Pancreatogenic Diabetes after Pancreatic Resection

Abstract

The loss of pancreatic parenchyma resulting from pancreatic resection causes an extreme disruption of glucose homeostasis known as pancreatogenic diabetes. This form of glucose intolerance is different from the other forms of diabetes mellitus in that affected individuals suffer frequent episodes of iatrogenic hypoglycemia. The development of sophisticated surgical procedures, improved postoperative care, and the capacity for early diagnosis of disease has prolonged life expectancy after pancreatic resection. For this reason, pancreatogenic diabetes is now attracting attention as the primary factor influencing quality of life in patients who have undergone this procedure. The incidence of new-onset diabetes mellitus after pancreatic resection increases as the follow-up period after surgery becomes longer and is related to the progression of underlying disease, the type of surgery, and the extent of resection. The pathophysiology of pancreatogenic diabetes is related to pancreatic hormone deficiency and the altered responses of the liver and peripheral organs to lower than normal hormone levels. Hyperglycemia occurs when the amount of insulin produced or administered is insufficient because of unsuppressed hepatic glucose production secondary to a deficiency in pancreatic polypeptide. In contrast, patients lapse into hypoglycemia when insulin is barely excessive because of enhanced peripheral insulin sensitivity and glucagon deficiency. Nutritional state, pancreatic exocrine function and intestinal function also affect glycemic control. Insulin replacement is considered to be the main treatment option for insulin dependent pancreatogenic diabetes. Pancreatic polypeptide replacement and islet autotransplantation have potential as new approaches to treating patients with pancreatogenic diabetes after pancreatic resection.