RIA. Assays using IA-2ic or full length IA-2 clones were more sensitive than those using IA-2bdc, with higher AUC (p = 0.004)., Conclusions/interpretation: GADA and IA-2A assays perform well in discriminating health and disease. The workshop format highlights systematic differences related to assay method and allows full evaluation of novel methods. The programme of autoantibody workshops in type 1 diabetes provides a model for other autoimmune diseases.
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- 2008
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27. Autoantibodies to IA-2beta improve diabetes risk assessment in high-risk relatives.
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Achenbach P, Bonifacio E, Williams AJ, Ziegler AG, Gale EA, and Bingley PJ
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- Analysis of Variance, Biomarkers blood, Diabetes Mellitus immunology, Diabetes Mellitus, Type 1 blood, Diabetes Mellitus, Type 1 epidemiology, Family, Glucose Tolerance Test, Humans, Radioligand Assay, Risk Assessment, Autoantibodies blood, Diabetes Mellitus epidemiology, Diabetes Mellitus, Type 1 immunology
- Abstract
Aims/hypothesis: The aim of this study was to evaluate the prognostic significance of autoantibodies to IA-2beta (IA2betaA) in a large, well-characterised population of islet cell antibody (ICA)-positive relatives followed for 5 years in the European Nicotinamide Diabetes Intervention Trial., Methods: Autoantibodies to insulin (IAA), glutamate decarboxylase (GADA) and IA-2 (IA2A) were measured in 549 participants at study entry, and IA2A-positive samples tested for IA2betaA. First-phase insulin response (FPIR) and oral glucose tolerance were determined at baseline., Results: Of 212 ICA/IA2A-positive participants (median age 12.1 years; 57% male), 113 developed diabetes (5 year cumulative risk 56%), and 148 were also GADA-positive and IAA-positive (4Ab-positive). IA2betaA were detected in 137 (65%) ICA/IA2A-positive participants and were associated with an increased 5 year diabetes risk (IA2betaA-positive 65 vs 39% in IA2betaA-negative, p=0.0002). The effect was most marked in 4Ab-positive relatives (72% vs 52%, p=0.003). Metabolic testing further refined risk assessment. Among 101 4Ab-positive relatives with IA2betaA, the 5 year risk was 94% in those with a low FPIR (vs 50% in those with a normal FPIR, p<0.0001), and 95% in those with impaired glucose tolerance (IGT) (vs 66% in those with normal glucose tolerance, p<0.0001). The median time to diagnosis of 4Ab/IA2betaA-positive participants with a low FPIR was 1.5 years. Multivariate analysis confirmed IA2betaA status, antibody number, young age, FPIR and IGT as independent determinants of risk., Conclusions/interpretation: IA2betaA are associated with a very high risk of diabetes in ICA/IA2A-positive relatives. Testing for IA2A/IA2betaA compares favourably with the IVGTT in identifying a subgroup of autoantibody-positive relatives at increased risk. IA2betaA determination should be added to screening protocols of future intervention trials.
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- 2008
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28. An association analysis of the HLA gene region in latent autoimmune diabetes in adults.
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Desai M, Zeggini E, Horton VA, Owen KR, Hattersley AT, Levy JC, Walker M, Gillespie KM, Bingley PJ, Hitman GA, Holman RR, McCarthy MI, and Clark A
- Subjects
- Adult, Aged, Aged, 80 and over, Case-Control Studies, Cohort Studies, Diabetes Mellitus, Type 1 ethnology, Diabetes Mellitus, Type 1 physiopathology, Female, Gene Frequency genetics, Genotype, HLA-DQ beta-Chains, HLA-DRB1 Chains, Haplotypes, Humans, Linear Models, Male, Middle Aged, United Kingdom, Diabetes Mellitus, Type 1 genetics, Genetic Predisposition to Disease genetics, HLA-DQ Antigens genetics, HLA-DR Antigens genetics
- Abstract
Aims/hypothesis: Pathophysiological similarities between latent autoimmune diabetes in adults (LADA) and type 1 diabetes indicate an overlap in genetic susceptibility. HLA-DRB1 and HLA-DQB1 are major susceptibility genes for type 1 diabetes but studies of these genes in LADA have been limited. Our aim was to define patterns of HLA-encoded susceptibility/protection in a large, well characterised LADA cohort, and to establish association with disease and age at diagnosis., Materials and Methods: Patients with LADA (n = 387, including 211 patients from the UK Prospective Diabetes Study) and non-diabetic control subjects (n = 327) were of British/Irish European origin. The HLA-DRB1 and -DQB1 genes were genotyped by sequence-specific PCR., Results: As in type 1 diabetes mellitus, DRB1 0301_DQB1 0201 (odds ratio [OR] = 3.08, 95% CI 2.32-4.12, p = 1.2 x 10(-16)) and DRB1 0401_DQB1 0302 (OR = 2.57, 95% CI 1.80-3.73, p = 4.5 x 10(-8)) were the main susceptibility haplotypes in LADA, and DRB1 1501_DQB1 0602 was protective (OR = 0.21, 95% CI 0.13-0.34, p = 4.2 x 10(-13)). Differential susceptibility was conferred by DR4 subtypes: DRB1 0401 was predisposing (OR = 1.79, 95% CI 1.35-2.38, p = 2.7 x 10(-5)) whereas DRB1 0403 was protective (OR = 0.37, 95% CI 0.13-0.97, p = 0.033). The highest-risk genotypes were DRB1 0301/DRB1 0401 and DQB1 0201/DQB1 0302 (OR = 5.14, 95% CI 2.68-10.69, p = 1.3 x 10(-8); and OR = 6.88, 95% CI 3.54-14.68, p = 1.2 x 10(-11), respectively). These genotypes and those containing DRB1 0401 and DQB1 0302 associated with a younger age at diagnosis in LADA, whereas genotypes containing DRB1 1501 and DQB1 0602 associated with an older age at diagnosis., Conclusions/interpretation: Patterns of susceptibility at the HLA-DRB1 and HLA-DQB1 loci in LADA are similar to those reported for type 1 diabetes, supporting the hypothesis that autoimmune diabetes occurring in adults is an age-related extension of the pathophysiological process presenting as childhood-onset type 1 diabetes.
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- 2007
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29. Presentation and progress of childhood diabetes mellitus: a prospective population-based study. The Bart's-Oxford Study Group.
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Pinkey JH, Bingley PJ, Sawtell PA, Dunger DB, and Gale EA
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- Adolescent, Adult, Age Factors, Child, Child, Preschool, Cohort Studies, Diabetes Mellitus, Type 1 physiopathology, Diabetic Ketoacidosis epidemiology, England epidemiology, Female, Humans, Hypoglycemia epidemiology, Infant, Male, Medical Records, Prospective Studies, Sex Factors, Surveys and Questionnaires, Diabetes Mellitus, Type 1 diagnosis, Diabetes Mellitus, Type 1 epidemiology
- Abstract
We surveyed the clinical presentation, initial management and subsequent course of a prospectively registered, population-based cohort of 230 patients with Type 1 (insulin-dependent) diabetes mellitus diagnosed before age 21 years in the Oxford Regional Health Authority area in 1985 and 1986. Clinical details from the time of diagnosis were available on 219 patients. Thirty-four (16%) were in severe ketoacidosis with pH less than 7.10 or plasma bicarbonate less than 10 mmol/l, and 21 (10%) had mild to moderate ketoacidosis with pH 7.10-7.35 or plasma bicarbonate 10-21 mmol/l. One child died in ketoacidosis. Presentation in severe ketoacidosis was most common in children under age 5 years (p < 0.05), and ketoacidosis of any degree was less frequent in older children (0.05 < p < 0.01) and those with a parent or sibling with diabetes (p < 0.01). Within 4 years of diagnosis, 55 of 211 patients (26%) experienced severe hypoglycaemia, which in 31 (15%) led to one or more admissions. Readmission for unstable glycaemic control excluding acute hypoglycaemia occurred at least once within 1 year of diagnosis in 13% and within 4 years in 28%, and was more common in girls, in children aged less than 10 years at diagnosis, and those with a history of severe hypoglycaemia. A second cohort of 97 similar patients was recruited in 1990. The rates of admission at diagnosis (79%), severe ketoacidosis (13%) and mild to moderate ketoacidosis (13%) did not differ from the 1985/1986 cohort.(ABSTRACT TRUNCATED AT 250 WORDS)
- Published
- 1994
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