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Open Access Research article

Sepsis induced changes of adipokines and cytokines - septic patients compared to morbidly obese patients

Andreas Hillenbrand1*, Uwe Knippschild1, Manfred Weiss2, Hubert Schrezenmeier3, Doris Henne-Bruns1, Markus Huber-Lang4 and Anna M Wolf1

Author affiliations

1 Department of General-, Visceral-, and Transplantation Surgery, University Hospital of Ulm, Steinhoevelstr. 9, 89075 Ulm, Germany

2 Department of Anesthesiology University Hospital of Ulm, Steinhoevelstr. 9, 89075 Ulm, Germany

3 Institute of Clinical Tranfusion Medicine and Immunogenetics, Helmholtzstr. 10; D-89081 Ulm; Germany

4 Department of Traumatology, Hand and Reconstructive Surgery, University Hospital of Ulm, Steinhoevelstr. 9, 89075 Ulm, Germany

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Citation and License

BMC Surgery 2010, 10:26  doi:10.1186/1471-2482-10-26

Published: 9 September 2010

Abstract

Background

Hyperglycemia and insulin resistance frequently occur in critically ill and in morbidly obese (MO) patients. Both conditions are associated with altered serum levels of cytokines and adipokines. In addition, obesity related alterations in adipokine expression contribute to insulin resistance in metabolic syndrome. In this study we examined the serum adipocytokine profile in critically ill patients, MO patients, and healthy blood donors.

Methods

33 patients who fulfilled the clinical criteria for severe sepsis or septic shock (SP) were prospectively enrolled in this study. A multiplex analysis was performed to evaluate plasma levels of adiponectin, resistin, leptin, active PAI-1, MCP-1, IL-1 alpha, IL-6, IL-8, IL-10, and TNF-alpha in 33 critically ill patients, 37 MO patients and 60 healthy blood donors (BD).

Results

In SP, adiponectin was significantly lowered and resistin, active PAI-1, MCP-1, IL-1 alpha, IL-6, IL-8, IL-10, and TNF-alpha were significantly elevated compared to BD. Leptin levels were unchanged. In MO, adiponectin and IL-8 were significantly lowered, leptin, active PAI-1, MCP-1, IL-1 alpha, IL-6, and IL-10 significantly elevated, whereas resistin was unaltered.

In SP, adiponectin correlated negatively with BMI, SAPS II and SOFA scores, while resistin correlated positively with SAPS II and SOFA scores and leptin correlated positively with the BMI. Adiponectin was approximately equally diminished in SP and MO compared to BD. With the exception of active PAI-1, cytokine levels in SP were clearly higher compared to MO.

Conclusion

A comparable adipocytokine profile was determined in critically ill and MO patients. As in MO, SP showed reduced adiponectin levels and elevated MCP-1, active PAI-1, IL-1 alpha, IL-6, and IL-10 levels. Leptin is only elevated in MO, while resistin, IL-8, and TNF-alpha is only elevated in SP. As in MO patients, increased levels of proinflammatory cytokines and altered levels of adipokines may contribute to the development of insulin resistance in critically ill patients.