Pancreas Allograft Failure Research Articles

Spectrum of Histopathological Changes in Pancreas Allograft Biopsies and Relationship to Graft Loss

Histological evaluation of pancreas allografts through the use of needle biopsies is of paramount importance for the determination of the etiology of graft dysfunction. In addition, pathological assessment of the overall status of the exocrine, endocrine, and vascular components provides invaluable information with regards to the prognosis of the graft. Pancreas allograft failure results from a variety of causes, highly dependent on the time posttransplantation, but after the first 6 months’ posttransplantation the most common cause of graft loss is chronic rejection. The main histological manifestations of chronic rejection are progressive graft sclerosis (increasing fibrosis and proportional atrophy of the glandular components), secondarily leading to endocrine failure. Evaluation of serial biopsies in patients with graft failure has shown that the most important histological predictors of chronic rejection/graft sclerosis are diffuse acinar inflammation and acute and chronic vascular injury in the form of intimal arteritis and proliferative transplant arteriopathy, respectively.

Combined analysis of autoantibodies against beta-cells for prediction of pancreas allograft failure

Combined analysis of autoantibodies against beta-cells for prediction of pancreas allograft failure

APPEARANCE OF TYPE II DIABETES MELLITUS IN TYPE I DIABETIC RECIPIENTS OF PANCREAS ALLOGRAFTS

To determine the cause of hyperglycemia appearing after pancreas transplantation in type I diabetic recipients, we performed 65 oral glucose tolerance tests with serum insulin and C-peptide determinations in 32 patients with pancreas grafts functioning two or more months following transplantation. We correlated these results with estimates of graft size obtained by magnetic resonance imaging (MRI) and values of urinary amylase as a measure of pancreatic exocrine function. A total of 33 studies were obtained in 20 patients at times of normal glucose tolerance, and normal ranges for serum insulin and C-peptide levels were established; 32 studies in 17 patients during periods of glucose intolerance revealed values of serum insulin and C-peptide that were within the normal range, though the time to peak values was delayed to 2 hr, characteristic of type II diabetes. Only 3 of 17 patients examined by MRI had significant pancreatic allograft atrophy. These patients also had low urinary amylase excretion, and the only values for serum C-peptide that were below the normal range. The other 14 hyperglycemic patients had normalized pancreas grafts, normal urinary amylase excretion, and normal values for serum insulin and C-peptide. In our experience, then, in 76% of patients with hyperglycemia more than 2 months following pancreas transplantation, the cause was appearance of type II diabetes rather than destruction of the allograft with recurrence of type I diabetes. This observation has important implications for the definition of pancreas allograft failure and for the management of pancreas allograft recipients with hyperglycemia.