Islet cell and insulin autoantibodies in organ-specific autoimmune patients. Their behaviour and predictive value for the development of Type 1 ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1987-05

AUTHORS

C. Betterle, F. Presotto, B. Pedini, L. Moro, R. S. Slack, F. Zanette, R. Zanchetta

ABSTRACT

To evaluate the behaviour and predictive value of islet cell and insulin autoantibodies in patients with organ-specific autoimmune diseases, we followed 21 non-diabetic subjects for a mean period of 84 +/- 27 months. Ten patients were persistently seropositive for complement-fixing islet cell antibodies and high titres of immunoglobulin G islet cell antibodies (greater than or equal to 1:8). The prevalence of persistent insulin autoantibodies in this group was 67%. Seven patients (70%) developed Type 1 (insulin-dependent) diabetes mellitus after a latency period of 2-60 months. The predictive value of complement-fixing islet cell antibodies was 65%, and in the presence of both complement-fixing islet cell and insulin autoantibodies the predictive value rose to 76%. Eleven patients were seronegative for complement-fixing islet cell antibodies and had low immunoglobulin G islet cell antibodies titres (less than 1:8) that were either persistent or transient, or that fluctuated during follow-up. The prevalence of persistent insulin autoantibodies in this group was 45%; only one subject developed Type 1 diabetes. The predictive value of persistent islet cell antibodies (complement-fixing positive/negative) was 54%, and it rose to 70% when both islet cell and insulin autoantibodies were present. Individuals with only insulin autoantibodies or immunoglobulin G islet cell antibodies did not develop diabetes mellitus. A high frequency of HLA-DR3 and/or DR4 was found in patients who developed diabetes mellitus. Thus, the presence of both islet cell and insulin autoantibodies in patients with organ-specific autoimmune disease appears to confer the highest risk of progression toward Type 1 diabetes. More... »

PAGES

292-297

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf00299020

DOI

http://dx.doi.org/10.1007/bf00299020

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050342703

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/3301480


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