Amylase α-2A Autoantibodies
Novel Marker of Autoimmune Pancreatitis and Fulminant Type 1 Diabetes
Novel Marker of Autoimmune Pancreatitis and Fulminant Type 1 Diabetes
Abstract
OBJECTIVE— The 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 METHODS— We have screened a λTriplEx2 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 α-2A. Using a recombinant COOH-terminal amylase α-2A protein, we developed an enzyme-linked immunosorbent assay system to detect autoantibodies against human amylase α-2A.
RESULTS— All 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 α-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).
CONCLUSIONS— These results suggest that an autoantibody against amylase α-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.
Footnotes
Published ahead of print at http://diabetes.diabetesjournals.org on 10 November 2008.
Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
See accompanying commentary, p. 520.
- Accepted October 31, 2008.
- Received April 11, 2008.
- DIABETES
