PMID- 8262322
OWN - NLM
STAT- MEDLINE
DCOM- 19940121
LR  - 20221207
IS  - 0012-1797 (Print)
IS  - 0012-1797 (Linking)
VI  - 43
IP  - 1
DP  - 1994 Jan
TI  - High genetic risk for IDDM in the Pacific Northwest. First report from the 
      Washington State Diabetes Prediction Study.
PG  - 87-94
AB  - A combination of immune, genetic, and metabolic markers potentially implicated in 
      the development of insulin-dependent diabetes mellitus (IDDM) was studied in the 
      general population. We screened 3,992 healthy schoolchildren, 12-18 years of age 
      with no family history of IDDM, for islet cell antibodies (ICAs). Of the 
      children, 69 (1.7%) were found to be ICA positive (ICA+), of whom 7 (0.17%) also 
      were positive for insulin autoantibodies (IAAs). ICA+ children (group 1) were 
      human leukocyte antigen (HLA) typed at the DQ locus along with 123 matched (group 
      2) and 235 random (group 3) control subjects (from the original cohort of 3,992). 
      Of the ICA+ children, 28 underwent beta-cell function (beta-CF) studies. 
      High-risk DQ types were surprisingly prevalent in all groups with 35.8% of random 
      control subjects carrying DQB1*0302 and 8.9% carrying the highest risk HLA type 
      for IDDM, DQB1*0302/*0201. Those individuals with higher ICA titer (> 19 Juvenile 
      Diabetes Foundation units [JDF U]) had a significantly higher prevalence of 
      DQB1*0302 than those with lower titer ICA or normal control subjects. Six of 7 
      individual positive for both ICA and IAA and typed at the DQ locus were 
      DQB1*0302/*0201 heterozygotes or DQB1*0302 or DQB1*0201 homozygotes, representing 
      three of the highest risk genotypes for IDDM. No correlation was observed between 
      ICA titer or DQ type and beta-CF except that all those with beta-CF below the 5th 
      percentile carried either DQB1*0302 or DQB1*0201. Prospective follow-up is 
      underway to determine if any combination of DQ type and immune markers predicts 
      decline in beta-CF and the development of IDDM.
FAU - Rowe, R E
AU  - Rowe RE
AD  - Virginia Mason Research Center, Seattle, Washington 98111.
FAU - Leech, N J
AU  - Leech NJ
FAU - Nepom, G T
AU  - Nepom GT
FAU - McCulloch, D K
AU  - McCulloch DK
LA  - eng
GR  - DK-17047/DK/NIDDK NIH HHS/United States
GR  - DK-40627/DK/NIDDK NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Diabetes
JT  - Diabetes
JID - 0372763
RN  - 0 (Autoantibodies)
RN  - 0 (Glycated Hemoglobin A)
RN  - 0 (HLA-DQ Antigens)
RN  - 0 (Insulin Antibodies)
RN  - 0 (islet cell antibody)
SB  - IM
MH  - Adolescent
MH  - Autoantibodies/blood
MH  - Child
MH  - Diabetes Mellitus, Type 1/blood/*epidemiology/*genetics
MH  - Female
MH  - Glycated Hemoglobin/analysis
MH  - HLA-DQ Antigens/analysis
MH  - Humans
MH  - Insulin Antibodies/blood
MH  - Islets of Langerhans/immunology
MH  - Male
MH  - Northwestern United States/epidemiology
MH  - Risk Factors
MH  - Washington/epidemiology
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.2337/diab.43.1.87 [doi]
PST - ppublish
SO  - Diabetes. 1994 Jan;43(1):87-94. doi: 10.2337/diab.43.1.87.