Effects of vacuum-assisted closure and Drotrecogin alpha on inflammatory markers in severe acute pancreatitis

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

Department of Chemistry, University of Guadalajara, Guadalajara, México.
Department of General Surgery, Specialties Hospital, National Occidental Medical Centre, Social Security Institute of México, Guadalajara, México.
Department of Physiology, University Health Sciences Centre, University of Guadalajara, Guadalajara, México.
Intensive Care Unit, Specialties Hospital, National Occidental Medical Centre, Social Security Institute of México, Guadalajara, México.
Occidental Biomedical Research Centre, Social Security Institute of México, Guadalajara, México.

DOI: 10.4236/abb.2013.48A2007                

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.

Keywords

Severe Acute Pancreatitis; Systemic Inflammation; Proinflammatory Cytokines

Conflicts of Interest

The authors declare no conflicts of interest.

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