This study presents a 2-yr follow-up of 281 patients, aged 15-34 yr, diagno
sed with diabetes between 1992 and 1993. At diagnosis, 224 (80%) patients w
ere positive for at least one of the following autoantibodies: islet cell a
ntibodies (ICAs), glutamic acid decarboxylase antibodies (GADAs), or tyrosi
ne phosphatase antibodies (IA-2As); the remaining 57 (20%) patients were ne
gative for all three autoantibodies. At diagnosis, C-peptide levels were lo
wer (0.27; 0.16-0.40 nmol/L) in autoantibody-positive patients compared wit
h autoantibody-negative patients (0.51; 0.28-0.78 nmol/L; P < 0.001). After
2 yr, C-peptide levels had decreased significantly in patients with autoim
mune diabetes (0.20; 0.10-0.37 nmol/L; P = 0.0018), but not in autoantibody
-negative patients. In patients with autoimmune diabetes, a low initial lev
el of C-peptide (odds ratio, 2.6; 95% confidence interval, 1.7-4.0) and a h
igh level of GADAs (odds ratio, 2.5; 95% confidence interval, 1.1-5.7) were
risk factors for a C-peptide level below the reference level of 0.25 nmol/
L 2 yr after diagnosis. Body mass index had a significant effect in the mul
tivariate analysis only when initial C-peptide was not considered. Factors
such as age, gender, levels of ICA or IA-2A or insulin autoantibodies (anal
yzed in a subset of 180 patients) had no effect on the decrease in <beta>-c
ell function.
It is concluded that the absence of pancreatic islet autoantibodies at diag
nosis were highly predictive for a maintained beta -cell function during th
e 2 yr after diagnosis, whereas high levels of GADA indicated a course of d
ecreased beta -cell function with low levels of C-peptide. In autoimmune di
abetes, an initial low level of C-peptide was a strong risk factor for a de
crease in beta -cell function and conversely high C-peptide levels were pro
tective. Other factors such as age, gender, body mass index, levels of ICA,
IA-2A or IAA had no prognostic importance.