Slow onset type 1 diabetes is an heterogeneous entity. its clinical feature
s may mimick type 2 diabetes but its pathophysiological mechanisms are clos
e to type 1 diabetes.
Aim of the study: To find out the frequencies, levels and associations of I
CA, GADab and IA-2ab in type 2 diabetic patients with atypical phenotype. T
o compare it to type 1 diabetes.
Patients and methods: 1CA, GADab and IA-2ab were determined in: -61 patient
s (age at diagnosis 48.2 +/- 10, range 36-73 years) with an initial diagnos
is of type 2 diabetes but having at least one symptom suggesting a slow typ
e 1 diabetes (loss of weight, absence of obesity at diagnosis or secondary
failure of oral hypoglycaemic agents). -70 patients with type 1 diabetes (a
ge 18 +/- 8.9, range 2-35 years). Clinical data evaluated in slow type 1 we
re maximal BMI, BMI and loss of weight at diagnosis and autoimmune disease.
Fasting C-peptide and insulinemia were also assessed.
Results: (Slow type 1 diabetes versus type 1 diabetes). ICA (43% vs 70%; p
< 0.01) and IA-2ab (16% vs 75%; p < 0.01) were more frequent in type 1. GAD
ab were as frequent (62% vs 74%). Association of the three antibodies 1:15.
7% vs 58.5%; p < 0.05) were more frequent in type 1. Prevalence of GADab al
one (27.5% vs 7.5%; p < 0.05) was higher in slow type 1 diabetes and with h
igher levels (median 55.5 UI/ml vs 17 UI/ml; p < 0.01). There was no differ
ence for levels of ICA (25.5 UJDF/ml vs 28 UJDF/ml) or IA-2ab (11.5 UI/ml v
s 38.5 UI/ml), BMI of GADab positive patients was lower. Delay of insulinot
herapy was shorter in GADab or ICA positive patients. We did not find any r
elationship between antibodies presence and fasting C-peptide or insulinemi
a.
Conclusion: Slow type 1 diabetes should be evoked in atypical type 2 diabet
es. Slow onset type 1 diabetic patients have different autoimmune patterns
suggesting a different pathophysiological process. GADab and ICA are useful
markers to predict future insulinopenia.