PMID- 16390391
OWN - NLM
STAT- MEDLINE
DCOM- 20060307
LR  - 20221207
IS  - 1399-543X (Print)
IS  - 1399-543X (Linking)
VI  - 6
IP  - 4
DP  - 2005 Dec
TI  - Slowly progressing form of type 1 diabetes mellitus in children: genetic analysis 
      compared with other forms of diabetes mellitus in Japanese children.
PG  - 221-9
AB  - AIMS: Slowly progressing insulin-dependent diabetes mellitus (SPIDDM, hereafter 
      referred to as IDDMS in this article) is a unique subtype of type 1 diabetes in 
      Japanese children. To clarify the genetic background of IDDMS, we analyzed 
      HLA-DRB1, -DQB1 and -DQA1 alleles, phenotypes, and genotypes and compared them 
      with acute-onset type 1 diabetes, non-insulin-dependent diabetes mellitus 
      (NIDDM), and control subjects. METHODS: HLA-DRB1, -DQA1, and -DQB1 types were 
      defined by DNA analysis using polymerase chain reaction (PCR), and typing for 
      human leukocyte antigen (HLA) was performed by the sequencing-based typing (SBT) 
      method using Match Maker and MT Navigator in combination. HLA-A24 was determined 
      by the PCR-sequence-specific oligo-nucleotide probe (PCR-SSOP) method. The 234 
      patients with type 1 diabetes were divided into three groups: 32 cases of IDDMS, 
      137 cases of acute-onset form aged more than 5 yr (IDDMA), and 65 cases of 
      acute-onset form less than 5 yr of age at onset (IDDME). In addition, we studied 
      55 children with type 2 diabetes (NIDDM) and 97 normal controls. RESULTS: The 
      patients with IDDMS were older at diagnosis and had a greater body mass index 
      (BMI) than those with IDDM (A + E). The prevalence of islet autoantbodies was not 
      significantly different from IDDMA. The allele frequencies of DRB1*0405, 
      DQA1*0302, and DQB1*0401 were significantly increased; however, DRB1*0901, 
      DQA1*03, DQB1*0303, and HLA-A24 were low and not significantly different from 
      control subjects. CONCLUSIONS: HLA phenotypes and genotypes in patients with 
      IDDMS were different from those in NIDDM and control subjects and were closer to 
      those of IDDMA. Together with a low prevalence of HLA-A24, the genetic features 
      are similar to those of SPIDDM and latent autoimmune diabetes in adults (LADA) in 
      adults. In our series, the clinical features such as lack of obesity and lack of 
      responsiveness to oral hypoglycemic agents were most different from those of 
      adults' onset.
FAU - Ohtsu, Shigeyuki
AU  - Ohtsu S
AD  - Department of Pediatrics, Kitasato University School of Medicine, Sagamihara, 
      Japan.
FAU - Takubo, Noriyuki
AU  - Takubo N
FAU - Kazahari, Mayumi
AU  - Kazahari M
FAU - Nomoto, Keiko
AU  - Nomoto K
FAU - Yokota, Fumiyuki
AU  - Yokota F
FAU - Kikuchi, Nobuyuki
AU  - Kikuchi N
FAU - Koike, Akemi
AU  - Koike A
FAU - Matsuura, Nobuo
AU  - Matsuura N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Denmark
TA  - Pediatr Diabetes
JT  - Pediatric diabetes
JID - 100939345
RN  - 0 (Autoantibodies)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 94ZLA3W45F (Arginine)
SB  - IM
MH  - Age of Onset
MH  - Arginine
MH  - Asian People/genetics
MH  - Aspartic Acid
MH  - Autoantibodies/analysis
MH  - Case-Control Studies
MH  - Child
MH  - Child, Preschool
MH  - Diabetes Mellitus, Type 1/epidemiology/*genetics/immunology
MH  - Diabetes Mellitus, Type 2/genetics/immunology
MH  - Disease Progression
MH  - Female
MH  - Gene Frequency
MH  - Genotype
MH  - Haplotypes
MH  - Humans
MH  - Japan/epidemiology
MH  - Male
MH  - Phenotype
EDAT- 2006/01/05 09:00
MHDA- 2006/03/08 09:00
CRDT- 2006/01/05 09:00
PHST- 2006/01/05 09:00 [pubmed]
PHST- 2006/03/08 09:00 [medline]
PHST- 2006/01/05 09:00 [entrez]
AID - PDI133 [pii]
AID - 10.1111/j.1399-543X.2005.00133.x [doi]
PST - ppublish
SO  - Pediatr Diabetes. 2005 Dec;6(4):221-9. doi: 10.1111/j.1399-543X.2005.00133.x.