Upregulated but insufficient generation of activated protein C is associated with development of multiorgan failure in severe acute pancreatitis

• Published in: Critical care (London, England) England), 2006-02, Vol.10 (1), p.R16-R16, Article R16
• Main Authors: Lindstrom, Outi, Kylanpaa, Leena, Mentula, Panu, Puolakkainen, Pauli, Kemppainen, Esko, Haapiainen, Reijo, Fernandez, Jose A, Griffin, John H, Repo, Heikki, Petaja, Jari
• Format: Article
• Language: English
• Subjects: Acute Disease; Adult; Aged; Aged, 80 and over; Female; Humans; Intensive Care Units; Male; Middle Aged; Multiple Organ Failure - blood; Multiple Organ Failure - etiology; Pancreatitis - blood; Pancreatitis - complications; Protein C - biosynthesis; Protein C - metabolism; Protein C - physiology; Severity of Illness Index; Signal Transduction - physiology; Up-Regulation - physiology
• ISSN: 1364-8535; 1466-609X; 1364-8535
• DOI: 10.1186/cc3966

Disturbed protein C (PC) pathway homeostasis might contribute to the development of multiple organ failure (MOF) in acute pancreatitis (AP). We therefore evaluated circulating levels of PC and activated protein C (APC), evaluated monocyte deactivation in AP patients, and determined the relationship of these parameters to MOF. Thirty-one patients in the intensive care unit were categorized as cases (n = 13, severe AP with MOF) or controls (n = 18, severe AP without MOF). Blood samples were drawn every second day to determine the platelet count, the levels of APC, PC, and D-dimer, and the monocyte HLA-DR expression using flow cytometry. The APC/PC ratio was used to evaluate turnover of PC to APC. During the initial two weeks of hospitalization, low PC levels (