Development of autoimmune-mediated β cell failure after total pancreatectomy with autologous islet transplantation

M. D. Bellin, A. Moran, J. J. Wilhelm, T. D. O'Brien, P. A. Gottlieb, L. Yu, T. B. Dunn

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Total pancreatectomy with islet autotransplantation (TPIAT) is performed for definitive treatment of chronic pancreatitis; patients are not diabetic before surgery, or have C-peptide positive pancreatogenous diabetes. Thus, TPIAT recipients are not traditionally considered at risk for autoimmune loss of the islet graft. We describe a 43-year-old female who underwent TPIAT with high mass islet graft of 6031-IEQ/kg, with no evidence of presurgical β cell autoimmunity who developed type 1 diabetes within the first year after TPIAT, resulting in complete loss of beta cell function. The patient had positive GAD and insulin autoantibodies at 1 year and 18 months after TPIAT, not present prior, and undetectable C-peptide after mixed meal and intravenous glucose tolerance testing at 18 months. Glucagon secretion was preserved, suggesting the transplanted alpha cell mass was intact. HLA typing revealed a DR3/DR4 class II haplotype. This case highlights the need to consider de novo type 1 diabetes in patients with unexpected islet graft failure after TPIAT. The authors report a novel case of rapid beta cell failure due to de novo type 1 diabetes presenting after total pancreatectomy and islet autotransplantation, highlighting the need to consider autoimmunity as a cause of unexpected graft failure in islet autotransplant recipients.

Original languageEnglish (US)
Pages (from-to)1991-1994
Number of pages4
JournalAmerican Journal of Transplantation
Volume15
Issue number7
DOIs
StatePublished - Jul 1 2015

Keywords

  • autoimmunity
  • autotransplantation
  • diabetes: type 1
  • insulin / C-peptide
  • islets of Langerhans

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