학술논문

Re-exposure to beta cell autoantigens in pancreatic allograft recipients with preexisting beta cell autoantibodies.
Document Type
Article
Source
Clinical Transplantation. Nov2015, Vol. 29 Issue 11, p991-996. 6p.
Subject
*PANCREATIC beta cells
*AUTOANTIGENS
*HOMOGRAFTS
*AUTOANTIBODIES
*PANCREAS transplantation
Language
ISSN
0902-0063
Abstract
Re-exposure to beta cell autoantigens and its relevance in the presence of donor-specific antibodies ( DSA) in pancreatic allograft recipients is not well known. Thirty-three patients requiring a pancreas transplant were enrolled in an IRB approved study. They underwent prospective monitoring for DSA and beta cell autoantibody ( BCAA) levels to GAD65, insulinoma-associated antigen 2 ( IA-2), insulin (micro- IAA [ mIAA]), and islet-specific zinc transporter isoform-8 (ZnT8). Twenty-five (75.7%) had pre-transplant BCAA. Twenty had a single antibody ( mIAA n = 15, GAD65 n = 5); five had two or more BCAA ( GAD65 + mIAA n = 2, GAD65 + mIAA+ IA-2 n = 2, GA65 + mIAA+ IA-2 + ZnT8 = 1). No changes in GAD65 (p > 0.29), IA-2 (>0.16), and ZnT8 (p > 0.07) were observed between pre-transplant and post-transplant at 6 or 12 months. A decrease in mIAA from pre- to post-6 months (p < 0.0001), 12 months (p < 0.0001), and from post-6 to post-12 months (p = 0.0002) was seen. No new BCAA was observed at one yr. Seven (21.0%) developed de novo DSA. The incidence of DSA was 24% in patients with BCAA vs. 25% in patients without BCAA (p = 0.69). Pancreatic allograft function of patients with vs. without BCAA, and with and without BCAA + DSA was comparable until last follow-up (three yr). Re-exposure to beta cell autoantigens by pancreas transplant may not lead to increased levels or development of new BCAA or pancreatic allograft dysfunction. [ABSTRACT FROM AUTHOR]