ASYMMETRIC (ADMA) AND SYMMETRIC (SDMA) DIMETHYLARGININE IN SEPTIC PATIENTS

Rationale: Endothelium-derived NO plays a critical rule in regulation of blood pressure, preservation of organ perfusion and interaction between vascular endothelium and blood platelets/leukocytes. ADMA is an endogenous nonselective inhibitor of nitric oxide (NO) synthase and SDMA competes with arginine for cellular transport. The aim of the study was to investigate if ADMA and SDMA are increased in ‘‘sepsis syndrome’’ due to protein catabolism and eventually to decreased epato-renal elimination. Methods: Twenty-nine consecutive septic patients, as defined by the ACCP/SCCM1 were enrolled. Blood sampling was performed on admission day (T0), 3rd(T3), 6th(T6), 9th(T9), 12th(T12). ADMA and SDMA (mmol/L)were measured by HPLC. ADMA and SDMA were also measured in 77 healthy volunteers. SAPSII at ICU admission, SOFA score, and sepsis status1 were recorded daily. Data are presented as mean7SD. Differences between groups were analysed with Student’s t-test, ANOVA and Scheffe` test. Significance was set at po0.05. Results: Mean ADMA (1.0470.44 vs 0.4670.13, n ¼ 116, po0.0000) and SDMA levels (2.271.3 vs 0.470.09, n ¼ 116, po0.0000), all samples together, are higher than in healthy volunteers. SDMA level during Severe Sepsis/Septic Shock(1)days is significantly higher than during Sirs/Sepsis days (2.471.35 vs 1.8871.22, n ¼ 116, p ¼ 0.038) while ADMA (1.170.51 vs 0.9570.29, n ¼ 116, p ¼ 0.07) shows a trend. Patients who developed Septic Shock along ICU stay have higher values of ADMA (1.1370.5, n ¼ 64 vs 0.937 0.32, n ¼ 52, po0.013) and SDMA (2.6271.48, n ¼ 64 vs 1.6970.86, n ¼ 52, p ¼ 0.0001). Conclusions: ADMA and SDMA levels are consistently higher in critically ill septic patients than in healthy volunteers. These values are even higher in Severe Sepsis/Septic Shock status.