Ketosis-prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta-cell functional classification, prospective analysis, and clinical outcomes
(2003) In Journal of Clinical Endocrinology and Metabolism 88(11). p.5090-5098- Abstract
 - Ketosis-prone diabetes is heterogeneous. Its causes could include novel beta-cell functional defects. To characterize such defects, 103 patients with diabetic ketoacidosis were evaluated for beta-cell autoimmunity and human leukocyte antigen (HLA) class II alleles, with longitudinal measurements of beta-cell function and biochemical and clinical parameters. They were classified into four A beta groups, based on the presence of glutamic acid decarboxylase (GAD)65, GAD67, or IA-2 autoantibodies (A+ or A-) and beta-cell functional reserve (beta+ or beta-). The group distribution was: 18 A+beta-, 23 A-beta-, 11 A+beta+, and 51 A-beta+. Collectively, the two beta- groups differed from the two beta+ groups in earlier onset and longer duration of... (More)
 - Ketosis-prone diabetes is heterogeneous. Its causes could include novel beta-cell functional defects. To characterize such defects, 103 patients with diabetic ketoacidosis were evaluated for beta-cell autoimmunity and human leukocyte antigen (HLA) class II alleles, with longitudinal measurements of beta-cell function and biochemical and clinical parameters. They were classified into four A beta groups, based on the presence of glutamic acid decarboxylase (GAD)65, GAD67, or IA-2 autoantibodies (A+ or A-) and beta-cell functional reserve (beta+ or beta-). The group distribution was: 18 A+beta-, 23 A-beta-, 11 A+beta+, and 51 A-beta+. Collectively, the two beta- groups differed from the two beta+ groups in earlier onset and longer duration of diabetes, lower body mass index, less glycemic improvement, and persistent insulin requirement. HLA class II genotyping showed that the A-beta- group differed from the A+beta- group in having lower frequencies of two alleles strongly associated with (Less)
 
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- author
 - organization
 - publishing date
 - 2003
 - type
 - Contribution to journal
 - publication status
 - published
 - subject
 - in
 - Journal of Clinical Endocrinology and Metabolism
 - volume
 - 88
 - issue
 - 11
 - pages
 - 5090 - 5098
 - publisher
 - Oxford University Press
 - external identifiers
 - 
                
- scopus:10744227156
 - pmid:14602731
 
 - ISSN
 - 1945-7197
 - DOI
 - 10.1210/jc.2003-030180
 - language
 - English
 - LU publication?
 - yes
 - id
 - 3d5a9e09-a8f7-4548-afe4-6752b7e33e8b (old id 1127391)
 - date added to LUP
 - 2016-04-01 17:01:11
 - date last changed
 - 2025-10-14 13:11:04
 
@article{3d5a9e09-a8f7-4548-afe4-6752b7e33e8b,
  abstract     = {{Ketosis-prone diabetes is heterogeneous. Its causes could include novel beta-cell functional defects. To characterize such defects, 103 patients with diabetic ketoacidosis were evaluated for beta-cell autoimmunity and human leukocyte antigen (HLA) class II alleles, with longitudinal measurements of beta-cell function and biochemical and clinical parameters. They were classified into four A beta groups, based on the presence of glutamic acid decarboxylase (GAD)65, GAD67, or IA-2 autoantibodies (A+ or A-) and beta-cell functional reserve (beta+ or beta-). The group distribution was: 18 A+beta-, 23 A-beta-, 11 A+beta+, and 51 A-beta+. Collectively, the two beta- groups differed from the two beta+ groups in earlier onset and longer duration of diabetes, lower body mass index, less glycemic improvement, and persistent insulin requirement. HLA class II genotyping showed that the A-beta- group differed from the A+beta- group in having lower frequencies of two alleles strongly associated with}},
  author       = {{Maldonado, Mario and Hampe, Christiane S and Gaur, Lakshmi K and D'Amico, Susana and Iyer, Dinakar and Hammerle, Lisa P and Bolgiano, Douglas and Rodriguez, Lucille and Rajan, Arun and Lernmark, Åke and Balasubramanyam, Ashok}},
  issn         = {{1945-7197}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{5090--5098}},
  publisher    = {{Oxford University Press}},
  series       = {{Journal of Clinical Endocrinology and Metabolism}},
  title        = {{Ketosis-prone diabetes: dissection of a heterogeneous syndrome using an immunogenetic and beta-cell functional classification, prospective analysis, and clinical outcomes}},
  url          = {{http://dx.doi.org/10.1210/jc.2003-030180}},
  doi          = {{10.1210/jc.2003-030180}},
  volume       = {{88}},
  year         = {{2003}},
}
