B. Lindberg et al., Islet autoantibodies in cord blood from children who developed Type I (insulin-dependent) diabetes mellitus before 15 years of age, DIABETOLOG, 42(2), 1999, pp. 181-187
Islet autoantibodies are early markers for Type I (insulin-dependent) diabe
tes mellitus. The aim of this study was to establish whether islet autoanti
bodies were present at birth in children who developed Type I diabetes befo
re 15 years of age. Cord blood sera from 81 children who developed Type I d
iabetes between 10 months and 14.9 years of age were tested for glutamic ac
id decarboxylase autoantibodies (GAD65Ab), islet cell antigen 512 autoantib
odies (ICA512Ab), insulin autoantibodies (IAA) all by quantitative radiolig
and binding assays and islet cell autoantibodies (ICA) by indirect immunofl
uorescence. Cord blood sera from 320 randomly selected matched children wer
e controls. The children who developed Type I diabetes had an increased fre
quency of cord blood islet autoantibodies compared with control subjects: G
lutamic acid decarboxylase autoantibodies were detected in 6% (5/81) patien
ts and 2% (5/320) control subjects (p = 0.03); islet cell antigen 512 autoa
ntibodies in 5% (4/73) patients and 1% (4/288) control subjects (p = 0.06);
insulin autoantibodies (IAA) in 0% (0/79) patients and 0.3% (1/320) contro
l subjects (p = 0.36); and islet cell autoantibodies in 10% (8/81) patients
compared with 0.6% (2/320) control subjects (p = 0.0001). Taken together,
17% (14/81) patients had one or more islet autoantibody compared with 4% (1
2/320) control subjects (p = 0.0001). Whereas none of the control children
had more than one antibody, 4% (3/81) children who later developed Type I d
iabetes were double positive (p = 0.002). Although glutamic acid decarboxyl
ase autoantibodies' concentrations in cord-blood correlated to those in the
mothers' blood at the time of delivery, no corresponding correlation was f
ound for the other two types of autoantibodies. The increased frequency of
cord blood islet autoantibodies suggests that the Type I diabetes process c
ould already be initiated in utero.