Abstract
Background and AimPartial pancreatic resection is accompanied not only by a reduction in the islet cell mass but also by a variety of other factors that are likely to interfere with glucose metabolism. The aim of this work was to characterize the patient dynamics of blood glucose homeostasis during the course of partial pancreatic resection and to specify the associated clinico-pathological variables.MethodsIn total, 84 individuals undergoing elective partial pancreatic resection were consecutively recruited into this observational trial. The individuals were assigned based on their fasting glucose or oral glucose tolerance testing results into one of the following groups: (I) deteriorated, (II) stable or (III) improved glucose homeostasis three months after surgery. Co-variables associated with blood glucose dynamics were identified.ResultsOf the 84 participants, 25 (30%) displayed a normal oGTT, 17 (20%) showed impaired glucose tolerance, and 10 (12%) exhibited pathological glucose tolerance. Elevated fasting glucose was present in 32 (38%) individuals before partial pancreatic resection. Three months after partial pancreatic resection, 14 (17%) patients deteriorated, 16 (19%) improved, and 54 (64%) retained stable glucose homeostasis.Stability and improvement was associated with tumor resection and postoperative normalization of recently diagnosed glucose dysregulation, preoperatively elevated tumor markers and markers for common bile duct obstruction, acute pancreatitis and liver cell damage. Improvement was linked to preoperatively elevated insulin resistance, which normalized after resection and was accompanied by a decrease in fasting- and glucose-stimulated insulin secretion.ConclusionsSurgically reversible blood glucose dysregulation diagnosed concomitantly with a (peri-) pancreatic tumor appears secondary to compromised liver function due to tumor compression of the common bile duct and the subsequent increase in insulin resistance. It can be categorized as “cholestasis-induced diabetes” and thereby distinguished from other forms of hyperglycemic disorders.
Highlights
The endocrine function of the pancreas is essential for blood glucose regulation
Total pancreatectomy leads to the complete absence of insulin and glucagon production, which is followed by severe dysregulation of blood glucose levels
It remains unclear whether diabetes is a predisposing factor for pancreatic neoplasms or a consequence of pancreatic pathology, a body of evidence points to a time-dependent association of new-onset diabetes and pancreatic ductal adenocarcinoma (PDAC) [1,2,3,4]
Summary
The endocrine function of the pancreas is essential for blood glucose regulation. Total pancreatectomy leads to the complete absence of insulin and glucagon production, which is followed by severe dysregulation of blood glucose levels. The resection of pancreatic carcinoma can be followed by a postoperative improvement in glucose homeostasis in diabetic patients, which is accompanied by an increase in peripheral insulin sensitivity [5] These observations have led to the hypothesis that a diabetogenic factor might result from the tumor, pancreatic ductal adenocarcinomas [6,7]. In the course of pancreatic resection, other variables, such as dynamics in body weight, alterations of the anatomy of the alimentary tract and changes of liver function and acute or chronic pancreatic inflammation, may interfere with blood glucose homeostasis In this light, the hypothesis that diabetes is induced by a tumor-intrinsic factor appears reductionist. The aim of this work was to characterize the patient dynamics of blood glucose homeostasis during the course of partial pancreatic resection and to specify the associated clinico-pathological variables
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