Journal of Antimicrobial Chemotherapy, Vol 41, 51-63, Copyright © 1998 by The British Society for Antimicrobial Chemotherapy
PG Wilson, M Manji and JP Neoptolemos
Severe acute pancreatitis has many similarities to sepsis syndrome and
septic shock. The haemodynamic features of cardiovascular instability,
reduced ejection fraction and decreased systemic vascular resistance are
indistinguishable in each of these conditions. In addition there are many
striking similarities in the cytokine and inflammatory mediator profiles,
suggesting that the haemodynamic abnormalities may result from the same
pathogenic mechanisms, albeit as a result of different inflammatory
stimuli. Although septic complications of severe acute pancreatitis do
arise these are usually late features and in the early phase of a severe
attack there is sterile pancreatic necrosis. Evidence suggests that the
important cytokines in the development of complications and multiple organ
failure in severe acute pancreatitis are tumour necrosis factor-alpha,
interleukin-1, interleukin-6 and interleukin-8. In addition, endotoxin and
other important inflammatory mediators including platelet activating factor
and phospholipase A2 are implicated in the development of complications in
both severe acute pancreatitis and sepsis. Patients with severe acute
pancreatitis are not an entirely homogeneous group but in terms of
pathogenesis and complications of their disease they have much more in
common with each other than the patients who are collected under the
unifying diagnosis of 'sepsis'. The similar clinical and biochemical
features between severe acute pancreatitis and sepsis make the former an
excellent model for studying the pathogenesis of the sepsis syndrome.
ORIGINAL ARTICLES
Acute pancreatitis as a model of sepsis
University Department of Medicine, Queen Elizabeth Hospital, Edgbaston, Birmingham, UK.
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