Clinical characteristics, and time course of pancreatic beta-cell functionand glutamic acid decarboxylase antibodies in Thai patients with adult-onset type 1 diabetes: Distinction between patients of rapid- and slow-onset

In order to study the clinical characteristics, time course of beta cell fu nction and glutamic acid decarboxylase antibodies (GAD(65)Ab) in Thai patie nts with adult-onset Type 1 diabetes and to examine the distinctive feature s between patients with rapid-and slow-onset, 61 Thai patients with Type 1 diabetes who had age of disease onset at or after 20 years were studied. Al l patients were treated with insulin at the time of study and had fasting C -peptide levels less than or equal to 0.33 nmol/l. Twenty-six (42.6 %) were in rapid-onset and 35 (57.4%) were in slow-onset groups. Fourty-four of 61 (70.5%) were male. About three-fourths had body mass index (BMI) < 19 kg/m (2) at the time of insulin therapy. Only 7 of 61 (11.5%) patients had ketoa cidosis at first presentation. Five patients had associated autoimmune thyr oid disease and 10 (16.7 %) patients had family history of diabetes in firs t-degree relatives. GAD(65)Ab was positive in 31 patients (50.8%); 10 (38.5 %) were in rapid-onset and 21 (60.0 %) were in slow-onset groups. GAD(65)A b particularly of high levels were persistently elevated during 3-4 years f ollow-up period. The persistence of GAD(65)Ab were not associated with chan ges in fasting C-peptide levels. At the time of insulin dependency, there w ere no distinctive clinical features between rapid- and slow-onset patients except higher fasting C-peptide (0.08 +/- 0.08 vs. 0.14 +/- 0.10 nmol/l; p = 0.023) and GAD(65)Ab levels (19.6 +/- 17.4 vs. 46.1 +/- 49.7 U/ml; p = 0 .036) in slow-onset patients. Fasting C-peptide levels of patients in the l atter group were also demonstrated to be higher after 3-4 years of follow-u p. In conclusion, most Thai patients with adult-onset Type 1 diabetes in th is study were male and had significant degree of weight loss and lean BMI p rior to insulin therapy. The presence of GAD(65)Ab did not predict clinical features or rate of p cell loss. Patients in rapid-onset group had lower f asting C-peptide and GAD(65)Ab levels than those of slow-onset group which confirms the slower process of beta cell failure in the latter.