Q J Med 2000; 93: 469-476
© 2000 Association of Physicians
Commentary papers |
Mast cell: pivotal player in lethal acute pancreatitis
In association with the Pancreato-Biliary Service, Manchester Royal Infirmary, Manchester, UK
Introduction
The fearful aura of acute pancreatitis stems from the imagery of an organ and organism under threat of cannibalization by pancreatic enzymes that have become active prematurely. This century-old autodigestion theory1 is all too plausible when one is confronted with the necrohaemorrhagic remains of the gland in a patient who succumbs from multisystem organ failure, as do 10–20% of cases. It was challenged2 when the average interval from onset of symptoms to death was found to be shorter (under 48 h) and the degree of initial shock greater with interstitial pancreatitis—which accounts for a quarter of the toll3—than with wholesale coagulative necrosis, an infarct-like lesion associated with hyaline occlusion of venules and capillaries.2
Progress on pathogenesis
The literature is colossal—4844 titles in a Medline search from 1966, and 260 in 1999—but the current position can be gleaned from a recent monograph,4 an assortment of reviews5–11 and supplementary papers. Of necessity, much reliance
Mast cell: the overlooked link
The evidence in question
Aetiology
Enzyme cascade activation
Inhibitor therapy
Concluding comments
Acknowledgments
Notes
References