TITLE:
Effects of vacuum-assisted closure and Drotrecogin alpha on inflammatory markers in severe acute pancreatitis
AUTHORS:
Oscar Arias-Carvajal, José Manuel Hermosillo-Sandoval, Carlos Alberto Gutiérrez-Martínez, Fermín Paul Pacheco-Moisés, Genaro Gabriel Ortiz, Adolfo Daniel Rodríguez-Carrizalez, Luis Miguel Román-Pintos, Alejandra Guillermina Miranda-Díaz
KEYWORDS:
Severe Acute Pancreatitis; Systemic Inflammation; Proinflammatory Cytokines
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.4 No.8B,
August
8,
2013
ABSTRACT: In severe acute pancreatitis
(SAP) inflammatory processes foster necrosis, cellular lysis and liberation
of vasoactive substances associated with multiple organ failure. The effects of
vacuum-assisted closure and Drotrecogin alpha on inflammatory cytokines were
evaluated in SAP patients with infected necrosis. Methods: Forty-six patients
were included in three groups: Group 1, necrosectomy and abdominal cavity
washing; Group 2, necrosectomy plus vacuum-assisted closure (VAC), and Group 3, necrossectomy
plus VAC plus Drotrecogin alpha. Immunoreactive IL-32, TNF-α, IL-6, TGF-β and
IL-2 cytokines were quantified with ELISA method. Results: IL-32 was significantly
increased in all patients, predominantly the non-survivor of Group 3 (p 0.0001). Group 2 maintained
increased IL-32 levels throughout. Peak TNF-α was
observed in non-survivors of Groups 1 and 2, with a frank tendency to decrease
in Group 3. The IL-6 was increased, sustained throughout the study, peaking at
the onset in non-survivors. At the end IL-6 tended to diminish, predominantly
in survivors. TNF-α and IL-6 were significantly increased on hospitalization, with a maximum peak in
non-survivors of all groups. Initial values of TGF-β were significantly increased in
survivors of the three groups, and were significantly diminished in
non-survivors; affecting pancreas regeneration and favoring systemic
inflammation, with possible multiple-organ repercussions. IL-2 levels were
elevated, predominantly in non-survivors of Group 1. There was positive
correlation between the increase IL-32 and TNF-α, and negative correlation between
the increase in TNF-α and
decrease in TGF-β; and, a tendency for negative correlation between the
IL-2 increased and TGF-β levels. Conclusion: We found a generalized, sustained
inflammatory state that fosters a torpid outcome in SAP patients.