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American Journal of Pathology, Vol 128, 151-170, Copyright © 1987 by American Society for Investigative Pathology

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Pancreas transplantation. An immunohistologic and histopathologic examination of 100 grafts

RK Sibley and DE Sutherland

The authors examined tissues obtained by biopsy, pancreatectomy, and autopsy from 100 pancreas grafts to determine the cause of dysfunction or failure of the graft. Immunohistologic examination of 42 tissues to determine the mononuclear cell phenotypes and Class I and II antigen expression was performed as well. Technical factors--infections, thrombosis, obstruction--accounted for a large number of graft losses, but immunologic-mediated mechanisms resulted in graft dysfunction and failure as well. Pleomorphic inflammatory infiltrates were present in grafts with acute rejection, as well as Silastic and Prolamine duct- obstructed grafts. Criteria useful in the identification of acute rejection from pancreatitis included a more intense, predominantly mononuclear cell infiltration of transformed lymphocytes in the exocrine pancreas and evidence of vascular rejection--endovasculitis or fibrinoid necrosis. Increased expression and/or induction of Class I and II antigens on pancreatic constituents occurred in grafts with evidence of acute rejection, but also with Silastic and prolamine duct- obstructed pancreatitis. An isletitis occurred in 25% of the grafts. Nine of the 25 grafts (36%) with isletitis also had selective loss of beta cells from the islets. Recurrent diabetes mellitus appeared to have developed in these cases, which accounted for loss of graft function.


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G. Tyden, F. P. Reinholt, G. Sundkvist, and J. Bolinder
Recurrence of Autoimmune Diabetes Mellitus in Recipients of Cadaveric Pancreatic Grafts
N. Engl. J. Med., September 19, 1996; 335(12): 860 - 863.
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Copyright © 1987 by the American Society for Investigative Pathology.