Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis

Citation
A. Hietaranta et al., Extracellular phospholipases A2 in relation to systemic inflammatory response syndrome (SIRS) and systemic complications in severe acute pancreatitis, PANCREAS, 18(4), 1999, pp. 385-391
Citations number
42
Categorie Soggetti
da verificare
Journal title
PANCREAS
ISSN journal
08853177 → ACNP
Volume
18
Issue
4
Year of publication
1999
Pages
385 - 391
Database
ISI
SICI code
0885-3177(199905)18:4<385:EPAIRT>2.0.ZU;2-V
Abstract
The pathophysiology of severe acute pancreatitis (AP) resembles other condi tions with systemic inflammatory response syndrome (SIRS) such as sepsis pr edisposing to remote organ failure. Because extracellular phospholipases A2 (PLA2) have been implicated in AP, their serum concentrations were analyze d with respect to SIPS and systemic complications in patients with severe A P. The serum samples were collected daily for 12 days in 57 patients with s evere AP. SIPS, early organ complications, local complications, and outcome of AP were recorded. Time-resolved fluoroimmunoassays were used for group I and group II PLA2 measurements. Thirty-nine (68.4%) patients fulfilled th e criteria of SIPS within 12 days from admission. Pancreatic necrosis was d etected in 43 (75.4%) patients. Infected necrosis was found preoperatively or at operation in five (8.8%) patients. Twenty-six (45.6%) and eight (14.0 %) patients had respiratory or renal failure, respectively. Seven (12.3%) p atients died of their disease. All patients with systemic complications ful filled the criteria of SIRS. The increasing number of positive SIPS criteri a was associated with increased frequency of systemic complications. Pancre atic ne crosis was not significantly associated with SIPS. The serum concen tration of group II PLA2 was significantly higher in patients with SIPS (p < 0.05) compared with patients without from day 7 onward. The concentration of group II PLA2 increased (p < 0.01) in patients with SIRS but decreased in patients without. The serum concentration of group II PLA2 did not diffe r significantly with respect to systemic complications. The concentration o f group I PLA2 decreased (p < 0.05) similarly in patients with and without SIRS or systemic complications during follow-up, respectively. Early system ic complications of severe AP are associated with SIPS with increasing freq uency as the number of positive SIRS criteria increases. Group II PI,A2 but not group I PLA2 may have pathophysiologic importance in severe AP-associa ted SIRS. Increasing serum concentration of group II PLA2 seems to reflect the ongoing systemic inflammation in severe AP-associated SIRS.