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Has the Time Come?

Jay S. Skyler, MD

JAMA. 2007;297:1599-1600.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Type 1 diabetes mellitus (DM) arises from selective immunologically mediated destruction of the insulin-producing beta cells in the pancreatic islets of Langerhans with consequent insulin deficiency.^1-2 This occurs in genetically susceptible individuals and is a cellular-mediated process, presumably a specific reaction to 1 or more beta cell proteins (autoantigens), although probably initiated by some environmental factors. There is consequent progressive impairment of beta cell function and decline in beta cell mass.

The immunologic nature of the type 1 DM disease process was firmly established in humans by studies in the late 1980s and early 1990s demonstrating that immune intervention in patients with newly diagnosed type 1 DM resulted in a slower decline in beta cell function than in control groups.^3-4 Over the last several years, there have been major efforts to interdict the type 1 DM disease process either in newly diagnosed patients^5-6 or in relatives . . . [Full Text of this Article]

Author Affiliation: Diabetes Research Institute, University of Miami Miller School of Medicine, Miami, Fla.

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