RELATIONSHIPS AMONG RESIDUAL BETA-CELLS, EXOCRINE PANCREAS, AND ISLET CELL ANTIBODIES IN INSULIN-DEPENDENT DIABETES-MELLITUS

Quantitative analysis was performed using computerized morphometry on the relationships between residual β cells, pancreatic exocrine glands, and islet cell antibodies (ICA) in 14 pancreata of insulin-dependent diabetic (IDDM) patients. Both pancreatic exocrine glands and β cells were markedly reduced in weight in IDDM patients compared with non-insulin-dependent diabetic (NIDDM) patients or nondiabetic controls. β cells were preserved in six cases and were completely abolished in eight cases. In nine IDDM pancreata weighed at autopsy, the weights of pancreatic exocrine glands in six patients with either no or virtually no residual β cells (32.3 ± 1.6 g) were greater than those in three patients with residual β cells (23.1 ± 2.5 g, P < .05). Infiltration of lymphocytes positive for leukocyte common antigen (LCA) around the islet was observed in only one case with ICA and residual β cells. Infiltration of LCA-positive lymphocytes around pancreatic acinar cells was observed in 50% (six of 12) of patients examined. The weight of pancreatic exocrine glands in patients with LCA-positive lymphocyte infiltration (26.2 ± 2.3 g) was lower than that in patients without this condition (33.2 ± 2.4 g, P < .05). Pancreatic cytokeratin autoantibodies (PKA) were detected in four of 10 patients examined. In addition, all four ICA-positive patients had residual β cells, while only one of seven ICA-negative patients had residual β cells (P = .03). The better preservation of exocrine pancreas glands in patients without residual β cells than in those with residual β cells cannot be explained by the hypothesis that atrophy of the pancreatic exocrine gland is due to loss of the trophic action of insulin on acinar cells. Exocrine pancreatic atrophy accompanied by infiltration of LCA-positive lymphocytes around the acinar cells suggests primary involvement of the exocrine pancreas in the autoimmune pathological process of IDDM. The contribution of residual β cells to the generation of ICA is also suggested. © 1993.