PMID- 8722065
OWN - NLM
STAT- MEDLINE
DCOM- 19961011
LR  - 20190515
IS  - 0149-5992 (Print)
IS  - 0149-5992 (Linking)
VI  - 18
IP  - 11
DP  - 1995 Nov
TI  - Immunogenetic, clinical, and demographic characterization of childhood type I 
      diabetes in New Zealand.
PG  - 1428-33
AB  - OBJECTIVE: To examine the relationship between genetic susceptibility alleles and 
      islet cell antibodies (ICAs) in type I diabetes. RESEARCH DESIGN AND METHODS: The 
      human leukocyte antigen (HLA)-DQB1 alleles and ICA levels of all incident type I 
      diabetic cases in patients < 20 years of age diagnosed in 1990 and 1991 in 
      Canterbury, New Zealand, were determined. RESULTS: The mean annual incidence rate 
      for type I diabetes over the 24 months was 19.0/100,000 patient-years (95% 
      confidence interval [CI] 13.5-26.0/100,000), which was considerably higher than 
      rates observed between 1982 and 1989 (11.7/100,000; 95% CI 9.6-14.3/100,000). 
      ICAs > or = 10 Juvenile Diabetes Foundation units (JDF U) were present in 84.6% 
      of the subjects, but there was a higher prevalence of ICA-negative (ICA-) 
      subjects among those diagnosed during the winter months. The frequencies of the 
      susceptibility allele DQB1*0302 and susceptibility genotype 0302/0201 were 71.8% 
      and 43.5%, respectively. Subjects with 0302 tended to be younger (mean age 8.3 
      +/- 5.1 years) than those with nonsusceptibility types (mean age 11.8 +/- 4.7 
      years, P = 0.056). The probability of being ICA positive (ICA+) was not 
      significantly different between subjects with allele 0302 (85.7%) and those 
      without it (81.8%). All seven patients negative for ICA were homozygous for DQB1 
      nonaspartate-57. There was no clustering of the immunogenetic markers with 
      demographic and clinical characteristics apart from age at diagnosis. 
      CONCLUSIONS: No direct relationship was observed between DQB1-defined genetic 
      susceptibility and ICA at diagnosis, suggesting that variations at the DQB1 locus 
      are not linked to the expression of this autoimmune marker of beta-cell 
      destruction.
FAU - Forbes, L V
AU  - Forbes LV
AD  - Lipid and Diabetes Research Group, Christchurch Hospital, New Zealand.
FAU - Scott, R S
AU  - Scott RS
FAU - Brown, L J
AU  - Brown LJ
FAU - Darlow, B A
AU  - Darlow BA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Diabetes Care
JT  - Diabetes care
JID - 7805975
RN  - 0 (Autoantibodies)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (HLA-DQ beta-Chains)
RN  - 0 (HLA-DQB1 antigen)
RN  - 0 (islet cell antibody)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Adolescent
MH  - Age Factors
MH  - Alleles
MH  - Autoantibodies/*blood
MH  - Child
MH  - Child, Preschool
MH  - Confidence Intervals
MH  - DNA/blood/isolation & purification
MH  - Demography
MH  - Diabetes Mellitus, Type 1/*epidemiology/genetics/*immunology
MH  - Disease Susceptibility
MH  - Female
MH  - Gene Frequency
MH  - Genotype
MH  - HLA-DQ Antigens/blood/genetics
MH  - HLA-DQ beta-Chains
MH  - Histocompatibility Testing
MH  - Humans
MH  - Incidence
MH  - Infant
MH  - Islets of Langerhans/immunology
MH  - Male
MH  - New Zealand/epidemiology
MH  - Polymerase Chain Reaction
MH  - Polymorphism, Restriction Fragment Length
MH  - Prevalence
MH  - Restriction Mapping
MH  - Seasons
EDAT- 1995/11/01 00:00
MHDA- 1995/11/01 00:01
CRDT- 1995/11/01 00:00
PHST- 1995/11/01 00:00 [pubmed]
PHST- 1995/11/01 00:01 [medline]
PHST- 1995/11/01 00:00 [entrez]
AID - 10.2337/diacare.18.11.1428 [doi]
PST - ppublish
SO  - Diabetes Care. 1995 Nov;18(11):1428-33. doi: 10.2337/diacare.18.11.1428.