Histologic findings in islets of whole pancreas allografts: lack of evidence for recurrent cell-mediated diabetes mellitus.

Cell-mediated cytotoxicity directed toward pancreatic islets plays a significant role in the pathogenesis of type 1 diabetes mellitus. Histologically, autoimmune insulitis appears as mononuclear infiltrates that precede actual beta cell loss. Experimental studies by Bartlett et al. on the BB rat model suggest that whole pancreas transplants are not susceptible to recurrent autoimmune diabetes. To test this hypothesis on clinical grounds, we evaluated the islets in pancreatectomies and percutaneous needle biopsies from 55 whole pancreas allografts. In this material, islet inflammation was never seen independently of allograft rejection, but was always associated with inflammation of the surrounding acinar structures. The degree of islet inflammation and the occasional presence of islet necrosis correlated well with the degree of rejection and only occurred in the higher grades of the latter (grades III-V). We did not observe isolated insulitis as a histological indication of selective cell-mediated cytotoxicity against beta cells.