Progression to insulin deficiency in Korean patients with Type 2 diabetes mellitus positive for anti-GAD antibody
- Authors
- Lee S.A.; Lee W.J.; Kim E.H.; Yu J.H.; Jung C.H.; Koh E.H.; Kim M.-S.; Park J.-Y.; Lee K.-U.
- Issue Date
- 2011
- Keywords
- Anti-GAD antibody; C-peptide; Insulin deficiency; Type2 diabetes mellitus
- Citation
- Diabetic Medicine, v.28, no.3, pp 319 - 324
- Pages
- 6
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- Diabetic Medicine
- Volume
- 28
- Number
- 3
- Start Page
- 319
- End Page
- 324
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/14115
- DOI
- 10.1111/j.1464-5491.2010.03186.x
- ISSN
- 0742-3071
1464-5491
- Abstract
- Aims To investigate the rate of progression to insulin deficiency in Korean patients with Type2 diabetes mellitus positive for anti-GAD antibody (GADA) and to determine the factors related to progression to insulin deficiency. Methods We retrospectively analysed data on 87 GADA-positive and 87 age- and sex-matched GADA-negative patients with Type2 diabetes. GADA-positive patients were further subclassified into high-titre (≥250 WHO units/ml) (n=24) and low-titre (<250 WHO units/ml) (n=63) subgroups. Cox proportional hazard analysis was used to identify factors associated with progression to insulin deficiency. Results Over a period of 6years, two of 87 (2.3%) GADA-negative and 37 of 87 (42.5%) GADA-positive patients had progressed to insulin deficiency. The rate of progression to insulin deficiency was higher in the high-titre than in the low-titre subgroup (75.0 vs. 30.2%). Multivariate analysis in GADA-positive patients showed that high-titre GADA and low BMI at diagnosis were independent factors significantly related to progression to insulin deficiency. Conclusions The presence of GADA predicted the progression to insulin deficiency in Korean patients with Type2 diabetes. In GADA-positive patients, high-titre GADA and low BMI were associated with this progression. © 2011 The Authors. Diabetic Medicine © 2011 Diabetes UK.
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Collections - 2. Clinical Science > Department of Endocrinology and Metabolism > 1. Journal Articles
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