Sepsis Clinical Trial
Official title:
Activity and Expression of Plasma Arginase in Patients With Severe Sepsis or Septic Shock as Prognostic Value
Sepsis is an acute pathology defined as an inappropriate response of the host to infection,
resulting in the onset of organ failure (Quick SOFA ≥2, or SOFA ≥2). Septic shock is a sepsis
associated with an elevation of lactate ≥ 2 mmol / l and an arterial hypotension requiring
vasoactive drugs. Several studies highlighted that sepsis is associated with a plasma
L-arginine deficiency. This deficiency induces a lower availability of L-arginine for
multiple metabolic pathways including those involved in the synthesis of nitric oxide (NO) in
the vascular endothelium via NO synthase. NO is the main endogenous vasodilator mediator, a
lower synthesis induces a vascular and endothelial dysfunction that can promote the
occurrence of an organic dysfunction during sepsis. Decrease in available NO was confirmed in
patients with sepsis and appears correlated with severity.
L-arginine deficiency can have multiple origins:
- L-arginine deficiency resulting from a decrease in endogenous production from citrulline
synthesized by the enterocytes. Such enterocyte dysfunction has been confirmed in
patients with sepsis and is characterized biologically by elevated plasma levels of
I-FABP (intestinal fatty acid binding protein - enterocyte-specific protein, cytolysis
marker) and lower than that of citrulline (hypocitrullinemia, marker of lower activity).
- L-arginine deficiency may also result from a catabolism increase via arginase activity
increased. This ubiquitous enzyme, having 2 isoforms (Arg1 and Arg2), allows the
synthesis of urea and ornithine from L-arginine. An increase in arginase activity would
decrease the available reserves of L-arginine for NO synthesis.
The objectives of this work is to evaluate, in patients with severe sepsis or septic shock,
the prognostic value of the plasma arginase activity and the plasma expression of 2 isoforms
Arg1 and Arg2, their kinetics, and the link between activity / expression of arginase and
enterocyte dysfunction.
n/a
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