A fresh approach to the pathogenesis of pancreatitis.

The pathogenesis of pancreatitis has remained a confused subject in spite of extensive investigation and the advancement of numerous theories. There are two main reasons for this. 1 The persistent belief that obstruction of the pancreatic duct is a major cause of pancreatitis when the bulk of experimental and pathological evidence is against this possibility. 2 The failure to distinguish between aetiological factors (alcohol, gallstones) and the mechanism by which these factors produce pancreatitis. Thus Warren (1961a) has suggested that 'the continued search for a single aetiological agent in the genesis of acute and chronic pancreatitis is illusory': this statement is obviously correct in relation to the aetiological factors mentioned but it may not be true for the mechanism. In this paper a unifying concept of pathogenesis is presented which is compatible with known clinical and experimental facts and suggests new possibilities in the relationship between biliary tract disease and pancreatitis. Many authors regard acuteand chronic pancreatitis as different stages of the one disease (Comfort, Gambill, and Baggenstoss, 1946; Hess, 1965): others have given evidence that these are separate entities with different aetiologies (Sarles, Sarles, Camatte, Muratore, Gaini, Guien, Pastor, and Le Roy, 1965). In view of this uncertainty and the fact that the mechanism of pathogenesis is obscure in both instances, both types must be considered in any discussion of the pathogenesis of pancreatitis. The simplest terminology to follow is that adopted by participants in the symposium held in Marseilles in 1963 (Bockus, 1965), namely, (1) acute pancreatitis and relapsing acute pancreatitis, and (2) chronic pancreatitis and relapsing chronic pancreatitis (chronic pancreatitis with acute exacerbations). The essential difference between 1 and 2 is the presence of permanent residual damage in both chronic varieties.