Tamion F, Le Cam-Duchez V, Menard J F, Girault C, Coquerel A, Bonmarchand G
Medical Intensive Care Unit, Radioanalysis Laboratory, Hematology Laboratory and Department of Biostatistics, Rouen University Hospital, France.
Anaesth Intensive Care. 2005 Oct;33(5):578-84. doi: 10.1177/0310057X0503300505.
Erythropoietin is a glycoprotein hormone mainly released by the kidney, which stimulates red blood cell production. However, in sepsis, the mechanisms responsible for the final increase in circulating erythropoietin remain unclear Seventeen critically ill patients with Simplified Acute Physiologic Score average 66 (range 43 to 103) were included in this study. Ten patients survived and seven died within 28 days. Blood samples obtained at different times were assayed for erythropoietin, cytokine levels and lactate measurements. PCO2 gap was assessed to detect the presence of gastric mucosal acidosis. Erythropoietin decreased in the patients who survived while it remained high or increased in non-survivors (37+/-6.5 vs 147+/-6. 7 UI/l respectively, P<0.05). Erythropoietin plasma levels were correlated with IL-6 levels (r=0.84, P<0.05) and TNFalpha levels (r=0.84, P<0.05). We observed a significant positive relationship between erythropoietin plasma levels and lactate concentrations (r= 0.89, P< 0. 05) and with PCO2 gap (r=0.9, P < 0.05). No correlation was found between erythropoietin concentration and the other parameters. High serum erythropoietin levels in non-survivors were observed with septic shock despite an increase in the levels of proinflammatory cytokines. We found a relationship between erythropoietin concentration and biological markers of tissue hypoperfusion i.e. lactate levels or PCO2 gap. This relationship could suggest tissue hypoperfusion as the stimulating factor for erythropoietin production in septic shock.
