We characterised a consecutive cohort of 132 youth onset diabetic individua
ls (age at onset < 30 years, mean duration of disease 5.5 +/- 6.0 years) fr
om North India, by serological determination of the determination of the is
let cell autoantibodies, GAD(65) and IA2, and clinically for coexisting aut
oimmune thyroid disease, malnutrition and pancreatic calcification. Five ty
pes of diabetes were delineated: Type 1 (37%), ketosis resistant (32%), Typ
e 2 (13%). fibrocalculous pancreatopathy (11%) and autoimmune polyglandular
syndrome (7%). C-peptide response to glucagon was assessed in a representa
tive subset of 50 patients with Type 1, ketosis resistant, and autoimmune p
olyglandular syndrome. A total of 22.4% of Type 1 and 30% of autoimmune pol
yglandular syndrome subjects showed both GAD(65) plus IA-2 autoantibody pos
itivity, significantly more than the 4.7% positivity shown by the ketosis r
esistant type. However, GAD(65) antibody positivity alone was seen in 38% o
f ketosis resistant subjects which was significantly more than the 14.2 and
10% positivity seen in Type 1 and autoimmune polyglandular groups, respect
ively. The fibrocalculous pancreatopathy group showed GAD(65) plus IA-2 aut
oantibody positivity in 14.2% and GAD(65) autoantibody alone positivity in
7.1%. 26 and 60%, respectively, of the Type 1 and autoimmune polyglandular
syndrome groups had thyroid microsomal autoantibody positivity. Type 1 show
ed significantly less C-peptide response to glucagon when compared to the k
etosis resistant and autoimmune polyglandular syndrome groups. The controls
and Type 2 diabetic individuals tested negative for islet cell autoimmunit
y markers. These findings demonstrate a role of islet cell autoimmunity in
the pathogenesis of four out of the five clinical types of youth onset diab
etes seen in North India. (C) 2001 Elsevier Science Ireland Ltd. All rights
reserved.