PMID- 8636356
OWN - NLM
STAT- MEDLINE
DCOM- 19960711
LR  - 20220310
IS  - 0021-972X (Print)
IS  - 0021-972X (Linking)
VI  - 81
IP  - 4
DP  - 1996 Apr
TI  - Antibodies to glutamic acid decarboxylase and insulin-dependent diabetes in 
      patients with autoimmune polyendocrine syndrome type I.
PG  - 1488-94
AB  - To evaluate the association of autoimmunity to glutamic acid decarboxylase (GAD) 
      with insulin-dependent diabetes mellitus (IDDM) and IDDM-associated human 
      leukocyte antigen (HLA) types, we studied a unique group of 47 patients with 
      autoimmune polyendocrine syndrome type 1, a recessive disease not associated with 
      HLA. GAD65 antibodies (GAD65-Ab), GAD67-Ab, islet cell antibodies, and HLA-DQA1, 
      -DQB1, and -DRB1 were analyzed in relation to IDDM or a decreased insulin 
      secretory capacity. GAD65-Ab were found in six of the eight diabetic patients 
      0.9-8.0 yr before the onset of IDDM and in 16 (41%) nondiabetic patients during a 
      follow-up of 2.4-19.5 yr. Eleven (28%) nondiabetic patients had GAD67-Ab and 
      islet cell antibodies. Fasting C peptide (mean +/- SD, 0.5 +/- 0.24 vs. 1.03 +/- 
      0.49 nmol/L; P = 0.003) and first phase insulin response (75.6 +/- 37.9 vs. 166.4 
      +/- 112.7 mU/L; P = 0.019) were lower in patients with than in those without 
      GAD65-Ab. No HLA genotype predominated in the IDDM patients or GAD65-Ab-positive 
      nondiabetic patients, but the IDDM high risk genotypes were decreased in 
      frequency among the patients with GAD65-Ab. In conclusion, nondiabetic autoimmune 
      polyendocrine syndrome type 1 patients frequently have GAD65-Ab together with a 
      decreased insulin secretory capacity, suggesting subclinical islet cell 
      inflammation not invariably progressing to diabetes. This is not associated with 
      HLA haplotypes conferring susceptibility to or protection from IDDM.
FAU - Tuomi, T
AU  - Tuomi T
AD  - Department of Endocrinology, Lund University, Malmo, Sweden.
FAU - Bjorses, P
AU  - Bjorses P
FAU - Falorni, A
AU  - Falorni A
FAU - Partanen, J
AU  - Partanen J
FAU - Perheentupa, J
AU  - Perheentupa J
FAU - Lernmark, A
AU  - Lernmark A
FAU - Miettinen, A
AU  - Miettinen A
LA  - eng
GR  - R01 DK026190/DK/NIDDK NIH HHS/United States
GR  - DK-42654/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Clin Endocrinol Metab
JT  - The Journal of clinical endocrinology and metabolism
JID - 0375362
RN  - 0 (Autoantibodies)
RN  - 0 (C-Peptide)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ alpha-Chains)
RN  - 0 (HLA-DQ beta-Chains)
RN  - 0 (HLA-DQA1 antigen)
RN  - 0 (HLA-DQB1 antigen)
RN  - 0 (HLA-DR Antigens)
RN  - 0 (HLA-DRB1 Chains)
RN  - 0 (Insulin)
RN  - 0 (islet cell antibody)
RN  - EC 4.1.1.15 (Glutamate Decarboxylase)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Autoantibodies/*blood
MH  - C-Peptide/blood
MH  - Child
MH  - Child, Preschool
MH  - Diabetes Mellitus, Type 1/*immunology
MH  - Female
MH  - Follow-Up Studies
MH  - Genes, MHC Class II
MH  - Genotype
MH  - Glutamate Decarboxylase/*immunology
MH  - HLA-DQ Antigens/blood
MH  - HLA-DQ alpha-Chains
MH  - HLA-DQ beta-Chains
MH  - HLA-DR Antigens/blood
MH  - HLA-DRB1 Chains
MH  - Histocompatibility Testing
MH  - Humans
MH  - Infant
MH  - Insulin/blood/metabolism
MH  - Insulin Secretion
MH  - Islets of Langerhans/immunology/metabolism
MH  - Male
MH  - Middle Aged
MH  - Polyendocrinopathies, Autoimmune/blood/diagnosis/*immunology
MH  - Polymerase Chain Reaction
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
AID - 10.1210/jcem.81.4.8636356 [doi]
PST - ppublish
SO  - J Clin Endocrinol Metab. 1996 Apr;81(4):1488-94. doi: 10.1210/jcem.81.4.8636356.