Insulin autoantibodies are associated with islet cell antibodies; their relation to insulin antibodies and B-cell function in diabetic children

Abstract

Blood was drawn from 74 children, 3-16 years old, at diagnosis of Type 1 (insulin-dependent) diabetes and before the first insulin injection. Insulin autoantibodies were detected with a polyethylen-glycol-method in 27/74 (36.4%) and with an immuno-electrophoretic method in 6/74 (8.1%). Islet cell cytoplasmic antibodies detected by indirect immuno-fluorescence were found in 49/74 patients (66.2%), who included as many as 23 of the 27 patients with insulin autoantibodies determined with the polyethylen-glycol-method (p less than 0.01). The proportion of insulin autoantibody-positive patients who developed insulin antibodies during the first 9 months of insulin treatment was not significantly greater (51.8%) than that of insulin autoantibody-negative patients (44.6%), but patients with both islet cell antibodies and insulin autoantibodies at diagnosis produced more insulin antibodies during the first 9 months (p less than 0.05). There was no difference in fasting or meal stimulated serum C-peptide after 3, 9 or 18 months as related to occurrence of insulin autoantibodies and/or islet cell antibodies. The correlation between insulin autoantibodies and islet cell antibodies indicates that both types of autoantibodies reflect the same immunological process, although the lack of correlation to C-peptide may indicate that they play a minor causal role. In addition, the results show that patients with an active autoimmune process evidently tend to produce more insulin antibodies during the first months of insulin treatment, but the islet cell antibodies and insulin autoantibodies-positive patients had at least as good residual B-cell function as patients without autoantibodies at diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Natural Course of Remission in IDDM During 1st yr After Diagnosis

“…Persistently ICA + patients show an increased reduction in fasting C-peptide 18-30 mo after diagnosis (20,21). Other studies were unable to demonstrate a more rapid loss of (3-cell function in ICA + patients (22)(23)(24). Probably because of the short observation period of 12 mo in this study, we did not find a more rapid loss of P-cell function in patients with ICA.…”

An 8‐year follow‐up of anti‐insulin antibodies in diabetic children: relation to insulin autoantibodies, HLA type, β‐cell function, clinical course and type of insulin therapy

“…Most of our findings on insulin autoantibodies in newly diagnosed type 1 diabetic patients are consistent with earlier studies. In particular, our data confirmed the high percentage of positivity, the influence of age on insulin binding level (3)(4)(5)(6) and the lack of correlation with C-peptide levels on diagnosis (7,9). However, we disagree with the findings of Ziegler et al (8) concerning the striking association with HLA DR4 encountered in newly diagnosed type 1 diabetic adults.…”

“…The lack of correlation with C-peptide levels (3,7,9) and the inability of these autoantibodies to predict the insulin antibody response to exogenous insulin (6,7,10) suggest that their main role is not so much as active participants in beta-cell destruction as serologic markers of autoimmune damage. Furthermore, the clinical importance of anti-insulin antibodies remains poorly defined at present, although they have been found in the serum of patients treated with exogenous insulin for a long period (1 1).…”

“…Finally, data on the long-term follow-up of these antibodies have not been published to date. Indeed, until now these antibodies have been investigated only in the very first few years of the disease, in patients treated with either porcine or human insulin (6,7,9,10,(19)(20)(21).…”

Etiopathogenesis of Insulin Autoimmunity

“…Such studies are also important as it has been suggested that the IAA levels may be the best predictor of clinical onset in young children [168] as well as in children born to mothers with T1D in the BABY DIAB study [87]. Further studies are also needed to determine epitope specificity in relation to the apparent polyclonal nature of IAA and their similarity to the insulin antibodies (IA) detected after insulin therapy has been initiated [174, 175]. …”