Optimising outcomes in acute pancreatitis

Citation
Id. Norton et Je. Clain, Optimising outcomes in acute pancreatitis, DRUGS, 61(11), 2001, pp. 1581-1591
Citations number
61
Categorie Soggetti
Pharmacology,"Pharmacology & Toxicology
Journal title
DRUGS
ISSN journal
00126667 → ACNP
Volume
61
Issue
11
Year of publication
2001
Pages
1581 - 1591
Database
ISI
SICI code
0012-6667(2001)61:11<1581:OOIAP>2.0.ZU;2-L
Abstract
Acute pancreatitis is a common cause for presentation to emergency departme nts. Common causes in Western societies include biliary pancreatitis and al cohol (the latter in the setting of chronic pancreatitis). Acute pancreatit is also follows endoscopic retrograde pancreatography in 5 to 10% of patien ts, a group that could potentially benefit from prophylactic treatment. Although episodes of pancreatitis usually run a relatively benign course, u p to 20% of patients have more severe disease, and this group has significa nt morbidity and mortality. Therefore, attempts have been made to identify, at or soon after presentation, those patients likely to have a poor outcom e and to channel resources to this group. The mainstay of treatment is aggressive support and monitoring of those pat ients likely to have a poor outcome. Pharmacotherapy for acute pancreatitis (both prophylactic and in the acute setting) has been generally disappoint ing. Efforts initially focused on protease inhibitors, of which gabexate sh ows some promise as a prophylactic agent. Agents that suppress pancreatic s ecretion have produced disappointing results in human studies. Infection of pancreatic necrosis is associated with high mortality and requ ires surgical intervention. In view of the seriousness of infected necrosis , the use of prophylactic antibacterials such as carbapenems and quinolones has been advocated in the setting of pancreatic necrosis. Similarly, data are accumulating to support the use of prophylactic antifungal therapy. Recently, it has become apparent that the intense inflammatory response ass ociated with acute pancreatitis is responsible for much of the local and sy stemic damage. With this realisation, future efforts in pharmacotherapy are likely to focus on suppression or antagonism of pro-inflammatory cytokines and other inflammatory mediators. Similarly, animal studies have demonstra ted the importance of oxidative stress in acute pancreatitis, although to d ate there is a paucity of information regarding the efficacy of antioxidant s. Although the clinical course for most patients with acute pancreatitis is m ild, severe acute pancreatitis continues to be a clinical challenge, requir ing a multidisciplinary approach of physician, intensivist and surgeon.