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  • Open Access

Serum insulin-like growth factor binding protein 1 and C-peptide to assess insulin resistance in septic patients

  • 1 and
  • 1
Critical Care200812 (Suppl 2) :P161

https://doi.org/10.1186/cc6382

  • Published:

Keywords

  • Insulin Resistance
  • Catecholamine
  • Hyperglycemia
  • Laboratory Finding
  • Definite Diagnosis

Introduction

Insulin resistance and hyperglycemia are important features of the care of the critically ill. They are part of the metabolic pathophysiology of acute conditions [1, 2]. In septic patients, insulin resistance is linked to the synergic effect of cytokines, bacterial products and catecholamines [3]. Laboratory findings include elevated C-peptide and serum insulin-like growth factor binding protein 1 (IGFBP-1) [4]. This is secreted by the liver and its secretion is inhibited by insulin. In the insulin-resistant patient, a rise in insulin fails to reduce its plasma levels. We dosed serum IGFBP-1 in samples of patients with sepsis and compared it with glycemia and serum C-peptide.

Methods

Only patients with a definite diagnosis of sepsis were included. Five blood samples were taken from each patient at the time of their entrance and every 24 hours for the next 96 hours. For each sample, glycemia, C-peptide and IGFBP-1 were dosed and their values compared.

Results

C-peptide levels constantly remained high, even in normoglycemic patients. Higher glycemias were associated with raised serum IGFBP-1 levels. Insulin increases could not inhibit IGFBP-1 and, hence, the worse the insulin resistance, the higher the glycemia, the higher the IGFBP-1. The relation between C-peptide and IGFBP-1 showed that higher levels of circulating insulin were associated with higher levels of IGFBP-1. This was thought as a direct sign of the existing insulin-resistant state.

Conclusion

IGFBP-1 can be used to asses insulin resistance in septic critical patients, particularly compared with glycemia. Its correlation with C-peptide might better define the severity of insulin resistance and, thus, of the underlying sepsis.

Authors’ Affiliations

(1)
University of Florence, Italy

References

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Copyright

© BioMed Central Ltd 2008

This article is published under license to BioMed Central Ltd.

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