A Novel Subtype of Type 1 Diabetes Mellitus Characterized by a Rapid Onset and an Absence of Diabetes-Related Antibodies

• Published in: The New England journal of medicine Vol. 342; no. 5; pp. 301 - 307
• Main Authors: Imagawa, Akihisa, Hanafusa, Toshiaki, Miyagawa, Jun-ichiro, Matsuzawa, Yuji
• Format: Journal Article
• Language: English
• Published: Boston, MA Massachusetts Medical Society 03.02.2000
• Subjects: Acids; Biological and medical sciences; Diabetes; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Japan; Medical sciences; Pancreas; Endocrinopathy; Human; Immunopathology; Glutamic acid; Decarboxylase; Enzyme; Autoimmune disease; Lyases; Serology; Pathology; Carbon-carbon lyases; Carboxy-lyases; Clinical biology; Insulin dependent diabetes; Adult; Evolution; Clinical investigation; Pancreas; Subtype
• ISSN: 0028-4793; 1533-4406
• DOI: 10.1056/NEJM200002033420501

Type 1 diabetes mellitus is caused by loss of insulin-secreting capacity due to selective autoimmune destruction of the pancreatic beta cells. 1 , 2 Insulitis (i.e., mononuclear-cell infiltration of the pancreatic islets) is the direct result of the autoimmune process. Antibodies to the cytoplasm of islet cells, glutamic acid decarboxylase, insulin, and tyrosine phosphatase–like protein (IA-2 or IA-2β), which appear before the clinical onset of diabetes, are good markers of the autoimmune process. 1 , 2 Several lines of evidence have suggested that autoimmunity is not the only cause of beta-cell destruction. We and others have described young patients who presented with the abrupt . . .