Why a detailed examination after acute pancreatitis?

During the 1965-9 period, we studied the consequences of acute pancreatitis in a group of 53 patients (1). Using the 1963 Marseille classification of pancreatitis (2), we pointed, inter alia, to the incidence of changes in exocrine and endocrine functions of the pancreas in some patients (something that we would refer to as residua after acute pancreatitis, today), and emphasized the need for a detailed examination of patients, following an attack of acute pancreatitis. In this article we wish to reemphasize the need for such detailed examination, this time in connection with new classifications of pancreatitis, i.e., the Revised Classification of Pancreatitis--Marseille, 1984 (3), and the Pancreatitis Classification of Marseille-Rome 1988 (4,5). The latter classification, based on studies of lesions and causes of pancreatitis, constitutes yet another attempt to integrate pathology into the prerequisites for clear-cut definition of the disease. However, a definition of pancreatitis, based on pathological findings, remains an aim yet to be attained in everyday clinical practice. That is why the clinician will rely on the Marseille classification (1984), taking into account the Marseille-Rome classification (1988).

Endocrine pancreatic secretion in patients after acute pancreatitis.

In 14 nonobese patients after acute pancreatitis and with normal oral glucose tolerance, the response of insulin, C-peptide, and pancreatic glucagon after 100 g of oral glucose was assessed. The curves of insulin and C-peptide were significantly raised compared with those of controls, and no difference was found between the response of patients with a negative (n = 8) and a positive (n = 6) family history of type II diabetes. The curves of pancreatic glucagon did not differ from those found in controls. Our results indicate that a normal response to glucose after recovery from an attack of acute pancreatitis is maintained at the cost of increased insulin secretion.

The effect of some N solutions for parenteral nutrition on gastric and pancreatic secretion.

In patients without pancreatic disease Aminofusin L forte infused for 1 h did not stimulate gastric or pancreatic secretion. On the other hand, infusion of casein by hydrolysate led to a significant increase in the concentration and total output of HCl. 4 h intravenous infusion of Aminofusin L forte caused a transient but significant rise of the bicarbonate concentration, amylase activity and above all trypsin activity and output. The results show that N solutions used for parenteral protein nutrition influence in a different way both gastric and pancreatic secretion.