Pancreatic secretions as a clue to the presence of pancreatic cancer

Abstract

Pancreatic secretory function is abnormal in at least 90% of patients with pancreatic cancer. These abnormalities may be due to direct involvement of the secretory cells by the malignant process and/or the effects of pancreatic duct obstruction. There is no specific stimulus (secretin and/or cholecystokinin, CCK, or CCK-like hormones) of pancreatic secretion that is clearly superior to any other as a test of pancreatic function. Pancreatic secretion is abnormal in animal models of pancreatic cancer and secretory abnormalities antedate the histologic appearance of the cancer. A decrease in protein secretion after CCK stimulation is the most significant finding in experimental partial pancreatic duct obstruction (the condition most commonly seen in pancreatic cancer). In the absence of any identifiable high-risk group within the population, it is unlikely that the testing of pancreatic function provides a means for the earlier diagnosis of pancreatic cancer.

Preoperative and operative diagnosis of pancreatic cancer

“…Pancreatic function is abnormal in about 90% of patients with pancreatic cancer, and there is reason to suspect that it deteriorates early in the course of the disease [6,7]. For detection of pancreatic disease, function tests are rather sensitive [4].…”

“…For detection of pancreatic disease, function tests are rather sensitive [4]. The inability of these tests to discriminate between cancer and chronic pancreatitis [6,7], however, seriously limits their practical usefulness, and for the diagnosis of pancreatic cancer they are, in their present-day designs, not sufficiently contributive to merit clinical use. Tumor markers, like carcinoembryonic antigen (CEA), may be of some help in the follow-up of treatment [8].…”

Membrane targetting of carbonic anhydrase II (CAII) in human pancreatic ductal Capan 1 cells in culture

“…Membrane targetting of CAI1 may favour the increase in the bicarbonate electrochemical gradient and thus facilitate the diffision of this anion through the HCO, channel which has already been described in polarized Capan 1 cells [5]. This phenomenon also takes place in the normal pancreas during digestion when HCO, of the fluid increases from about 25mEqflitre (basal secretion) to 150mEqflitre [6]. The membrane targetting of CAI1 could be one of the response mechanisms following stimulation of ductal cells by secretin released from mucosal cells of the proximal intestine, triggered by intraluminal HCI.…”