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- Toyoshi Endo, Soichi Takizawa, Shoichiro Tanaka, Masashi Takahashi, Hideki Fujii, Terumi Kamisawa, and Tetsuro Kobayashi.
- Third Department of Internal Medicine, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Chuo City, Yamanashi, Japan. endot@yamanashi.ac.jp
- Diabetes. 2009 Mar 1; 58 (3): 732-7.
ObjectiveThe pathogenesis of autoimmune pancreatitis (AIP) and fulminant type 1 diabetes remains unclear, although it is known that immune-mediated processes severely compromise the endocrine and exocrine functions in both diseases.Research Design And MethodsWe have screened a lambdaTriplEx2 human pancreas cDNA library with serum from a patient with AIP and obtained positive clones. Sequence analysis revealed that 7 of 10 clones were identical to human amylase alpha-2A. Using a recombinant COOH-terminal amylase alpha-2A protein, we developed an enzyme-linked immunosorbent assay system to detect autoantibodies against human amylase alpha-2A.ResultsAll 15 serum samples from patients with AIP recognized the recombinant protein, whereas sera from 25 patients with chronic alcoholic pancreatitis and sera from 25 patients with a pancreas tumor did not. Interestingly, 88% (15/17) of patients with fulminant type 1 diabetes were positive for an autoantibody against amylase alpha-2A. These antibodies were detected in 21% of patients with acute-onset type 1 diabetes (9 of 42) and 6% of type 2 diabetic patients (4 of 67).ConclusionsThese results suggest that an autoantibody against amylase alpha-2A is a novel diagnostic marker for both AIP and fulminant type 1 diabetes and that, clinically and immunologically, AIP and fulminant type 1 diabetes are closely related.
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