Late-onset type 1 diabetes

Abstract

Insulin-dependent diabetes mellitus (IDDM) and non-insulin dependent diabetes mellitus (NIDDM) are generally phenotypically different and are thought to be caused by separate and distinct disease processes: type 1 and type 2 diabetes, respectively. The finding of islet cell antibodies and glutamic acid decarboxylase antibodies in 10% to 30% of patients with phenotypic NIDDM has raised the possibility that the type 1 diabetes disease process is much more common than previously assumed; this subset has been referred to as late-onset type 1 diabetes or slowly progressive IDDM. Our ability to distinguish the type 1 versus the type 2 disease process has limitations because of genetic, immunologic, and functional complexity. In this review, we summarize the current understanding of the clinical characteristics, autoimmunity, genetic susceptibility, and protection of late-onset type 1 diabetes, and we discuss the implications for therapy and prevention.