Register for email alerts and news feeds:
This journal | BMJ Group
rss
Gut 1994;35:552-556; doi:10.1136/gut.35.4.552
Copyright © 1994 BMJ Publishing Group Ltd & British Society of Gastroenterology.

Progression of alcoholic acute to chronic pancreatitis.

R W Ammann, B Muellhaupt

Department of Medicine, University Hospital, Zurich, Switzerland.

Alcoholic chronic pancreatitis usually progresses from acute attacks to chronic pancreatitis within one to 19 years. The factors responsible for the appreciable variability in progression are unclear. In this study the relation between progression and the incidence and severity of acute episodes in a large cohort of patients with alcoholic chronic pancreatitis was analysed. All patients with at least one documented episode of acute pancreatitis have been studied prospectively over the past 30 years according to our protocol. Patients were classified according to their long term course into (a) calcific (n = 185), (b) non-calcific (n = 30), and (c) non-progressive (n = 39) chronic pancreatitis groups. The yearly incidence of acute attacks of pancreatitis was significantly higher in groups (a) and (b) than in group (c). Furthermore, the progression rate to advanced chronic pancreatitis (groups (a) and (b)) correlated with the incidence of severe pancreatitis (associated with pseudocysts in more than 55%). Pseudocysts were located primarily in the cephalic pancreas in groups (a) and (b) (58-71%) and in the pancreatic tail in group (c) (61%). In conclusion, these data suggest that the progression of acute to chronic pancreatitis is closely related to the incidence and severity of acute attacks. This finding and the primary location of pseudocysts in the cephalic pancreas (groups (a) plus (b)) are compatible with the 'necrosis-fibrosis' pathogenetic hypothesis.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?

This article has been cited by other articles:

  • Church, N I, Pereira, S P, Churchill, D, Cairns, S, Hatfield, A R W, Webster, G J M (2007). Chronic pancreatitis: diagnosis and management of complications. Gut 56: 1189-1190 [Full Text]  
  • Nagashio, Y., Asaumi, H., Watanabe, S., Nomiyama, Y., Taguchi, M., Tashiro, M., Sugaya, T., Otsuki, M. (2004). Angiotensin II type 1 receptor interaction is an important regulator for the development of pancreatic fibrosis in mice. Am. J. Physiol. Gastrointest. Liver Physiol. 287: G170-G177 [Abstract] [Full Text]  
  • Demols, A., Van Laethem, J.-L., Quertinmont, E., Degraef, C., Delhaye, M., Geerts, A., Deviere, J. (2002). Endogenous interleukin-10 modulates fibrosis and regeneration in experimental chronic pancreatitis. Am. J. Physiol. Gastrointest. Liver Physiol. 282: G1105-G1112 [Abstract] [Full Text]  
  • Mews, P, Phillips, P, Fahmy, R, Korsten, M, Pirola, R, Wilson, J, Apte, M (2002). Pancreatic stellate cells respond to inflammatory cytokines: potential role in chronic pancreatitis. Gut 50: 535-541 [Abstract] [Full Text]  
  • McCutcheon, A. D. (2000). Neurological Damage and Duodenopancreatic Reflux in the Pathogenesis of Alcoholic Pancreatitis. Arch Surg 135: 278-285 [Abstract] [Full Text]  

This Article

Services
Citing Articles
Google Scholar
PubMed
Topic Collections
Bookmark with

Register for free content

The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.

Cardiology Jobs

Gastroenterology Jobs