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Open Access Research

Hypoxia-inducible factor (HIF1α) gene expression in human shock states

Julien Textoris12*, Nathalie Beaufils3, Gabrielle Quintana1, Amin Ben Lassoued3, Laurent Zieleskiewicz1, Sandrine Wiramus1, Valéry Blasco1, Nathalie Lesavre4, Claude Martin1, Jean Gabert3 and Marc Leone12

Author Affiliations

1 Service d'anesthésie et de réanimation, Hôpital Nord, Assistance Publique-Hôpitaux de Marseille, Chemin des bourrely, 13915, Marseille, France

2 URMITE, CNRS U7278, INSERM U1095, Faculté de médecine Timone, Aix-Marseille Univ, Boulevard Jean Moulin, 13385, Marseille, France

3 Laboratoire de Biochimie et Biologie Moléculaire, Hôpital Nord, Assistance Publique-Hôpitaux de Marseille, Chemin des bourrely, 13915, Marseille, France

4 Centre d'Investigation Clinique, Hôpital Nord, Assistance Publique-Hôpitaux de Marseille, Chemin des bourrely, 13915, Marseille, France

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Critical Care 2012, 16:R120  doi:10.1186/cc11414

Published: 10 July 2012

Abstract

Introduction

Hypoxia-inducible factor-1 (HIF1) controls the expression of genes involved in the cellular response to hypoxia. No information is available on its expression in critically ill patients. Thus, we designed the first clinical study in order to evaluate the role of HIF1α as a prognosis marker in patients suffering from shock.

Methods

Fifty consecutive adult patients with shock and 11 healthy volunteers were prospectively enrolled in the study. RNA was extracted from whole blood samples and expression of HIF1α was assessed over the first four hours of shock. The primary objective was to assess HIF1α as a prognostic marker in shock. Secondary objectives were to evaluate the role of HIF1α as a diagnostic and follow-up marker. Patient survival was evaluated at day 28.

Results

The causes of shock were sepsis (78%), hemorrhage (18%), and cardiac dysfunction (4%). HIF1α expression was significantly higher in the shock patients than in the healthy volunteers (121 (range: 72-168) versus 48 (range: 38-54) normalized copies, P <0.01), whatever the measured isoforms. It was similar in non-survivors and survivors (108 (range 84-183) versus 121(range 72-185) normalized copies, P = 0.92), and did not significantly change within the study period.

Conclusions

The present study is the first to demonstrate an increased expression of HIF1α in patients with shock. Further studies are needed to clarify the potential association with outcome. Our findings reinforce the value of monitoring plasma lactate levels to guide the treatment of shock.