Diabetes mellitus secondary to chronic pancreatitis.

From the present review it appears that insulin-dependent diabetes is a common finding in chronic pancreatitis, and impaired secretion of insulin from beta-cells of the pancreatic islets is essential for the development of this form of secondary diabetes. Judged from a positive correlation between insulin secretory capacity and stimulated pancreatic enzyme output, beta-cell function may decrease in parallel with exocrine pancreatic function. However, in patients with insulin-dependent diabetes secondary to chronic pancreatitis beta-cell function was preserved to a greater extent and glucoregulation was better than in comparable Type 1 (insulin-dependent) diabetic patients. Immunological phenomena and associations with certain HLA-alleles characterizing Type 1 diabetes mellitus were not found in insulin-dependent diabetes secondary to chronic pancreatitis. This may contribute to the slower destruction of the beta-cells in chronic pancreatitis than encountered in Type 1 diabetes. The small number of chronic pancreatitis patients who developed totally absence of endogenous insulin production still have some alpha-cell function during i.v. arginine and meal stimulation. However, insulin-induced hypoglycemia and insulin withdrawal did not stimulate glucagon secretion in the secondary diabetic patients in contrast to comparable Type 1 diabetics. Nevertheless, blood glucose counterregulation is intact in the secondary diabetics due to preserved catecholamine secretion. Furthermore, ketonemia develops during dissipation of insulin, in spite of absence of increased glucagon secretion, emphasizing the role of insulin dissipation for the development of ketoacidosis in this form of diabetes. The suggested increased susceptibility to severe hypoglycemia and less tendency to development of ketonemia may further be influenced by altered insulin sensitivity, nutritional factors and concomitant hepatic failure in diabetes secondary to chronic pancreatitis. Pancreatic polypeptide secretion was absent in chronic pancreatitis without endogenous insulin production. Pancreatic polypeptide secreting cells thus seem to be at least as vulnerable as the beta-cells to the destructive processes characterizing chronic pancreatitis, whereas glucagon secreting alpha-cells preserve secretory capacity to a greater extent than PP-cells and beta-cells. No data, however, favour the view that absent pancreatic polypeptide secretion has any major effect on the glucoregulation in diabetes secondary to chronic pancreatitis. Increased plasma concentration of somatostatin was found in patients with insulin-dependent diabetes secondary to chronic pancreatitis. The source of somatostatin in the patients is unknown, but somatostatin may contribute to a reduction in overall blood glucose level in patients without endogenous insulin secretion due to inhibition of glucagon secretion.(ABSTRACT TRUNCATED AT 400 WORDS)