Introduction Both C-reactive protein (CRP) and procalcitonin (PCT) are accepted sepsis markers. However, there is still some debate concerning the correlation between their serum concentrations and sepsis severity. We hypothesised that PCT and CRP concentrations are different in patients with infection or with no infection at a similar severity of organ dysfunction or of systemic inflammatory response. Patients and methods One hundred and fifty adult intensive care unit patients were observed consecutively over a period of 10 days. PCT, CRP and infection parameters were compared among the following groups: no systemic inflammatory response syndrome (SIRS) (n = 15), SIRS (n = 15), sepsis/SS (n = 71) (including sepsis, severe sepsis and septic shock [n = 34, n = 22 and n = 15]), and trauma patients (n = 49, no infection). Results PCT and CRP concentrations were higher in patients in whom infection was diagnosed at comparable levels of organ dysfunction (infected patients, regression of median [ng/ml] PCT = -0.848 + 1.526 sequential organ failure assessment [SOFA] score, median [mg/l] CRP = 105.58 + 0.72 SOFA score; non-infected patients, PCT = 0.27 + 0.02 SOFA score, P < 0.0001; CRP = 84.53 -0.19 SOFA score, P < 0.005), although correlation with the SOFA score was weak (R = 0.254, P < 0.001 for PCT, and R = 0.292, P < 0.001 for CRP). CRP levels were near their maximum already during lower SOFA scores, whereas maximum PCT concentrations were found at higher score levels (SOFA score > 12). PCT and CRP concentrations were 1.58 ng/ml and 150 mg/l in patients with sepsis, 0.38 ng/ml and 51 mg/l in the SIRS patients (P < 0.05, Mann-Whitney U-test), and 0.14 ng/ml and 72 mg/l in the patients with no SIRS (P < 0.05). The kinetics of both parameters were also different, and PCT concentrations reacted more quickly than CRP.
PCT plasma reinduction marks possible septic complication during systemic inflammatory response syndrome after major trauma. In addition, high PCT concentration at admission after trauma in ICU patients indicates an increased risk of septic complications.
The variation in ATIII activity in the post prostatectomy period is examined by the Authors and is correlated with pulmonary embolism. Type of anaesthesia, blood transfusion and modality of blood transfusion (autotransfusion V/S homologous transfusion) were the parameters considered. In the post surgery period, the ATIII level decreases and afterwards slowly recovers. ATIII variations were similar in both auto transfused and non-transfused patients. The ATIII level decreased more in transfused patients than in those auto or not transfused. Other factors lowering the ATIII level were suprapubic prostatectomy and loco-regional anaesthesia; TURP or general anaesthesia were less influential. In the patients with pulmonary embolism ATIII activity decreased to below 70%. The Authors correlate these data with the risk of embolism.
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