[Secondary diabetes in pancreatic carcinoma and after pancreatectomy: pathophysiology, therapeutic peculiarities and prognosis]

Abstract

Diabetes and pancreatic cancer are known to be associated. The relative risk for pancreatic carcinoma is dependent on the time after onset of diabetes. Diabetes in patients with pancreatic carcinoma is frequently of recent onset and partially caused by the tumor. Diabetes in a patient without obesity, no family history and unusual requirement for aggressive management including a rapid start of insulin treatment, may be early symptoms of pancreatic cancer. Recognition of atypical diabetes as an early symptom of pancreatic cancer may lead to earlier diagnosis and improved survival in these patients. Pancreatic carcinoma and chronic pancreatitis with untractable, incapacitating pain are the main reasons for (partial) pancreas resection. Pancreas resection may lead to a deterioration of pancreatic endocrine function. In healthy humans, hemipancreatectomy leads to impaired glucose tolerance after oral stimulation in 25% of the patients. To reduce morbidity resulting from operation, several operation techniques have been developed. Postoperative glucose metabolism is primarily dependent on the degree of preexisting endocrine function and on the amount of pancreatic tissue being resected. Early surgical intervention may, on the other hand, prevent the progression of endocrine insufficiency in the course of chronic pancreatitis. Good results of resective procedures now allow earlier operation. Any operative technique should aim on stopping the inflammatory process while preserving as much pancreatic tissue as possible. The choice of operation to be performed is dependent of morphological changes and individual local complications of the patient.